A model for enhancing software project management using software agent technology

The present study has originated from the realisation that numerous software development projects either do not live up to expectations or fail outright. The scope, environment and implementation of traditional software projects have changed due to various reasons such as globalisation, advances in computing technologies and, last but not least, the development and deployment of software projects in distributed, collaborative and virtual environments. As a result, traditional project management methods cannot and do not address the added complexities found in this ever-changing environment. In this study the processes and procedures associated with software project management (SPM) were explored. SPM can be defined as the process of planning, organising, staffing, monitoring, controlling and leading a software project. The current study is principally aimed at making a contribution to enhancing and supporting SPM. A thorough investigation into software agent computing resulted in the realisation that software agent technology can be regarded as a new paradigm that may be used to support the SPM processes. A software agent is an autonomous system that forms part of an environment, can sense the environment and act on it over a period of time, in pursuit of its own agenda. The software agent can also perceive, reason and act by selecting and executing an appropriate action. The unique requirements of SPM and the ways in which agent technology may address these were subsequently identified. It was concluded that agent technology is specifically suited to geographically distributed systems, large network systems and mobile devices. Agents provide a natural metaphor for support in a team environment where cooperation and the coordination of actions toward a common goal, as well as the monitoring and controlling of actions are strongly supported. Although it became evident that agent technology is indeed being applied to areas and sections of the SPM environment, it is not being applied to the whole spectrum, i.e. to all core and facilitating functions of SPM. If software agents were to be used across the whole spectrum of SPM processes, this could provide a significant advantage to software project managers who are currently using other contemporary methods. The "SPMSA" model (Software Project Management supported by Software Agents) was therefore proposed. This model aims to enhance SPM by taking into account the unique nature and changing environment of software projects. The SPMSA model is unique as it supports the entire spectrum of SPM functionality, thus supporting and enhancing each key function with a team of software agents. Both the project manager and individual team members will be supported during software project management processes to simplify their tasks, eliminate the complexities, automate actions and enhance coordination and communication. Virtual teamwork, knowledge management, automated workflow management and process and task coordination will also be supported. A prototype of a section of the risk management key function of the SPMSA model was implemented as `proof of concept'. This prototype may be expanded to include the entire SPMSA model and cover all areas of SPM. Finally, the SPMSA model was verified by comparing the SPM phases of the model to the Plan-Do-Check-Act (PDCA) cycle. These phases of the SPMSA model were furthermore compared to the basic phases of software development as prescribed by the ISO 10006:2003 standard for projects. In both cases the SPMSA model compared favourably. Hence it can be concluded that the SPMSA model makes a fresh contribution to the enhancement of SPM by utilising software agent technology.School of ComputingPh. D. (Computer Science

Pharmacogenomics of non-steroidal antiinflammatory drug-induced gastrointestinal complications

Over 30 million people worldwide use aspirin and other non-aspirin non-steroidal antiinflammatory drugs (NSAID) on a daily basis. It is estimated that over 25% of patients treated for arthritis with NSAIDs have experienced gastrointestinal (GI) complications that required hospital admission and 60% of deaths from adverse drug reactions (ADRs) are attributable to NSAID use. Significant non-genetic risk factors for the development of NSAID-related gastrointestinal complications include gender, H. pylori infection, and concomitant medications. Three genes (UGT1A6, PAI-1 and EYA1) with biological plausibility for roles in NSAID-related ulcers were analysed. Our analysis of genetic risk factors for NSAID-related GI complications in 1197 case-control subjects showed no association between a UGT1A6 polymorphism and NSAIDinduced GI toxicity (p=0.052). Furthermore, a meta-analysis of UGT1A6 studies confirmed that there was no association between NSAID-related GI complications and UGT1A6. The PAI-1 4G/5G polymorphism was also not associated with NSAID-related ulcers and bleeding (n=756), while the EYA1 rs12678747 single nucleotide polymorphism (SNP) was significantly (p<0.05, OR 1.52; 95% CI 1.21, 1.91) associated with binary ulcer status. In healthy volunteers, EYA1 gene expression in gastric biopsies was not related to the carriage of this SNP; this contrasts with the difference observed in patients with ulceration suggesting that there may be a SNP-disease interaction, which needs further study. EYA1 was found to be expressed in atypical gastrin secreting (AGS) cells, but the relative expression was significantly (p<0.05) lower than in healthy human gastric epithelial cells and in renal cortical epithelial cells. Functional assays performed to explore the mechanism of NSAID-related gastric cell death and validate a plausible role for EYA1 in this process showed that there are multiple cell death pathways occurring concurrently in this cell model depending on the concentration of aspirin. At lower concentrations (10-20mM), PARP cleavage was observed suggestive of an apoptotic process, while at 50mM, necrotic cell death was the predominant mode of cell death. There was a significant (p<0.05) concentration-dependent decrease in the caspase 3 and 7 activity in AGS cells despite a significant (p<0.05) fall in the viability of the cells compared to the controls, suggesting that there is a role for non-caspase dependent mechanisms in the cell death. In summary, the thesis has focused on the clinical, molecular and functional aspects of peptic ulceration caused by NSAIDs (including aspirin). A novel pathway involving EYA1 has been investigated; this needs further work to define the exact mechanisms by which EYA1 leads to cell death and gastrointestinal injury in patients taking NSAIDs (including aspirin)