In order to facilitate the process of safety analysis of an evolving software system, this paper presents an architectural approach that enhances the safety analysis by providing appropriate abstractions for modelling and analysing interactions between components, since faulty interactions are the usual cause of accidents.
Previous studies have suggested that the αB-R120G mutation causes DRM and cataracts due to faulty interactions between αB-crystallin and intermediate filament proteins such as vimentin [12], [31].
When a substantial number of chromosomes are engaged in these faulty interactions on both sister kinetochores, plus-end directed CENP-E-dependent forces exerted on stabilized lateral KT-MT attachments produce a net pulling force on centrosomes which disrupts the innermost centrosomal structure and generate multipolar spindles (Figure 8C).
An abnormally large fraction of Mia1p-MutNES4 cells (∼10%) showed the spindle assembly checkpoint (SAC) protein Mad2p present at kinetochores, indicative of faulty microtubule/kinetochore interaction and metaphase delay (Fig. 3C).
A faulty morphogenic interaction next takes place, most likely between the degenerated radial fibre network and the delayed replacement GPT neurons, which then fail to emit long projection axons (Xie et al., 2009).
A faulty trophic interaction then occurs between the impoverished terminal fields of long axonal projections and neurons in mature neocortex, which curtail the outgrowth and branching of their dendrites and local axonal collaterals (Adams et al., 1997; Xie et al., 2009).
A final faulty trophic interaction proceeds between the inadequate synaptic connectivity conveyed by axons (afferent projection and local fibers) and neocortical neurons, which accelerates the pace of neuronal apoptosis and reduces growth in the somatic and neuropil tissue compartments during the third phase of the ablation (Cowan et al., 1984; Xie et al., 2002, 2009).
This compensatory recruitment is accompanied by faulty morphogenic interactions that reconstitute the VZ proliferative array and further disrupt the radial fibre network (Xie et al., 2002, 2009).
Instead, the pattern of substantial, progressive reduction of growth in the ablated pallium indicates that the initial defect introduced by the specific killing of GPT cells is amplified by subsequent, faulty cellular interactions.
