Simulation Tools for Inclusive Design Solutions.

Disability has been redefined by the World Health Organization as a function of a person's interaction with the environment and not merely an innate part of a person. This redefinition highlights the need for inclusiveness in design solutions. To aid this, we apply and test the potential of different tools that restrict designers' physical abilities at deriving inclusive design perspectives among designers. Various tools and simulated conditions are often adopted in user-centered design to sup-port need-finding by eliciting rich data on users' needs and guide designers to empathize with users. Simulation tools that restrict designers' physical abilities have been applied to understand certain perspectives of people with physical challenges, yet these tools lack the ability to evoke an inclusive design perspective among designers. Through a co-creation workshop, participants were exposed to two forms of simulations: direct and situational physical impairments. This was achieved using different tools that simulate the same physical restriction. In this study, a noise- canceller and earphones were used to simulate a reduced hearing attention. Participants were asked to generate user needs and design functions by applying both the simulation tools. The study results comprise the outcomes of 33 participants who volunteered to participate in a co-design workshop that provided a venue for them to interact and work alongside users with physical challenges. This paper analyses the inclusiveness attained through different types of simulated conditions. With a growing need to create tools and technologies that delight the user, it is necessary to equip designers with the tools that would help them with the process. The study demonstrates the application and impact of one such tool.

Age-related alteration in hepatic disposition of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and pesticides.

Idiopathic Parkinson's disease may be caused by environmental neurotoxins such as pesticides, however the major risk factor is old age. We postulated that the high incidence of Parkinson's disease in older people is secondary to age-related impairment of the hepatic detoxification of xenobiotics. Previously, we have shown that there are significant differences between the hepatic disposition of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and pesticides. Here, we investigated whether there are age-related differences in the hepatic disposition of MPTP and pesticides, putatively associated with the pathogenesis of Parkinson's disease. We measured the hepatic disposition of paraquat, dichlorodiphenyltrichloroethane (DDT), malathion and MPTP using the multiple indicator dilution technique in the perfused livers of Fischer F344 rats aged 3 and 18 months. The recoveries of MPTP, DDT and malathion were increased from the livers of the older rats (by 258%, 253% and 134% compared with young rats, respectively). The hepatic transport of DDT and malathion into hepatocytes was reduced with age suggesting that part of the impaired uptake of neurotoxins may be secondary to an age-related barrier to influx. Ageing may increase risk of Parkinson's disease by altering hepatic detoxification and increasing systemic bioavailability of neurotoxins.

Age-environment and gene-environment interactions in the pathogenesis of Parkinson's disease.

Parkinson's disease (PD) is a common neurodegenerative disease characterized by dopaminergic cell death and deposition of Lewy bodies within the substantia nigra of the midbrain. Although the major risk factors for PD are aging and environmental factors, there is an important genetic component. An age-related change in xenobiotic metabolism alters the metabolism of and net exposure to, environmental neurotoxins. Genetic variability in xenobiotic metabolism may similarly increase the susceptibility to PD by altering the metabolism of neurotoxins. Genetic studies of rare familial cases of PD indicate a central mechanistic role for the aggregation of alpha-synuclein, a protein found in Lewy bodies. Environmental factors like pesticides and heavy metals can also influence alpha-synuclein aggregation. Common final pathways for aging, environmental, and genetic mechanisms can thus exist, involving both direct neurotoxicity and alpha-synuclein aggregation.