A framework for collecting inclusive design data for the UK population.

Successful inclusive product design requires knowledge about the capabilities, needs and aspirations of potential users and should cater for the different scenarios in which people will use products, systems and services. This should include: the individual at home; in the workplace; for businesses, and for products in these contexts. It needs to reflect the development of theory, tools and techniques as research moves on. And it must also to draw in wider psychological, social, and economic considerations in order to gain a more accurate understanding of users' interactions with products and technology. However, recent research suggests that although a number of national disability surveys have been carried out, no such knowledge currently exists as information to support the design of products, systems and services for heterogeneous users. This paper outlines the strategy behind specific inclusive design research that is aimed at creating the foundations for measuring inclusion in product designs. A key outcome of this future research will be specifying and operationalising capability, and psychological, social and economic context measures for inclusive design. This paper proposes a framework for capturing such information, describes an early pilot study, and makes recommendations for better practice.

Population of nonnative states of lysozyme variants drives amyloid fibril formation.

The propensity of protein molecules to self-assemble into highly ordered, fibrillar aggregates lies at the heart of understanding many disorders ranging from Alzheimer's disease to systemic lysozyme amyloidosis. In this paper we use highly accurate kinetic measurements of amyloid fibril growth in combination with spectroscopic tools to quantify the effect of modifications in solution conditions and in the amino acid sequence of human lysozyme on its propensity to form amyloid fibrils under acidic conditions. We elucidate and quantify the correlation between the rate of amyloid growth and the population of nonnative states, and we show that changes in amyloidogenicity are almost entirely due to alterations in the stability of the native state, while other regions of the global free-energy surface remain largely unmodified. These results provide insight into the complex dynamics of a macromolecule on a multidimensional energy landscape and point the way for a better understanding of amyloid diseases.