Component level strategies for exploiting the lifespan of steel in products

Approximately 40% of annual demand for steel worldwide is used to replace products that have failed. With this percentage set to rise, extending the lifespan of steel in products presents a significant opportunity to reduce demand and thus decrease carbon dioxide emissions from steel production. This article presents a new, simplified framework with which to analyse product failure. When applied to the products that dominate steel use, this framework reveals that they are often replaced because a component/sub-assembly becomes degraded, inferior, unsuitable or worthless. In light of this, four products, which are representative of high steel content products in general, are analysed at the component level, determining steel mass and cost profiles over the lifespan of each product. The results show that the majority of the steel components are underexploited - still functioning when the product is discarded; in particular, the potential lifespan of the steel-rich structure is typically much greater than its actual lifespan. Twelve case studies, in which product or component life has been increased, are then presented. The resulting evidence is used to tailor life-extension strategies to each reason for product failure and to identify the economic motivations for implementing these strategies. The results suggest that a product template in which the long-lived structure accounts for a relatively high share of costs while short-lived components can be easily replaced (offering profit to the producer and enhanced utility to owners) encourages product life extension. © 2013 The Author.

Cell shape changes indicate a role for extrinsic tensile forces in Drosophila germ-band extension.

Drosophila germ-band extension (GBE) is an example of the convergence and extension movements that elongate and narrow embryonic tissues. To understand the collective cell behaviours underlying tissue morphogenesis, we have continuously quantified cell intercalation and cell shape change during GBE. We show that the fast, early phase of GBE depends on cell shape change in addition to cell intercalation. In antero-posterior patterning mutants such as those for the gap gene Krüppel, defective polarized cell intercalation is compensated for by an increase in antero-posterior cell elongation, such that the initial rate of extension remains the same. Spatio-temporal patterns of cell behaviours indicate that an antero-posterior tensile force deforms the germ band, causing the cells to change shape passively. The rate of antero-posterior cell elongation is reduced in twist mutant embryos, which lack mesoderm. We propose that cell shape change contributing to germ-band extension is a passive response to mechanical forces caused by the invaginating mesoderm.