Numerical Method for Cost-Weight Optimisation of Stringer-Skin Panels

The need to integrate cost into the early product definition process as an engineering parameter is addressed. The application studied is a fuselage panel that is typical for commercial transport regional jets. Consequently, a semi-empirical numerical analysis using reference data was coupled to model the structural integrity of thin-walled structures with regard to material failure and buckling: skin, stringer, flexural, and interrivet. The optimization process focuses on direct operating cost (DOC) as a function of acquisition cost and fuel burn. It was found that the ratio of acquisition cost to fuel burn was typically 4:3 and that there was a 10% improvement in the DOC for the minimal DOC condition over the minimal weight condition because of the manufacturing cost saving from having a reduced number of larger-area stringers and a slightly thicker skin than that preferred by the minimal weight condition. Also note that the minimal manufacturing cost condition was slightly better than the minimal weight condition, which highlights the key finding: The traditional minimal weight condition is a dated and suboptimal approach to airframe structural design.

alpha-Synuclein aggregation in neurodegenerative diseases and its inhibition as a potential therapeutic strategy

There is strong evidence for the involvement of alpha-synuclein in the pathologies of several neurodegenerative disorders, including PD (Parkinson's disease). Development of disease appears to be linked to processes that increase the rate at which alpha-synuclein forms aggregates. These processes include increased protein concentration (via either increased rate of synthesis or decreased rate of degradation), and altered forms of alpha-synuclein (such as truncations, missense mutations, or chemical modifications by oxidative reactions). Aggregated forms of the protein are toxic to cells and one therapeutic strategy would be to reduce the rate at which aggregation occurs. To this end we have designed several peptides that reduce alpha-synuclein aggregation. A cell-permeable version of one such peptide was able to inhibit the DNA damage induced by Fe(II) in neuronal cells transfected with alpha-synuclein (A53T), a familial PD-associated mutation.