Positioning variation modeling for aircraft panels assembly based on elastic deformation theory

Dimensional variation in aircraft panel assembly is one of the most critical issues that affects the aerodynamic performance of aircraft, due to elastic deformation of parts during the positioning and clamping process. This paper proposes an assembly deformation prediction model and a variation propagation model to predict the assembly variation of aircraft panels, and derives consecutive 3-D deformation expressions which explicitly describe the nonlinear behavior of physical interaction occurring in compliant components assembly. An assembly deformation prediction model is derived from equations of statics of elastic beam to calculate the elastic deformation of panel component resulted from positioning error and clamping force. A variation propagation model is used to describe the relationship between local variations and overall assembly variations. Assembly variations of aircraft panels due to positioning error are obtained by solving differential equations of statics and operating spatial transformations of the coordinate. The calculated results show a good prediction of variation in the experiment. The proposed method provides a better understanding of the panel assembly process and creates an analytical foundation for further work on variation control and tolerance optimization

Novel disease-causing mutations in the dihydropyrimidine dehydrogenase gene interpreted by analysis of the three-dimensional protein structure.

Dihydropyrimidine dehydrogenase (DPD) deficiency is an autosomal recessive disease characterized by thymine-uraciluria in homozygous deficient patients. Cancer patients with a partial deficiency of DPD are at risk of developing severe life-threatening toxicities after the administration of 5-fluorouracil. Thus, identification of novel disease-causing mutations is of the utmost importance to allow screening of patients at risk. In eight patients presenting with a complete DPD deficiency, a considerable variation in the clinical presentation was noted. Whereas motor retardation was observed in all patients, no patients presented with convulsive disorders. In this group of patients, nine novel mutations were identified including one deletion of two nucleotides [1039-1042delTG] and eight missense mutations. Analysis of the crystal structure of pig DPD suggested that five out of eight amino acid exchanges present in these patients with a complete DPD deficiency, Pro86Leu, Ser201Arg, Ser492Leu, Asp949Val and His978Arg, interfered directly or indirectly with cofactor binding or electron transport. Furthermore, the mutations Ile560Ser and Tyr211Cys most likely affected the structural integrity of the DPD protein. Only the effect of the Ile370Val and a previously identified Cys29Arg mutation could not be readily explained by analysis of the three-dimensional structure of the DPD enzyme, suggesting that at least the latter might be a common polymorphism. Our data demonstrate for the first time the possible consequences of missense mutations in the DPD gene on the function and stability of the DPD enzyme