ABSTRACT
Designing a high-strength node is significant for space structures. Topological optimization can optimally allocate the material distribution of components to meet performance requirements. Although the material distribution after topology optimization is optimum, the structure becomes complicated to manufacture. By using additive manufacturing technology, this problem can be well solved. At present, both topology optimization technology and additive manufacturing technology are quite mature, but their application in the design of spatial nodes is very recent and less researched. This paper involves the study and improvement of the node optimization design-manufacturing integrated method. This study used the BESO optimization algorithm as the research algorithm. Through a reasonable improvement of the material interpolation method, the algorithm's dependence on the experience of selecting the material penalty index P was reduced. On this basis, the secondary development was carried out, and a multisoftware integration was carried out for optimization and manufacturing. The spatial node was taken as the research object, and the calculation results of the commercial finite element software were compared. The comparison showed that the algorithm used in this paper was better. Not only was it not trapped in a local optimum, but the maximum stress was also lower. In addition, this paper proposed a practical finite element geometric model extraction method and smoothing of the optimized nodes, completing the experiment of the additive manufacturing forming of the nodes. It provides ideas for processing jagged edges brought by the BESO algorithm. This paper verified the feasibility of the multisoftware integration method of optimized manufacturing.
ABSTRACT
OBJECTIVE: To understand the relationship between the HIV-1 viral sequence variation and host factors associated with HIV-1 disease progression. METHODS: Env and gag fragments of HIV-1 were amplified with PCR, cloned and sequenced. Bioinformatics was employed to find the genetic variation, N-linked glycosylation, hypermutation etc. Host gene polymorphism was analysed by using restricted fragment length polymorphism (RFLP). RESULTS: Significant difference was found in genetic divergence between Env PCR dominant and clonal sequences (0.1 and 0.06, respectively) in non-treated group, but no significant difference was found in the HAART treated group. V3 GPGQ accounted for the most part in both treated and nontreated groups, rare V3 loop such as GPGH, GQGR and GLGR was found in treated group, V3 substitutions of I/V (position 12) and Y/H (position 21) was associated with the relatively rapid progression (RRP). Glycosylation was significantly higher in RRP than in TP for Env region, GA substitution in RRP was also significantly higher than that in TP group. SDF1-3primeA and CCR2 V64I gene frequency was higher in TP than in RRP, but the difference was not significant. CONCLUSION: Disease progression was associated with V3 AA change, glycosylation and GA substitution in env gene. SDF1-3primeA, CCR2 V64I and CX3CR1 V249I/M280T was not associated with disease progression significantly.
