As a typical, discrete, and NP-hard problem, assembly sequence planning (ASP) has direct impact on assembly quality and costs. So far, lots of graph-based and meta-heuristic approaches cannot solve this problem effectively. This paper proposes an effective ASP algorithm based on the harmony search (HS) algorithm, which has an outstanding global search ability to obtain the global optimum more efficiently. To solve the ASP problem, an improved harmony search (IHS) algorithm is proposed mainly in four aspects: (1) an encoding of harmony is designed based on ASP problems; (2) an initial harmony memory (HM) is established using the opposition-based learning (OBL) strategy; (3) a particular way to improvise a new harmony is developed; and (4) a local search strategy is introduced to accelerate the convergence speed. Finally, the advantage of the proposed ASP algorithm over the competing algorithms in solving ASP problems is verified by two experiments. Moreover, the proposed ASP algorithm is applied to a practical problem, a propeller of azimuth thruster to verify its practicability.

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Regulatory T cells (Tregs) play critical roles in restricting inflammatory pathogenesis and limiting undesirable Th2 response to environmental allergens. However, the role of miR-181a in regulating acute gouty arthritis (AGA) and Treg function remains unclear. This study aimed to investigate the potential roles of miR-181a in Treg immunity and the associated signaling pathway in the AGA mouse model. A solution with monosodium urate (MSU) crystals was injected into the joint tissue of mice to induce AGA. ELISA was used to examine inflammatory factors in blood samples, and flow cytometry was used to analyze Treg profile in mice with MSU-induced AGA. Cell proliferation and viability were assessed by CCK-8 assay. TGF-β1/Smad signaling activation was detected by western blot. We found that miR-181a expression showed a positive correlation with the changes of splenic Tregs percentage in AGA mice. miR-181a regulated the TGF-β1/Smad axis, since the transfection of miR-181a mimic increased the level of TGF-β1 and the phosphorylation of Smad2/3 in Tregs in AGA mice. Additionally, miR-181a mimic also promoted responses of Tregs via TGF-β1 in vitro and in vivo . Our work uncovered a vital role of miR-181a in the immune function of Treg cells by mediating the activity of the TGF-β1/Smad pathway in the AGA mouse model induced by MSU.