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This article presents an accurate and efficient optimization method for heat exchanger. The structure of the original heat exchanger was optimized by combining LHS sampling, CFD simulation, radical basis function, and multi‐objective optimization. Since the Colburn factor j and the friction factor f are a pair of conflicting goals, so the multi‐objective optimization is adopted. The optimization results showed that the Colburn factor j increased by 5.43% and the friction factor f decreased by 23.31%, indicating that the optimized structure had higher heat transfer efficiency and lower resistance performance. The heat transfer mechanism and optimization effect of heat exchanger are explained by using the field synergy principle, which provides a theoretical basis for the structural design optimization of heat exchanger.

Circular RNAs (circRNAs) play vital roles in the pathogenesis and development of multiple cancers, including hepatocellular carcinoma (HCC). Nevertheless, the regulatory mechanisms of circ‐SPECC1 in HCC remain poorly understood. In our study, we found that circ‐SPECC1 was apparently downregulated in H2O2‐treated HCC cells. Additionally, knockdown of circ‐SPECC1 inhibited cell proliferation and promoted cell apoptosis of HCC cells under H2O2 treatment. Moreover, circ‐SPECC1 inhibited miR‐33a expression by direct interaction, and miR‐33a inhibitor partially reversed the effect of circ‐SPECC1 knockdown on proliferation and apoptosis of H2O2‐treated HCC cells. Furthermore, TGFβ2 was demonstrated to be a target gene of miR‐33a and TGFβ2 overexpression rescued the phenotypes of HCC cells attenuated by miR‐33a mimics. Meanwhile, autophagy inhibition by 3‐methyladenine (3‐MA) abrogated the effect of miR‐33a mimics on proliferation and apoptosis of H2O2‐treated HCC cells. Finally, knockdown of circ‐SPECC1 hindered tumor growth in vivo. In conclusion, our study demonstrated that circ‐SPECC1 regulated TGFβ2 and autophagy to promote HCC tumorigenesis under oxidative stress via miR‐33a. These findings might provide potential treatment strategies for patients with HCC., We confirmed the specific role and molecular mechanism of circ‐SPECC1 in HCC and discovered that circ‐SPECC1 modulated TGFβ2 and autophagy under oxidative stress by sponging miR‐33a to promote HCC tumorigenesis.