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A Fast Anti-jamming Decision Method Based on the Rule-Reduced Genetic Algorithm
( Jin Hui ),( Song Xiaoqin ),( Wang Miao ),( Niu Yingtao ),( Li Ke ) 한국인터넷정보학회 2016 KSII Transactions on Internet and Information Syst Vol.10 No.9
To cope with the complex electromagnetic environment of wireless communication systems, anti-jamming decision methods are necessary to keep the reliability of communication. Basing on the rule-reduced genetic algorithm (RRGA), an anti-jamming decision method is proposed in this paper to adapt to the fast channel variations. Firstly, the reduced decision rules are obtained according to the rough set (RS) theory. Secondly, the randomly generated initial population of the genetic algorithm (GA) is screened and the individuals are preserved in accordance with the reduced decision rules. Finally, the initial population after screening is utilized in the genetic algorithm to optimize the communication parameters. In order to remove the dependency on the weights, this paper deploys an anti-jamming decision objective function, which aims at maximizing the normalized transmission rate under the constraints of minimizing the normalized transmitting power with the pre-defined bit error rate (BER). Simulations are carried out to verify the performance of both the traditional genetic algorithm and the adaptive genetic algorithm. Simulation results show that the convergence rates of the two algorithms increase significantly thanks to the initial population determined by the reduced-rules, without losing the accuracy of the decision-making. Meanwhile, the weight-independent objective function makes the algorithm more practical than the traditional methods.
Lu Yanyang,Wei Ying,Shen Xiaoqin,Tong Yixi,Lu Jin,Zhang Yahui,Ma Yun,Zhang Rong 한국유전학회 2023 Genes & Genomics Vol.45 No.11
Background Endometrial carcinoma (EC) is the most prevalent gynecological cancer. Transcription factor (TF) regulates a large number of downstream target genes and is a key determinant of all physiological activities, including cell proliferation, differentiation, apoptosis, and cell cycle. The transcription factor E2F1 shows prominent roles in EC. BMI1 is a member of Polycomb suppressor Complex 1 (PRC1) and has been shown to be associated with EC invasiveness. It is currently unclear whether E2F1 can participate in the proliferation, migration, and invasion processes of EC cells by regulating BMI1 transcription. Objective We investigated whether E2F1 could participate in the proliferation, migration, and invasion processes of EC cells by regulating BMI1 transcription, in order to further clarify the pathogenesis and etiology of EC, and provide reference for identifying potential therapeutic targets and developing effective prevention and treatment strategies for this disease. Methods Human endometrial epithelial cells (hEECs) and human EC cell lines were selected. E2F1 expression was assessed by Western blot. E2F1 was silenced in AN3CA or overexpressed in HEC-1 by transfections, or E2F1 was silenced and BMI1 was overexpressed in AN3CA by cotransfection. Cell proliferation, migration, and invasion were detected by MTT, wound healing, and Transwell assays. The binding sites between E2F1 and BMI1 promoters were predicted through JASPAR website, and the targeted binding was verified by dual-luciferase report and ChIP assays. Results E2F1 was up-regulated in human EC cell lines, with its expression highest in AN3CA, and lowest in HEC-1. AN3CA invasion, migration, and proliferation were repressed by E2F1 knockdown, while those of HEC-1 cells were promoted by E2F1 overexpression. E2F1 overexpression increased the activity of wild type BMI1 reporter vector promoter, while this promotion was weakened after mutation of the predicted binding site in the BMI1 promoter. In the precipitated E2F1, BMI1 promoter site level was higher than that of IgG immunoprecipitant. BMI1 silencing suppressed AN3CA cell growth. BMI1 overexpression partially abrogated E2F1 silencing-inhibited EC cell growth. Conclusion E2F1 promoted EC cell proliferation, invasion, and migration by promoting the transcription of BMI1.