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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. [ABSTRACT FROM AUTHOR]

This paper is concerned with the measurement outlier (MO)-resistant mobile robot localization (MRL) problem. For the purpose of mitigating the effect of the MOs, a time-varying state estimator is constructed containing a saturation function with variable saturation level. The purpose of this paper is mainly to seek an effective solution to the addressed MRL problem by devising the desired time-varying state estimator which ensures that, over a finite horizon, the estimation error dynamics satisfies the H∞ performance constraint. By constructing an appropriate Lyapunov function, the existing condition of the estimator is first obtained. Then, the desired state estimator gain is given through the solution to a set of certain matrix inequalities and the MO-resistant MRL algorithm is presented. Finally, an example is conducted to testify the usefulness of the MRL algorithm proposed. [ABSTRACT FROM AUTHOR]

In this study, we propose a localization method based on multipath time-delay difference (MTD). We extract the time-delay difference of the direct and sea surface-reflected sound rays by the signal from hydrophones in deep sea to establish the MTD matching vector. The predicted matching vectors are obtained using Bellhop to build an ocean acoustic field model. The spatial distribution of MTD are simulated and analyzed. The matching ambiguity plane is obtained by the objective function. The maximum point of ambiguity plane is the position of the sound source. We show that the sound field propagation error can be replaced by the geometric error. We then analyze the influence of the received position error on the localization accuracy. The effects of errors caused by skewing of hydrophone and horizontal variation in SSP are studied. Simulation and experimental results at sea show that the proposed method is robust and can locate the sound source with a small aperture array of two hydrophones. [ABSTRACT FROM AUTHOR]