ABSTRACT
The direction estimation of the coherent source in a uniform circular array is an essential part of the signal processing area of the array, but the traditional uniform circular array algorithm has a low localization accuracy and a poor localization effect on the coherent source. To solve this problem, this paper proposes a two-dimensional direction of arrival (DOA) estimation for the coherent source in broadband. Firstly, the central frequency of the coherent sound source is estimated using the frequency estimation method of the delayed data, and a real-valued beamformer is constructed using the concept of the multiloop phase mode. Then, the cost function in the beam space is obtained. Finally, the cost function is searched in two dimensions to locate the sound source. In this paper, we simulate the DOA of the sound source at different frequencies and signal-to-noise ratios and analyze the resolution of the circular array. The simulation results show that the proposed algorithm can estimate the direction of arrival with high precision and achieve the desired results.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) is one of the major malignancies and the second most common cause of cancer-related death worldwide. Sorafenib, an approved first-line systematic treatment agent for HCC, is capable to effectively improve the survival of patients with advanced HCC. The long-noncoding RNA (lncRNA) differentiation antagonizing non-protein coding RNA (DANCR) has been reported to exert oncogenic functions in several kinds of human cancers. However, the role of lncRNA DANCR in sorafenib resistance in HCC remains unknown. METHODS: The expression levels of DANCR in HCC tissues were detected by qRT-PCR. DANCR overexpression and knockdown models were established and utilized to investigate the functional role of DANCR on sorafenib resistance in HCC cells. The MS2-binding sequences-MS2-binding protein-based RNA immunoprecipitation assay, RNA pull-down and luciferase reporter assay was used to detect the association between DANCR and PSMD10 mRNA. The activation of DANCR transcription mediated by STAT3 was assessed by luciferase reporter and chromatin immunoprecipitation assays. RESULTS: We found that DANCR was significantly overexpressed in HCC tissues and associated with prognosis of HCC patients. Overexpression and knockdown experiments demonstrated that DANCR promoted sorafenib resistance in HCC cells in vitro and in vivo. Mechanistically, the role of DANCR relied largely on the association with PSMD10. DANCR stabilized PSMD10 mRNA through blocking the repressing effect of several microRNAs on PSMD10. Besides, DANCR activated IL-6/STAT3 signaling via PSMD10. Furthermore, we revealed that DANCR transcription was enhanced by the activation of IL-6/STAT3 signaling, indicating a positive feedback loop of DANCR and IL-6/STAT3 signaling. CONCLUSION: Collectively, our study is the first to elucidate the mechanism of DANCR-mediated sorafenib resistance via PSMD10-IL-6/STAT3 signaling axis, which provides a promising target for developing new therapeutic strategy for sorafenib tolerance of HCC.