H∞ filter for flexure deformation and lever arm effect compensation in M/S INS integration

Xixiang Liu,Xiaosu Xu,Lihui Wang,Yiting Liu 대한조선학회 2014 International Journal of Naval Architecture and Oc Vol.6 No.3

On ship, especially on large ship, the flexure deformation between Master (M)/Slave (S) Inertial Naviga-tion System (INS) is a key factor which determines the accuracy of the integrated system of M/S INS. In engineering this flexure deformation will be increased with the added ship size. In the M/S INS integrated system, the attitude error between MINS and SINS cannot really reflect the misalignment angle change of SINS due to the flexure deformation. At the same time, the flexure deformation will bring the change of the lever arm size, which further induces the uncertainty of lever arm velocity, resulting in the velocity matching error. To solve this problem, a H∞ algorithm is proposed, in which the attitude and velocity matching error caused by deformation is considered as measurement noise with limited energy, and measurement noise will be restrained by the robustness of H∞ filter. Based on the classical “attitude plus velocity” matching method, the progress of M/S INS information fusion is simulated and compared by using three kinds of schemes, which are known and unknown flexure deformation with standard Kalman filter, and unknown flexure deformation with H∞ filter, respectively. Simulation results indicate that H∞ filter can effectively improve the accuracy of information fusion when flexure deformation is unknown but non-ignorable.

H<SUB>∞</SUB> filter for flexure deformation and lever arm effect compensation in M/S INS integration

Xixiang Liu,Xiaosu Xu,Lihui Wang,Yinyin Li,Yiting Liu 대한조선학회 2014 International Journal of Naval Architecture and Oc Vol.6 No.3

On ship, especially on large ship, the flexure deformation between Master (M)/Slave (S) Inertial Navigation System (INS) is a key factor which determines the accuracy of the integrated system of M/S INS. In engineering this flexure deformation will be increased with the added ship size. In the M/S INS integrated system, the attitude error between MINS and SINS cannot really reflect the misalignment angle change of SINS due to the flexure deformation. At the same time, the flexure deformation will bring the change of the lever arm size, which further induces the uncertainty of lever arm velocity, resulting in the velocity matching error. To solve this problem, a H∞ algorithm is proposed, in which the attitude and velocity matching error caused by deformation is considered as measurement noise with limited energy, and measurement noise will be restrained by the robustness of H∞ filter. Based on the classical “attitude plus velocity” matching method, the progress of M/S INS information fusion is simulated and compared by using three kinds of schemes, which are known and unknown flexure deformation with standard Kalman filter, and unknown flexure deformation with H∞ filter, respectively. Simulation results indicate that H∞ filter can effectively improve the accuracy of information fusion when flexure deformation is unknown but non-ignorable.

$H_{\infty}$ filter for flexure deformation and lever arm effect compensation in M/S INS integration

Liu, Xixiang,Xu, Xiaosu,Wang, Lihui,Li, Yinyin,Liu, Yiting The Society of Naval Architects of Korea 2014 International Journal of Naval Architecture and Oc Vol.6 No.3

On ship, especially on large ship, the flexure deformation between Master (M)/Slave (S) Inertial Navigation System (INS) is a key factor which determines the accuracy of the integrated system of M/S INS. In engineering this flexure deformation will be increased with the added ship size. In the M/S INS integrated system, the attitude error between MINS and SINS cannot really reflect the misalignment angle change of SINS due to the flexure deformation. At the same time, the flexure deformation will bring the change of the lever arm size, which further induces the uncertainty of lever arm velocity, resulting in the velocity matching error. To solve this problem, a $H_{\infty}$ algorithm is proposed, in which the attitude and velocity matching error caused by deformation is considered as measurement noise with limited energy, and measurement noise will be restrained by the robustness of $H_{\infty}$ filter. Based on the classical "attitude plus velocity" matching method, the progress of M/S INS information fusion is simulated and compared by using three kinds of schemes, which are known and unknown flexure deformation with standard Kalman filter, and unknown flexure deformation with $H_{\infty}$ filter, respectively. Simulation results indicate that $H_{\infty}$ filter can effectively improve the accuracy of information fusion when flexure deformation is unknown but non-ignorable.

Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p

Yuan Donglan,Zhu Dandan,Yin Boyu,Ge Hongshan,Zhao Yinling,Huang Aihua,Wang Xiaosu,Cao Xiuhong,Xia Nan,Qian Hua 한국유전학회 2022 Genes & Genomics Vol.44 No.5

Background: Endometriosis (EM) is a gynecological disease that poses severe health risks to women, although its pathogenesis has yet to be fully elucidated. It has been shown that long non-coding RNAs (lncRNAs) are closely associated with EM initiation and have a role in the development of this disease. Previous studies exploring the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) have shown that this lncRNA functions as a tumor promoter in endometrial cancer. However, its exact mechanism of action in EM remains unclear. Objective: This report was designed to illustrate the potential molecular mechanisms of lncRNA NEAT1 on EM. Methods: Endometrial tissues were extracted from EM model rats and patients with EM. Hematoxylin and eosin staining was applied to detect the morphological changes that occurred in rats after construction of the model. Endometrial stromal cells (ESCs) were extracted from either ectopic endometrium (EC) or eutopic endometrium (EU) tissues from patients with EM. LncRNA NEAT1 and miR-124-3p expression in EM tissues and cells were subsequently evaluated by reverse transcription-quantitative (RT-q)PCR analysis. MTT assay, flow cytometric analysis, western blot assay and Transwell assay were then employed to examine the effect of NEAT1 and miR-124-3p on EC-ESC proliferation, apoptosis, migration and invasion, respectively. The targeted relationship between lncRNA NEAT1 and miR-124-3p was subsequently confirmed by dual-luciferase and co-transfection assays. Results: MiR-124-3p was identified as a target of NEAT1, and could be negatively regulated by NEAT1 in EC-ESCs. The expression level of NEAT1 was evidently increased, whereas that of miR-124-3p was decreased, in the EM in vivo model, EM tissues and EC-ESCs from patients with EM. The loss-of-function assays further established that silencing of NEAT1 could inhibit EC-ESC proliferation, migration, and invasion, but it led to the promotion of apoptosis via targeting miR-124-3p. Conclusions: NEAT1 is significantly upregulated in EM, promoting malignant behavior in EM through targeting miR-124-3p expression.

Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia

Lei Zhou,Lin Fu,Na Lv,Jing Liu,Yan Li,Xiaosu Chen,Qingyu Xu,Guofeng Chen,Baoxu Pang,Lili Wang,Yonghui Li,Xiaodong Zhang,Li Yu 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-

The AML1-ETO fusion protein (A/E), which results from the t(8;21) translocation, is considered to be a leukemiainitiating event. Identifying the mechanisms underlying the oncogenic activity of A/E remains a major challenge. In this study, we identified a specific down-regulation of brain acid-soluble protein 1 (BASP1) in t(8;21) acute myeloid leukemia (AML). A/E recognized AML1-binding sites and recruited DNA methyltransferase 3a (DNMT3a) to the BASP1 promoter sequence, which triggered DNA methylation-mediated silencing of BASP1. Ectopic expression of BASP1 inhibited proliferation and the colony-forming ability of A/E-positive AML cell lines and led to apoptosis and cell cycle arrest. The DNMT inhibitor decitabine up-regulated the expression of BASP1 in A/E-positive AML cell lines. In conclusion, our data suggest that BASP1 silencing via promoter methylation may be involved in A/E-mediated leukemogenesis and that BASP1 targeting may be an actionable therapeutic strategy in t(8;21) AML.