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The problem of state estimation based on bearing-only sensors is increasingly important while existing research on distributed filtering solutions is rather limited. Therefore, this paper proposed the novel distributed cubature information filtering (DCIF) method for addressing the state estimation challenge in bearing-only sensor networks. Firstly, the system model of the bearing-only sensor network was constructed, and the observability of the system was analyzed. The sensor nodes are paired to measure relative angle information. Subsequently, the coordinated consistency theory is employed to achieve a unified state estimation of the maneuvering target. The DCIF method enhances the observability of the system, addressing the issues of large accuracy errors and divergence in traditional nonlinear filtering algorithms. Building upon the theoretical proof of consistency convergence in DCIF, four simulation experiments were conducted for comparison. These experiments validate the effectiveness and superiority of the DCIF method in bearing-only sensor networks.
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[This corrects the article DOI: 10.3389/fonc.2023.1093063.].
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Background: It is poorly understood what cellular types participate in ductular reaction (DR) and whether DR facilitates recovery from injury or accelerates hepatic fibrosis. The aim of this study is to gain insights into the role of hepatic progenitor cell (HPC)-originated DR during fibrotic progression. Methods: DR in liver specimens of PBC, chronic HBV infection (CHB) or NAFLD, and four rodent fibrotic models by different pathogenic processes was evaluated. Gli1 expression was inhibited in rodent models or cell culture and organoid models by AAV-shGli1 or treating with GANT61. Results: Severity of liver fibrosis was positively correlated with DR extent in patients with PBC, CHB or NAFLD. HPCs were activated, expanded, differentiated into reactive cholangiocytes and constituted "HPC-originated DR", accompanying with exacerbated fibrosis in rodent models of HPC activation & proliferation (CCl4/2-AAF-treated), Μdr2-/- spontaneous PSC, BDL-cholestatic fibrosis or WD-fed/CCl4-treated NASH-fibrosis. Gli1 expression was significantly increased in enriched pathways in vivo and in vitro. Enhanced Gli1 expression was identified in KRT19+-reactive cholangiocytes. Suppressing Gli1 expression by administration of AAV-shGli1 or GANT61 ameliorated HPC-originated DR and fibrotic extent. KRT19 expression was reduced after GANT61 treatment in sodium butyrate-stimulated WB-F344 cells or organoids or in cells transduced with Gli1 knockdown lentiviral vectors. In contrast, KRT19 expression was elevated after transducing Gli1 overexpression lentiviral vectors in these cells. Conclusions: During various modes of chronic injury, Gli1 acted as an important mediator of HPC activation, expansion, differentiation into reactive cholangiocytes that formed DR, and subsequently provoked hepatic fibrogenesis.