This paper investigates the trajectory tracking problem of the quadrotor unmanned aerial vehicles (UAV) with consideration of both attitude and position dynamics. First of all, the trajectory tracking problem are divided into the commands tracking in position and attitude loops by introducing the virtual attitude angle commands. Secondly, the high-order sliding mode observers (HSMOs) are introduced to estimate the lumped disturbances in position loop and the derivatives of the attitude angle tracking errors, the lumped disturbances in the attitude loop. And then the composite nonlinear dynamical inversion controller in position loop and the composite nonsingular terminal sliding mode controller in attitude loop are constructed by introducing the es-

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Background & Aims Although the prognosis of patients with occult hepatitis B virus (HBV) infection (OBI) is usually benign, a small portion may undergo cirrhosis and subsequently hepatocellular carcinoma (HCC). We studied the mechanism of life-long Integration of virus DNA into OBI host’s genome, of which may induce hepatocyte transformation. Methods We applied HBV capture sequencing on single cells from an OBI patient who, developed multiple HCC tumors and underwent liver resection in May 2013 at Tongji Hospital in China. Despite with the undetectable virus DNA in serum, we determined the pattern of viral integration in tumor cells and adjacent non-tumor cells and obtained the details of the viral arrangement in host genome, and furthermore the HBV integrated region in cancer genome. Results HBV captured sequencing of tissues and individual cells revealed that samples from multiple tumors shared two viral integration sites that could affect three host genes, including CSMD2 on chr1 and MED30 / EXT1 on chr8. Whole genome sequencing further indicated one hybrid chromosome formed by HBV integrations between chr1 and chr8 that was shared by multiple tumors. Additional 50 poorly differentiated liver tumors and the paired adjacent non-tumors were evaluated and functional studies suggested up-regulated EXT1 expression promoted HCC growth. We further observed that the most somatic mutations within the tumor cell genome were common among the multiple tumors, suggesting that HBV associated, multifocal HCC is monoclonal in origin. Conclusion Through analyzing the HBV integration sites in multifocal HCC, our data suggested that the tumor cells were monoclonal in origin and formed in the absence of active viral replication, whereas the affected host genes may subsequently contribute to carcinogenesis. Electronic supplementary material The online version of this article (10.1186/s13046-019-1273-1) contains supplementary material, which is available to authorized users.

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