ECM-OPCC: Efficient Context Model for Octree-based Point Cloud Compression

Recently, deep learning methods have shown promising results in point cloud compression. For octree-based point cloud compression, previous works show that the information of ancestor nodes and sibling nodes are equally important for predicting current node. However, those works either adopt insufficient context or bring intolerable decoding complexity (e.g. >600s). To address this problem, we propose a sufficient yet efficient context model and design an efficient deep learning codec for point clouds. Specifically, we first propose a window-constrained multi-group coding strategy to exploit the autoregressive context while maintaining decoding efficiency. Then, we propose a dual transformer architecture to utilize the dependency of current node on its ancestors and siblings. We also propose a random-masking pre-train method to enhance our model. Experimental results show that our approach achieves state-of-the-art performance for both lossy and lossless point cloud compression. Moreover, our multi-group coding strategy saves 98% decoding time compared with previous octree-based compression method

Hepatitis B virus induces G1 phase arrest by regulating cell cycle genes in HepG2.2.15 cells

<p>Abstract</p> <p>Background</p> <p>To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism.</p> <p>Methods</p> <p>MTT, colony formation assay and tumourigenicity in nude mice were performed to investigate the effect of HBV on the proliferative capability of host cells. In order to explore the potential mechanism, cell cycle and apoptosis were analysed. The cell cycle genes controlling the G1/S phase transition were detected by immunohistochemistry, westernblot and RT-PCR.</p> <p>Results</p> <p>HepG2.2.15 cells showed decreased proliferation ability compared to HepG2 cells. G1 phase arrest was the main cause but was not associated with apoptosis. p53, p21 and total retinoblastoma (Rb) were determined to be up-regulated, whereas cyclinE was down-regulated at both the protein and mRNA levels in HepG2.2.15 cells. The phosphorylated Rb in HepG2.2.15 cells was decreased.</p> <p>Conclusions</p> <p>Our results suggested that HBV inhibited the capability of proliferation of HepG2.2.15 cells by regulating cell cycle genes expression and inducing G1 arrest.</p

Hepatitis B virus induces G1 phase arrest by regulating cell cycle genes in HepG2.2.15 cells

<p>Abstract</p> <p>Background</p> <p>To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism.</p> <p>Methods</p> <p>MTT, colony formation assay and tumourigenicity in nude mice were performed to investigate the effect of HBV on the proliferative capability of host cells. In order to explore the potential mechanism, cell cycle and apoptosis were analysed. The cell cycle genes controlling the G1/S phase transition were detected by immunohistochemistry, westernblot and RT-PCR.</p> <p>Results</p> <p>HepG2.2.15 cells showed decreased proliferation ability compared to HepG2 cells. G1 phase arrest was the main cause but was not associated with apoptosis. p53, p21 and total retinoblastoma (Rb) were determined to be up-regulated, whereas cyclinE was down-regulated at both the protein and mRNA levels in HepG2.2.15 cells. The phosphorylated Rb in HepG2.2.15 cells was decreased.</p> <p>Conclusions</p> <p>Our results suggested that HBV inhibited the capability of proliferation of HepG2.2.15 cells by regulating cell cycle genes expression and inducing G1 arrest.</p