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        An Optimized Mass-spring Model with Shape Restoration Ability Based on Volume Conservation

        ( Xiaorui Zhang ),( Hailun Wu ),( Wei Sun ),( Chengsheng Yuan ) 한국인터넷정보학회 2020 KSII Transactions on Internet and Information Syst Vol.14 No.4

        To improve the accuracy and realism of the virtual surgical simulation system, this paper proposes an optimized mass-spring model with shape restoration ability based on volume conservation to simulate soft tissue deformation. The proposed method constructs a soft tissue surface model that adopts a new flexion spring for resisting bending and incorporates it into the mass-spring model (MSM) to restore the original shape. Then, we employ the particle swarm optimization algorithm to achieve the optimal solution of the model parameters. Besides, the volume conservation constraint is applied to the position-based dynamics (PBD) approach to maintain the volume of the deformable object for constructing the soft tissue volumetric model base on tetrahedrons. Finally, we built a simulation system on the PHANTOM OMNI force tactile interaction device to realize the deformation simulation of the virtual liver. Experimental results show that the proposed model has a good shape restoration ability and incompressibility, which can enhance the deformation accuracy and interactive realism.

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        Amplification of transglutaminase 2 enhances tumor-promoting inflammation in gastric cancers

        Cho Sung-Yup,오유미,Jeong Eui Man,박상희,Dakeun Lee,Xiaorui Wang,Qiqi Zeng,Hongyu Qin,Fang Hu,Hui Gong,Xi Liu,Guanjun Zhang,나득채,이지은,채지수,서윤석,공성호,Hyuk-Joon Lee,Jong-Il Kim,박한수,Chengsheng Zhang,양한광,Charles Lee 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

        Tumor-promoting inflammation is a hallmark of cancer and is highly associated with tumor progression, angiogenesis, and metastasis. Tumor-associated macrophages (TAMs) are major drivers of tumor-promoting inflammation, but due to the complexity of the tumor microenvironment, the detailed regulatory mechanisms are still under investigation. Here, we investigated a novel role for transglutaminase 2 (TGM2) in the development of tumor-promoting inflammation and recruitment of TAMs to gastric cancer (GC) tissues. When estimated by array comparative genomic hybridization and droplet digital PCR, the copy numbers of the TGM2 gene were amplified in 13.6% (14/103) of GC patients and positively associated with TGM2 expression. Gene set enrichment analysis of expression microarray data for GC samples with high or low TGM2 expression showed that increased TGM2 expression was associated with tumor-promoting inflammation in GC. In addition, the expression of TGM2 was correlated with the expression of markers for macrophages, neutrophils, blood vessels, and lymphatic vessels. Overexpression of TGM2 in GC cells augmented the IL-1β-induced secretion of macrophage-recruiting chemokines and NF-κB activation. TGM2 protein levels were associated with the expression levels of the macrophage marker CD163 in human GC tissue samples. Moreover, GC patients with high expression of TGM2 had a worse prognosis than those with low expression of TGM2. These results suggest TGM2 as a novel regulator of the tumor microenvironment of GC and provide a promising target for constraining tumor-promoting inflammation.

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