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To evaluate the damage capability of circumferential multiple explosive formed projectiles (MEFPs), it is required to predict the EFP forming velocity accurately and quickly. According to the circumferential MEFP liner characteristics of uniform circumferential distribution and layered axial structure, a simplified physical model of circumferential MEFPs is put forward innovatively. The Lagrange and Euler coupling algorithm is selected to simulate the simulation model, which is verified as equivalent to the circumferential MEFPs. Based on the energy conservation principle and the simplified equivalent physical model, the calculating model of the circumferential MEFP forming velocity is derived. The correctness and accuracy of the calculation model are verified by using the numerical simulation software and the test device of the round-shaped charge model.

Additional file 4: Table S1. List of primers used for qPCR analysis in this study.

Additional file 1: Figure S1. Iron deprivation drives the immunosuppressive polarization of macrophages. (A) Cell viability was measured in BMDMs and PMs with indicated treatment by CCK-8 assay. (B) The mRNA expression of M1 signature genes in PMs with indicated treatment using qPCR. The fold changes in expression level relative to control were expressed as 2−ΔΔCt. (C) The mRNA expression of M2 signature genes in RAW264.7 cells with indicated treatment using qPCR. The fold changes in expression level relative to control were expressed as 2−ΔΔCt. (D–G) The surface expression of CD206 and PD-L1 with indicated treatment in RAW264.7 cells using FACS. The results were shown as relative fold changes in MFI of CD206 and PD-L1 normalized to their corresponding controls. All data are representative of three independent experiments and presented as mean ± SD. *p

Additional file 3: Figure S3. Iron deprivation drives macrophage M2 polarization through induction of Hif-1α. (A, B) The mRNA expression of Hif-1α and Hif-2α in PMs with indicated treatment using qPCR. The fold changes in expression level relative to control were expressed as 2−ΔΔCt. (C) The protein expression of HIF-2α in PMs with indicated treatment was detected by Western blot. (D) The mRNA expression of Arg1, Vegfa, and Pd-l1 by qPCR in BMDMs with either Hif-2α knockdown or its control counterpart upon indicated treatment. The fold changes in expression level relative to control were expressed as 2−ΔΔCt. (E) The concentration of lactate in the supernatants of Hepa1-6/shNT and Hepa1-6/shTfrc cells was measured by lactate assay kit.

Additional file 2: Figure S2. Tumor cells fail to educate macrophages toward an iron-releasing phenotype but instead an iron starvation response. (A) The mRNA expression of Tfrc, Fth1, and SLC40A1 in PMs co-cultured with indicated cells or DMEM alone using qPCR. The fold changes in expression level relative to control were expressed as 2−ΔΔCt. (B) Heat map of iron metabolism-related genes in THP-1 monocyte-derived macrophages based on RNA-seq data from GSE159254. (C) BMDMs and Hepa1-6 cells in the co-culture system were allowed to grow in DMEM media containing 50 ng/mL FITC-labeled holo-transferrin, and then in vitro holo-transferrin uptake assay was performed. BMDMs were collected 2 h later, and the MFI of FITC-transferrin was measured by FACS. All data are representative of three independent experiments and presented as mean ± SD. *p

Li-Li Liu,1,2,* Ji-Min Zhu,1,2,* Xiang-Nan Yu,1,2 Hai-Rong Zhu,1,2 Xuan Shi,1,2 Enkhnaran Bilegsaikhan,1,2 Hong-Ying Guo,1,2 Jian Wu,1–3 Xi-Zhong Shen1–3 1Department of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, People’s Republic of China; 2Shanghai Institute of Liver Diseases, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai 200032, People’s Republic of China; 3Department of Medical Microbiology and Parasitology, Ministry of Education/National Health Commission/Chinese Academy of Medical Sciences, Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai 200032, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xi-Zhong ShenDepartment of Gastroenterology and Hepatology, Zhongshan Hospital of Fudan University, 180 Fenglin Road, Shanghai 200032, People’s Republic of ChinaTel +86 216 404 1990Email shen.xizhong@zs-hospital.sh.cn Jian WuDepartment of Medical Microbiology and Parasitology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, 138 Yixue Yuan Road, P.O. Box 228, Shanghai 200032, People’s Republic of ChinaTel +86 21 5423 7705Email jian.wu@fudan.edu.cnBackground: Growing evidence suggests that the ubiquitin-proteasome system is involved in the pathogenesis and recurrence of hepatocellular carcinoma (HCC); yet, little is known about the role of ubiquitin-conjugating enzyme E2T (UBE2T) in HCC.Materials and methods: UBE2T levels were detected in HCC tissues and hepatoma cell lines using quantitative reserve transcriptase-polymerase chain reaction and Western blot analysis. Next, the changes of phenotypes after UBE2T knockdown or overexpression were evaluated using in vitro methods. Finally, the mechanism of UBE2T in HCC was tested using ex vivo and in vivo methods.Results: In the present study, we reported that UBE2T mRNA and protein levels were significantly upregulated in HCC tissues compared to adjacent non-tumor tissues. Additionally, suppression of UBE2T expression inhibited proliferation, colony formation, tumorigenesis, migration, and invasion of hepatoma cells, whereas UBE2T overexpression led to the opposite outcomes. Moreover, suppression of UBE2T expression resulted in an increase in G2/M phase and a decrease in the percentage of cells in G1 phase, which indicated a cell cycle arrest at the G2/M phase. In contrast, the percentage of cells in G2/M phase decreased following UBE2T overexpression. Further study indicated that UBE2T regulated the G2/M transition by modulating cyclin B1 and cyclin-dependent kinase 1.Conclusion: Taken together, the findings of the present study uncover biological functions of UBE2T in hepatoma cells, and delineate preliminary molecular mechanisms of UBE2T in modulating HCC development and progression.Keywords: hepatocellular carcinoma, UBE2T, ubiquitination, cell cycle

Hong Chen,1 Hai-Rong Zhu,2 Xiang-Nan Yu,2 Xuan Shi,2 Enkhnaran Bilegsaikhan,2 Hong-Ying Guo,2 Ren-Zheng Huang,2 Tao-Tao Liu,2 Xi-Zhong Shen,2–4 Ji-Min Zhu2,31Department of Endocrinology, Zhongshan Hospital of Fudan University, Shanghai, People’s Republic of China; 2Department of Gastroenterologyand Hepatology, Zhongshan Hospital of Fudan University, Shanghai, People’s Republic of China; 3Shanghai Institute of Liver Disease, Zhongshan Hospital of Fudan University, Shanghai, People’s Republic of China; 4Key Laboratory of Medical Molecular Virology, Shanghai Medical College of Fudan University, Shanghai, People’s Republic of ChinaBackground: Aberrant expression of pepsinogen C (PGC) has been observed in human cancers. However, its role in hepatocellular carcinoma (HCC) remains to be established. The goal of this study is to illustrate PGC expression and to evaluate its clinical relevance in HCC.Materials and methods: PGC expression was examined in 75 pairs of HCC and adjacent non-tumor tissues using tissue microarray. The correlations between its expression and clinical parameters were also analyzed.Results: PGC overexpression was significantly associated with larger tumor size (≥5 cm; P=0.017) and incomplete encapsulation (P