Submission of Evidence on Online Violence Against Women to the UN Special Rapporteur on Violence Against Women, its Causes and Consequences, Dr Dubravka Šimonović

Figure S1. B3GALNT2 levels determined by W.B. and ROC curve. a–c Relative mRNA expression of B3GALNT2 in HCC tumor tissues and normal liver tissues obtained from GSE76427, GSE36376, and TCGA-LIHC datasets. d Western blot analysis of B3GALNT2 levels in 24 pairs of HCC tissues. T HCC tumor tissue, N adjacent non-tumor tissue. e ROC curve analysis of the sensitivity and specificity for the predictive value of TNM model, B3GALNT2 expression, and the combination model. (TIFF 546 kb

In Situ FT-IR Spectroscopic Studies of CO Adsorption on Fresh Mo₂C/Al₂O₃ Catalyst

The surface sites of supported molybdenum carbide catalyst derived from different synthesis stages have been studied by in situ FT-IR spectroscopy using CO as the probe molecule. Adsorbed CO on the reduced passivated Mo2C/Al2O3 catalyst gives a main band at 2180 cm-1, which can be assigned to linearly adsorbed CO on Mo4+ sites. The IR results show that the surface of reduced passivated sample is dominated by molybdenum oxycarbide. However, a characteristic IR band at 2054 cm-1 was observed for the adsorbed CO on MoO3/Al2O3 carburized with CH4/H2 mixture at 1033 K (fresh Mo2C/Al2O3), which can be assigned to linearly adsorbed CO on Moδ+ (0 2C/Al2O3. Unlike adsorbed CO on reduced passivated Mo2C/Al2O3 catalyst, the IR spectra of adsorbed CO on fresh Mo2C/Al2O3 shows similarity to that on some of the group VIII metals (such as Pt and Pd), suggesting that fresh carbide resembles noble metals. To study the stability of Mo2C catalyst during H2 treatment and find proper conditions to remove the deposited carbon species, H2 treatment of fresh Mo2C/Al2O3 catalyst at different temperatures was conducted. Partial amounts of carbon atoms in Mo2C along with some surface-deposited carbon species can be removed by the H2 treatment even at 450 K. Both the surface-deposited carbon species and carbon atoms in carbide can be extensively removed at temperatures above 873 K

In Situ FT-IR Spectroscopic Studies of CO Adsorption on Fresh Mo₂C/Al₂O₃ Catalyst

The surface sites of supported molybdenum carbide catalyst derived from different synthesis stages have been studied by in situ FT-IR spectroscopy using CO as the probe molecule. Adsorbed CO on the reduced passivated Mo2C/Al2O3 catalyst gives a main band at 2180 cm-1, which can be assigned to linearly adsorbed CO on Mo4+ sites. The IR results show that the surface of reduced passivated sample is dominated by molybdenum oxycarbide. However, a characteristic IR band at 2054 cm-1 was observed for the adsorbed CO on MoO3/Al2O3 carburized with CH4/H2 mixture at 1033 K (fresh Mo2C/Al2O3), which can be assigned to linearly adsorbed CO on Moδ+ (0 2C/Al2O3. Unlike adsorbed CO on reduced passivated Mo2C/Al2O3 catalyst, the IR spectra of adsorbed CO on fresh Mo2C/Al2O3 shows similarity to that on some of the group VIII metals (such as Pt and Pd), suggesting that fresh carbide resembles noble metals. To study the stability of Mo2C catalyst during H2 treatment and find proper conditions to remove the deposited carbon species, H2 treatment of fresh Mo2C/Al2O3 catalyst at different temperatures was conducted. Partial amounts of carbon atoms in Mo2C along with some surface-deposited carbon species can be removed by the H2 treatment even at 450 K. Both the surface-deposited carbon species and carbon atoms in carbide can be extensively removed at temperatures above 873 K

In Situ FT-IR Spectroscopic Studies of CO Adsorption on Fresh Mo₂C/Al₂O₃ Catalyst

The surface sites of supported molybdenum carbide catalyst derived from different synthesis stages have been studied by in situ FT-IR spectroscopy using CO as the probe molecule. Adsorbed CO on the reduced passivated Mo2C/Al2O3 catalyst gives a main band at 2180 cm-1, which can be assigned to linearly adsorbed CO on Mo4+ sites. The IR results show that the surface of reduced passivated sample is dominated by molybdenum oxycarbide. However, a characteristic IR band at 2054 cm-1 was observed for the adsorbed CO on MoO3/Al2O3 carburized with CH4/H2 mixture at 1033 K (fresh Mo2C/Al2O3), which can be assigned to linearly adsorbed CO on Moδ+ (0 2C/Al2O3. Unlike adsorbed CO on reduced passivated Mo2C/Al2O3 catalyst, the IR spectra of adsorbed CO on fresh Mo2C/Al2O3 shows similarity to that on some of the group VIII metals (such as Pt and Pd), suggesting that fresh carbide resembles noble metals. To study the stability of Mo2C catalyst during H2 treatment and find proper conditions to remove the deposited carbon species, H2 treatment of fresh Mo2C/Al2O3 catalyst at different temperatures was conducted. Partial amounts of carbon atoms in Mo2C along with some surface-deposited carbon species can be removed by the H2 treatment even at 450 K. Both the surface-deposited carbon species and carbon atoms in carbide can be extensively removed at temperatures above 873 K

Additional file 10: of Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals

Table S3. Genes correlated to CLEC3B in TCGA database. (XLSX 1010 kb

Additional file 2: of Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals

Figure S2. Correlation between CLEC3B expression and clinicopathological characteristic, and improvement of the TNM staging prognostic model with CLEC3B expression. (A) Receiver operating characteristic (ROC) curve analyses of different cutoff values of composite expression score (CES), and the area under the ROC curve (AUC), 95% confident interval (95% CI) and P-value are shown. (B, C) The disease free time in IHC staining (n = 80, P < 0.0001) (B) and TCGA-LIHC database (n = 315, P < 0.0001) (C), based on CLEC3B expression level, were calculated by Kaplan–Meier. (D) The relative proportion of patients with low CLEC3B expression is increased with the tumor progression in hepatocellular carcinoma (P = 0.006). (E) Multivariate Cox analysis was conducted to analyze independent prognostic factors in patients with hepatocellular carcinoma. (F) ROC analysis of the sensitivity and specificity for the predictive value of CLEC3B expression model, TNM model and the combined model of CLEC3B and TNM. (G) AIC and C-index, another prognostic predicting model nomogram for overall survival, were performed to analyze the predictive accuracies of TNM stage, CLEC3B expression and the combined model of CLEC3B and TNM. (H) Nomogram was built to quantify the combined effect of the proven independent prognostic factors for overall survival. (I) Calibration plot of the nomogram for 5-year survival. (J) Of all patients, three groups were divided according to the total points in the nomogram which range of 0–40, 41–120, 121–160, was refined as low risk, medium and high risk subgroup (P < 0.0001). Kaplan–Meier analysis was used to test the correlation of the risk with overall survival. *, P < 0.05; **, P < 0.01; ***, P < 0.001; n.s., not significant. (TIF 827 kb

Additional file 14: of Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals

Figure S10. Exosomal CLEC3B inhibiting migration, invasion and EMT were AMPK signaling-independent in ECs. (A) Representative images and relative migratory number of ECs incubated with CC and exosomes from tumor cells, Exo-3B (no CC, P = 0.0003; CC, P = 0.3142) and Exo-3B-KD (no CC, P = 0.0389; CC, P = 0.4269). (B) Representative images and relative invasive number of ECs incubated with CC and Exo-3B (no CC, P = 0.0029; CC, P = 0.2830) or Exo-3B-KD (no CC, P = 0.0011; CC, P = 0.0733). (C) Relative mRNA expression of E-cad (Exo-3B, no CC, P = 0.0002; CC, P = 0.4442; Exo-3B-KD, no CC, P = 0.0509; CC, P = 0.0002), Slug (Exo-3B, P = 0.0159, P = 0.0030; Exo-3B-KD, no CC, P < 0.0001; CC, P = 0.0920) and ZO-1 (Exo-3B, no CC, P = 0.0002; CC, P < 0.0001; Exo-3B-KD, no CC, P = 0.0110; CC, P = 0.0134) in ECs treated with CC and Exo-3B or Exo-3B-KD. (D) Expression of E-cad, Slug and ZO-1 in ECs treated with CC and Exo-3B or Exo-3B-KD. *, P < 0.05; **, P < 0.01; ***, P < 0.001; n.s., not significant. (TIF 4765 kb

Additional file 8: of Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals

Figure S6. Exosomal CLEC3B inhibited EMT of HCC cells. (A) Analysis of correlation of CLEC3B with E-cad (R = 0.107, P = 0.04), ZO-1 (R = 0.002, P = 0.972), N-cad (R = − 0.116, P = 0.026), Snai1 (R = 0.438, P < 0.001), Slug (R = 0.147, P = 0.005),β-catenin (R = − 0.101, P = 0.051) and Vimentin (R = 0.401, P < 0.001) in TCGA-LIHC database. (B) The relative mRNA expression of EMT relative molecules in HCC cells transfected with 3B (Snai1, P = 0.0010; Slug, P = 0.0002; Vimentin, P = 0.0107; β-catenin, P = 0.0023) or 3B-KD (Snai1, P = 0.7509; Slug, P = 0.0100; Vimentin, P = 0.6157; β-catenin, P = 0.7604) plasmids. (C) The protein expression of EMT relative molecules in HCC cells transfected with 3B or 3B-KD plasmids. (D) The mRNA expression of N-cad (Exo-3B, P < 0.0001; Exo-3B-KD, P = 0.0015), Snai1 (Exo-3B, P = 0.0011; Exo-3B-KD, P = 0.0010), β-catenin (Exo-3B, P = 0.0015; Exo-3B-KD, P = 0.1158) and Vimentin (Exo-3B, P = 0.1211; Exo-3B-KD, P = 0.7113) in tumor cells, which were treated with exosomes. (E) Levels of protein related to EMT in tumor cells treated with Exo-3B or Exo-3B-KD. *, P < 0.05; **, P < 0.01; ***, P < 0.001; n.s., not significant. (TIF 1974 kb

Additional file 3: of Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals

Table S1. CLEC3B expression and relative factors. (DOCX 15 kb

Additional file 4: of Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals

Table S2. Survival time of HCC patients and relative factors. (DOCX 16 kb