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

Predictions of the Geometries and Fluorescence Emission Energies of Oxyluciferins

The complete active space self-consistent field (CASSCF) method and multiconfigurational second-order perturbation theory (CASPT2) have been used to study the structures and spectra of oxyluciferins (OxyLH2). The ground and lowest-lying singlet excited states geometries have been optimized using CASSCF. CASPT2 has been used to predict relaxed emission energies. The focus is on the lowest-lying singlet excited states of the anionic keto and enol forms of OxyLH2(−1) at the optimized excited-state geometries. The planar keto and enol forms of OxyLH2(−1) are minima on both the S0 and the S1 potential energy surfaces. The twisted keto and enol forms of OxyLH2(−1) are transition states on the S0 and S1 potential energy surfaces. The S1 → S0 fluorescence emission energies are in the range of 54.2−58.4 kcal/mol for the anionic planar keto forms of OxyLH2, and in the range of 55.7−63.2 kcal/mol for the anionic enol forms of OxyLH2. S0 and S1 potential energy surfaces and thus are not implicated in the emission spectra in the gas phase

Nonsmooth dynamic tracking control for nonlinear systems with mismatched disturbances: Algorithm and practice

This article addresses a dynamic tracking control issue for a class of nonlinear systems subject to mismatched disturbances. As an alternative control design algorithm for practitioners, a simple nonsmooth tracking scheme with a self-tuning scaling gain is proposed under a nonrecursive synthesis framework. In reference to the existing related works, a main distinguishable feature is that the scaling gain of the proposed regulation law can be adaptively adjusted subject to different perturbation levels; therefore, the control system is able to achieve an improved transient-time control performance while an accurate tracking objective is guaranteed. In addition, the proposed nonrecursive design philosophy is able to obtain the simplest state-feedback expression of the controller through essentially detaching the stability analysis with controller design procedure, i.e., without going through recursive determination steps of classical virtual controllers. The efficacy of the proposed method is validated by an illustrative numerical example and a real-life application to a dc-dc boost converter system

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 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 1 of 16S rRNA sequencing-based evaluation of the protective effects of Hua-Zhuo-Jie-Du on rats with chronic atrophic gastritis

Additional file 1

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