Pengaruh Kenaikan Penghasilan Tidak Kena Pajak (Ptkp) terhadap Peningkatan Daya Beli Masyarakat di Daerah Kabupaten Kediri (Studi Kasus di Desa Sambireksik Kecamatan Gampengrejo)

Developing countries such as Indonesia\u27s state government development is necessary in order to make this country better and grow into a developed country. Income tax article 21, the biggest contributor of government revenue. Itself taxable income is income that is not taxed. Policy PTKP rise in 2013 was taken by the government for fiscal stimulus in anticipation of a global economic slowdown. The purpose of this study is the effect of the increase in taxable income to purchasing power in the region, especially the village of Kediri District Gampengrejo Sambiresik. Researchers wanted to examine the truth by raising the taxable income will increase purchasing power also appropriate government said. This type of research used in this study is a quantitative approach. Data collection techniques used questionnaire study. This study used a Likert scale scores of the questionnaire. Analysis of the data used is descriptive analysis. The results of this research is that if the independent variable (PTKP) worth (0) then the dependent variable (Purchasing Power) worth 3,938. Leverage the value of coefficient for the variable X is equal to -180. In the regression tests are sig 0.140, then H0 is accepted. Advice from research that more closely if the government wants to increase the amount of taxable income to increase purchasing power. The government can increase people\u27s purchasing power by raising the taxable income but also control the prices of basic necessities

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

New Polymorphs of Huperzine A: Preparation, Structures, and Physicochemical Properties of Anhydrous Crystal Forms

Three new polymorphs (forms I, II, and III) of natural cholinesterase inhibitor Huperzine A were discovered through a comprehensive polymorph screening experiment. Their structures were elucidated by single-crystal structure analysis and characterized by powder X-ray diffraction, Fourier transform-infrared spectroscopy, and DXR Raman microscope. The physicochemical properties of these new forms were investigated by thermal analysis (TGA and DSC) and dynamic vapor sorption (DVS) isotherms. The powder dissolution rates were compared with the marketed monohydrate form. Thermodynamic stability, phase transformation, E–T diagram, and drugability properties are also discussed in detail

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

Figure S3. CLEC3B was significantly decreased in HCC cells. (A, B) The mRNA and protein level of CLEC3B in different hepatocellular carcinoma cell lines were analyzed by real-time polymerase chain reaction (RT-PCR) (A) and western blot (B). (C) The overexpression (P = 0.0005) and knockdown (P = 0.0018) efficiency of relative mRNA expression of plasmids in HCC cells. (D) The overexpression and knockdown efficiency of protein expression of plasmids in HCC cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001; n.s., not significant. (TIF 657 kb

Additional file 13: of Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals

Table S4. The functional enrichment of KEGG pathway. (XLSX 27 kb