Theoretically and Experimentally Exploring the Isobaric Vapor–Liquid Associating Behavior for Binary and Ternary Mixtures Containing Methanol, Water, and Ethanoic Acid

It is a formidable dilemma for vapor–liquid equilibrium (VLE) association behavior in chemical separation procedures to correlate and predict binary and ternary mixtures containing associated components, since the form of components is completely unknown, such as monomers, homogeneous or heterogeneous dimers, trimers, and even polymers, and so on. Herein, the VLE data for the binary and ternary mixtures, including methanol, water, and ethanoic acid, were measured via the various liquid- and vapor-phase compositions using a Fisher ebulliometer at 101.33 kPa. The geometric configurations and distributions of diverse clusters in methanol, water, and ethanoic acid systems were wholly optimized at the B3LYP/6-31+G(d) level of theory using Gaussian 09. Then, we established a strategy for computing the liquid activity coefficients by pondering the various association species in the associating system. The approach is named the discrete clusters (DC) model, and the comparison is also provided between the calculating results for the binary systems of the DC model and the UNIQUAC, NRTL, and Wilson models. Moreover, the ternary system’s phase behavior was investigated by using the DC, UNIQUAC, NRTL, and Wilson models without further adjusting model parameters. The DC model conveyed the number of various clusters, indicating better consistency and a smaller deviation from the measured data. These VLE data originating from the DC model can be applied to the design and simulation of the chemical separation process of the binary and ternary association systems

CCR6 is Upregulated in Primary Human CRC Samples.

<p>(A) Immunohistochemical staining of CCR6 in primary CRC derived from 191 CRC patients with clinical stage I–IV. (B) Digital image analysis was performed to count staining intensity of CCR6 area fraction (CCR6-AF) values of paired para-tumor/tumor samples in each clinical stage, Wilcoxon test.</p

Additional file 2: of Physical interaction of STAT1 isoforms with TGF-β receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer

Figure S1. STAT1 expression in human epithelial-type ovarian tumors. Tissue microarray shows the immunohistochemical (IHC) staining of pSTAT1-Y701, pSTAT1-S727, and total STAT1 in serous, mucinous, endometrioid, transitional cell, and metastatic tumors. Figure S2. STAT1 expression in ovarian surface epithelial cells. a STAT1 mRNA expression detected by quantitative RT-PCR. b STAT1 protein expression detected by immunoblotting. c Densitometric analysis of the gels. Figure S3. Effect of TGF-β1 on the phosphorylation of STAT1. (DOCX 1304 kb

Increased Metastasis of CRC Cells with Overexpressed CCR6 <i>in vivo</i>.

<p>(A) Number of metastatic nodules (indicated by white arrows) formed in the liver of BALB/c nude mice 5 weeks after spleen injection of HCT116^Ctr (upper panel) or HCT116^CCR6 (lower panel) cells (six mice per group). (B) <i>In vivo</i> metastasis assays of Luc-HCT116^Ctr and Luc-HCT116^CCR6 cells by tail vein injection. The whole body metastasis burden of xenografted animals was monitored at 6 weeks after CRC cell injection using the IVIS Imaging System. Statistical analysis of luciferase intensity from mice injected with Luc-HCT116^Ctr or Luc-HCT116^CCR6 cells was shown in the right panel. (C) Representative images of H&E staining of lungs prepared from mice injected with Luc-HCT116^Ctr or Luc-HCT116^CCR6 cells at ×5 (left panel) and ×10 (right panel) magnification. Statistical analysis of the number or mitosis by mm² in each metastatic nodule in the five lung H&E staining from mice injected with Luc-HCT116^Ctr or Luc-HCT116^CCR6 cells was shown in the right panel. *<i>p</i><0.05, **<i>p</i><0.01, U-mann whitney test.</p

Stimuli-Responsive Nanocarrier for Co-delivery of MiR-31 and Doxorubicin To Suppress High MtEF4 Cancer

Gene interference-based therapeutics represent a fascinating challenge and show enormous potential for cancer treatment, in which microRNA is used to correct abnormal gene. On the basis of the above, we introduced microRNA-31 to bind to 3′-untranslated region of mtEF4, resulting in the downregulation of its messenger RNA and protein to trigger cancer cells apoptosis through mitochondria-related pathway. To achieve better therapeutic effect, a mesoporous silica nanoparticle-based controlled nanoplatform had been developed. This system was fabricated by conjugation of microRNA-31 onto doxorubicin-loaded mesoporous silica nanoparticles with a poly­(ethyleneimine)/hyaluronic acid coating, and drug release was triggered by acidic environment of tumors. By feat of surface functionalization and tumor-specific conjugation to nanoparticles, our drug delivery system could promote intracellular accumulation of drugs via the active transport at tumor site. More importantly, microRNA-31 not only directly targeted to mtEF4 to promote cell’s death, but had synergistic effects when used in combination with doxorubicin, and achieved excellent superadditive effects. As such, our research might provide new insights toward detecting high mtEF4 cancer and exploiting highly effective anticancer drugs

Signaling Pathway Involved in the Aggressiveness of HCT116^CCR6.

<p>(A, B) Western blotting analysis of Erk1/2 or phospho-Erk1/2 and Akt, phosphorylated Akt (Ser473) or phosphorylated Akt (Ser308) in HCT116^CCR6 and HCT116^Ctr cells. Values were expressed as fold changes relative to HCT116^Ctr, and normalized to β-actin. (C) Upregulated (FXYD5 and SYK) or down-regulated genes (CDH1, KISS1 and TIMP2) in HCT116^CCR6 cells screening with a human tumor metastasis RT² profiler PCR Array. (D) Western blotting analysis of changed FXYD5, SYK, CDH1, KISS1 and TIMP2 genes in HCT116^CCR6 and HCT116^Ctr cells. Values were expressed as fold changes relative to HCT116^Ctr, and normalized to β-actin.</p

Inhibition of Mouse CRC Progression by Targeting Tumor-expressing CCR6.

<p>(A) Western blotting analysis of CCR6 in murine CMT93 colorectal tumor cell line and CRC tissue derived from CCR6^−/− mice grafted with CMT93 at day10. (B) Statistical analysis of tumor weight in each group treated with IgG or anti-CCR6. (C) Western blotting of CCR6 in murine CT26 colorectal tumor cell line and CRC tissue derived from Balb/c mice grafted with CT26 at day 10. (D) Statistical analysis of tumor weight in each group treated with IgG or anti-CCR6. *<i>p</i><0.05, **<i>p</i><0.01, U-mann whitney test.</p

Additional file 1: of Physical interaction of STAT1 isoforms with TGF-β receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer

Table S1. PCR primer and siRNA sequence used in experiments. Table S2. Comparison of pSTAT1-Y701, pSTAT1-S727, and STAT1 immunostaining in the ovarian tissues. Table S3. The expression of pSTAT1-Y701, pSTAT1-S727, and STAT1 in human ovarian tissues. (DOCX 50 kb

Survival Analysis of CRC Patients with Low versus High Expression of CCR6.

<p>(A) Kaplan-Meier curves of CRC patients with low versus high expression of CCR6 (n = 191, <i>p</i><0.001, log-rank test). (B) Kaplan-Meier curves of CRC patients with low versus high expression of CCR6 in clinical stage I (n = 14, <i>p</i> = 0.0679, log-rank test). (C) Kaplan-Meier curves of CRC patients with low versus high expression of CCR6 in clinical stage II (n = 104, <i>p</i> = 0.0738, log-rank test). (D) Kaplan-Meier curves of CRC patients with low versus high expression of CCR6 in clinical stage III (n = 57, <i>p</i> = 0.1749, log-rank test). (E) Kaplan-Meier curves of CRC patients with low versus high expression of CCR6 in clinical stage IV (n = 16, <i>p</i> = 0.0429, log-rank test).</p

Enhanced Proliferation and Migration of CRC cells with Overexpressed CCR6.

<p>(A) Western blotting analysis of ectopic expression of CCR6 in HCT116^Ctr and HCT116^CCR6 cells or Caco-2^Ctr and Caco-2^CCR6 or SW1116^Ctr and SW1116^CCR6 cells. β-actin served as a loading control. Values were expressed as fold changes relative to controls (Ctr), and normalized to β-actin. (B) Wound-healing assay for motility of HCT116^Ctr and HCT116^CCR6 or Caco-2^Ctr and Caco-2^CCR6 or SW1116^Ctr and SW1116^CCR6 cells. Representative pictures of one field at the beginning (t = 0) (upper panel) and at the end of the recording (t = 24 h) (lower panel) in each condition are shown. The relative cell migration in CCR6 and control groups are shown in the right panel. (C) Representative images of transwell migrated cells in stably transfected HCT116^Ctr, Caco-2^Ctr, SW1116^Ctr (upper panel) or HCT116^CCR6, Caco-2^CCR6, SW1116^CCR6 (lower panel) cells. Average number of migrated cells of HCT116^Ctr and HCT116^CCR6 or Caco-2^Ctr and Caco-2^CCR6 or SW1116^Ctr and SW1116^CCR6 cells are shown in the right panel. (D) Representative image of colony formation in HCT116^Ctr, Caco-2^Ctr, SW1116^Ctr (upper panel) or HCT116^CCR6, Caco-2^CCR6, SW1116^CCR6 cells (lower panel). Values represent mean from triplicate wells, ± S.D. *<i>p</i><0.05, **<i>p</i><0.01, Wilcoxon test. Data are representative of at least three independent experiments.</p