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BACKGROUND: The tetrahydrofuran–ethanol azeotrope cannot be separated by common distillation, but can be effectively separated by extractive distillation. Extractive distillation can be simulated by Aspen Plus software. The minimum annual cost of the process can be calculated to assess ionic liquid separation ability. The interaction energy can be used to explain the separation mechanism. RESULTS: The non‐random two‐liquid model parameters of ternary mixtures for tetrahydrofuran and ethanol containing tributylmethylammonium acetate or 1‐octyl‐3‐methylimidazolium acetate were obtained. Thermodynamic property databases of tributylmethylammonium acetate, 1‐hexyl‐2,3‐dimethylimidazolium acetate and 1‐octyl‐3‐methylimidazolium acetate were established. Based on the thermodynamic model parameters and properties, the sequential iterative method was used to determine the best operating conditions and minimum total annual cost the of extractive distillation process. The interaction energy was calculated to explain the separation mechanism. CONCLUSIONS: The separation performance of tributylmethylammonium acetate is better than that of 1‐hexyl‐2,3‐dimethylimidazolium acetate or 1‐octyl‐3‐methylimidazolium acetate. The selection and design of the ionic liquids can be conducted in terms of the interaction energy. © 2023 Society of Chemical Industry (SCI). [ABSTRACT FROM AUTHOR]

The corresponding author explained that 10 mice were used in each group whilst performing liver ischemia/reperfusion experiments, but that two liver samples of the Ago-mir-NC group were damaged during embedding or sectioning, and as a result this group only contained 8 samples. Specifically, the Fig 6D Ago-mir-146a panel appeared similar to the Fig 6G Ago-mir-146a panel despite being used to represent different experimental conditions. They provided an updated Fig 6 with the correct Fig 6D Ago-mir-146a image obtained in the original experiment, as well as the individual level data underlying the published results (S1 File). [Extracted from the article]

Nectins are Ca2+‑independent immunoglobulin‑like cell adhesion molecules that belong to a family of four members that function in a number of biological cellular activities. Nectin‑4 is overexpressed in several types of human cancer; however, the functional and prognostic significance of Nectin‑4 in gastric cancer (GC) remains unclear. In the present study, the reverse transcription‑quantitative polymerase chain reaction and tissue microarray immunohistochemical analysis were used to investigate the expression of Nectin‑4 in GC as well as its function in the prognosis of patients with GC. The results indicated that mRNA and protein expression of Nectin‑4 were increased in tumor tissues compared with the matched non‑tumor tissues. Expression of Nectin‑4 was closely associated with differentiation (P=0.004), primary tumor (P=0.001), lymph node metastasis (P<0.001) and tumor‑node‑metastasis (TNM) stage (P<0.001). Positive Nectin‑4 expression (P=0.001) and advanced TNM stage (P<0.001) were demonstrated to be associated with overall survival time in multivariate analyses. These results suggest that Nectin‑4 may serve a significant function in GC and may serve as a novel clinic pathological biomarker and therapeutic target in GC. [ABSTRACT FROM AUTHOR]

Background & Aims A critical role of the Toll-like receptor ( TLR)-4 and its downstream mediators in the pathogenesis of small-for-size liver graft injury has been documented. Recently, the micro RNA-146 (miR-146) was identified as a potent negative regulator of the TLR4 signalling pathway. In this study, the role of miR-146a and miR-146b in the attenuation of TLR-4 signalling and small-for-size liver graft injury was investigated. Methods The expression levels of miR-146a and miR-146b during small-for-size liver graft injury were studied in vivo. In addition, the effects of miR-146a and miR-146b on the expression of IRAK1 and TRAF6 in the rat macrophage cell line NR8383 and rat liver kupffer cells were studied in vitro. The in vivo effect of miR-146a and miR-146b on small-for-size liver graft injury was studied by the tail vein injection of miR-146a mimics and miR-146b mimics. Results The levels of miR-146a and miR-146b decreased with a small-for-size liver graft. MiR-146a and miR-146b inhibited IRAK1 and TRAF6 expression by binding to the 3′ UTR of IRAK1 or TRAF6, respectively, in the rat macrophage cell line NR8383. The administration of miR-146a mimics and miR-146b mimics prevented liver graft injury in small-for-size liver graft injury via the inactivation of IRAK1 and TRAF6 in vivo. Conclusions miR-146a and miR-146b prevent liver injury in small-for-size liver graft injury via the inactivation of IRAK1 and TRAF6. [ABSTRACT FROM AUTHOR]

A critical role of the Toll-like receptor(TLR) and its downstream molecules, including IL-1 receptor-associated kinase 1(IRAK1) and tumor necrosis factor receptor– associated factor 6(TRAF6), in the pathogenesis of liver ischemia/reperfusion (I/R) injury has been documented. Recently a microRNA, miR-146a, was identified as a potent negative regulator of the TLR signaling pathway. In this study, we investigated the role of miR-146a to attenuate TLR signaling and liver I/R injury invivo and invitro. miR-146a was decreased in mice Kupffer cells following hepatic I/R, whereas IRAK1 and TRAF6 increased. Overexpression of miR-146a directly decreased IRAK1 and TRAF6 expression and attenuated the release of proinflammatory cytokines through the inactivation of NF-κB P65 in hypoxia/reoxygenation (H/R)-induced macrophages, RAW264.7 cells. Knockdown experiments demonstrated that IRAK1 and TRAF6 are two potential targets for reducing the release of proinflammatory cytokines. Moreover, co-culture assays indicated that miR-146a decreases the apoptosis of hepatocytes after H/R. In vivo administration of Ago-miR-146a, a stable version of miR-146a invivo, protected against liver injury in mice after I/R via inactivation of the TLR signaling pathway. We conclude that miR-146a ameliorates liver ischemia/reperfusion injury invivo and hypoxia/reoxygenation injury invitro by directly suppressing IRAK1 and TRAF6. [ABSTRACT FROM AUTHOR]

Gastric cancer (GC) is one of the most common aggressive cancers. The discovery of an effective biomarker is necessary for GC diagnosis. In this study, we confirmed that Paired box gene 4 (PAX4) is up-regulated in GC tissues and cells via quantitative real time polymerase chain reaction (qRT-PCR), western blot and immunohistochemical staining. It was also identified that PAX4 contributed to GC cell proliferation, migration and invasion through Cell Counting Kit-8, BrdU, flow cytometry assay, colony formation assay, transwell assays, and wound healing assay. miR-27b-3p was confirmed with the binding site with PAX4 using ChIP assay and served as a tumor suppressor that inhibiting GC cell growth and metastasis, and reversed the effect of PAX4. Bioinformatics prediction and dual luciferase assay results demonstrated that miR-27b-3p targeted Grb2, which could alter the function of miR-27b-3p. Furthermore, the transcriptional control of PAX4-regulated miR-27b-3p activated the Ras-ERK pathway. Taken together, the PAX4/miR-27b-3p/Grb2 loop is known to be involved in GC cell promotion, and can be seen as a promising target for GC therapy.

MicroRNAs (miRNAs) are thought to be involved in the development of cisplatin (DDP) resistance in gastric cancer (GC). Using RNA sequencing analysis (RNA-seq), we found that miR-95-3p is associated with DDP resistance in GC. We discovered that miR-95-3p is highly expressed in DDP-resistant GC tissues and cell lines (SGC7901/DDP and AGS/DDP). Furthermore, results from the BrdU and MTT assays indicated that miR-95-3p promotes GC cell proliferation. Additionally, data from transwell chamber assay, wound healing test and in vivo experiments illustrated that miR-95-3p can effectively promote invasion, migration and tumorigenic capacity, respectively, of DDP-resistant GC cells. Subsequently, results from dual luciferase assay and qRT-PCR collectively indicated that EMP1 is a target of miR-95-3p with inhibitory function through suppression of the EMT process and drug-resistance proteins. Furthermore, PI3K/AKT was identified as a downstream pathway of miR-95-3p, which promotes DDP resistance in GC. In summary, miR-95-3p helped develop DDP-resistance through down-regulation of EMP1 and increasing phosphorylation of the PI3K/Akt pathway in GC.

The aim of this study is to   investigate the effect of miRNA-92a on GC cell proliferation, migration and invasiveness, and the mechanism(s) involved.  Four GC cell lines (SGC-7901, BGC-823, MKN45 and HGC-27) and normal human gastric epithelial cells (GES1) were used in this study. MicroRNA-92a mimics or inhibitor were transfected into the cells. The results of transfection were assessed using real-time quantitative polymerase chain reaction (qRT-PCR). Cell proliferation, migration, invasiveness and apoptosis were determined using cell counting kit 8 (CCK-8), scratch test, Transwell invasion assay, and flow cytometric analysis, respectively. The protein target of miRNA-92a was predicted using Bioinformatics. The expression of FOXO1 protein was measured using Western blotting. The expression of miRNA-92a was significantly upregulated in GC cells, relative to normal gastric epithelial cells (p &lt; 0.05). Overexpression of miRNA-92a significantly promoted the proliferation, migration and invasiveness of GC cells, but significantly inhibited their apoptosis (p &lt; 0.05). MicroRNA-92a directly targeted FOXO1 gene, and significantly reduced its protein expression. Overexpression of miRNA-92a promotes the proliferation, migration and invasiveness of GC cells, and plays a role similar to that of oncogene. It directly targets FOXO1 gene by inhibiting its protein expression.

Objective: Astrocyte elevated gene-1 (AEG-1) and Cyclin D1 is associated with tumorigenesis and progression. The aim of this study is to investigate the expression of AEG-1 and Cyclin D1 in human bladder urothelial carcinoma (BUC) and explore their clinical and pathological significance., Methods: The expression of AEG-1 and Cyclin D1 protein were detected in 85 cases of human BUC and 16 cases of tumor-adjacent tissues by the immunohistochemical method., Results: The positive expression level of AEG-1 was 61.2% in human BUC which was higher than that in tumor-adjacent tissues (18.8%), P=0.002. The high expression of AEG-1 protein was correlated with the recurrence group (P=0.004). The positive rate of AEG-1 protein in superficial carcinoma group was lower than that of invasive cancer group (P=0.014). The positive expression level of Cyclin D1 was 56.5% in BUC, which was higher than that in tumor-adjacent tissues (12.5%). P=0.001. The high expression of Cyclin D1 protein was correlated with the recurrence group (P=0.024). The positive rate of Cyclin D1 protein in low grade group was lower than that of high grade group (P=0.001). The positive rate of Cyclin D1 protein in superficial carcinoma group was lower than that of invasive carcinoma group, (P=0.012). AEG-1 protein was positively correlated with Cyclin D1 protein (r=0.567, P<0.001). The log-rank test statistical analysis suggested that patients with higher AEG-1 or Cyclin D1 expression had shorter overall survival time, while patients with lower AEG-1 or Cyclin D1 expression had better survival., Conclusion: Overexpression of AEG-1 and Cyclin D1 are markedly correlated with TNM stage and recurrence of BUC. Cyclin D1 are markedly correlated with grade of BUC. Detection of AEG-1 and Cyclin D1 may be helpful to evaluate prognosis and infiltrative capability of BUC.

The cell division cycle-associated 7-like protein (CDCA7L) is a recently-identified target gene of c-Myc which can also interact with c-Myc. It is known to be upregulated in many tumors, however, its role in tumor progression remains unclear. We investigated the role of CDCA7L expression in hepatocellular carcinoma (HCC). We confirmed that CDCA7L is strongly upregulated in human HCC, and demonstrated that ectopic overexpression of CDCA7L promotes HCC cell proliferation and colony formation. Conversely, knockdown of CDCA7L inhibits these malignant phenotypes. In an in vivo model, subcutaneous transplantation of the tumor in nude mice showed that overexpression of CDCA7L can accelerate the tumor growth rate. Mechanistic analyses indicated that CDCA7L was able to activate the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and regulate the cell cycle, thus promoting HCC progression. Collectively, these findings show that CDCA7L plays a role in promoting the development of HCC and may constitute a potential therapeutic target in HCC.