996 research outputs found

    3D hydrogel-based salt resistant self-floating solar-driven interfacial evaporator with efficient water-lifting capacity for desalination

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    Solar desalination has been extensively researched as a promising way to address freshwater shortages. However, developing a salt resistant solar evaporator that can be easily extended and manufactured is still a challenge in practical applications. In this work, a 3D hydrogel-based salt resistant self-floating solar-driven interfacial evaporator with efficient water-lifting capacity was proposed using the prepared hydrogel with carbon black (CB) nanoparticles and extruded polystyrene (XPS) board as raw materials. The experimental results implied that the developed evaporator had the highest evaporation rate and evaporation efficiency at 0.05 g CB loading, which were 1.70 kg m- 2h- 1 and 92.8 % at a light intensity of 1 kW m- 2. Moreover, the evaporator also displayed prominent salt resistance in the evaporation of brine with high salinity and outstanding stability after 10 cycles. Significantly, the outdoor experiment demonstrated that 1 m2 evaporator can generate 5923.5 g freshwater per day, which was enough to meet the daily requirement of two adults for drinking water. In addition, the physical fields of the hydrogel with CB nanoparticles of the evaporator at evaporation equilibrium were simulated to analyze its long-term and high-performance operation capability. All in all, the 3D hydrogel-based salt resistant self-floating solar-driven interfacial evaporator with efficient water-lifting capacity presented an enormous application prospect in the field of solar desalination

    sj-pdf-1-jva-10.1177_11297298221115003 – Supplemental material for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis

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    Supplemental material, sj-pdf-1-jva-10.1177_11297298221115003 for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis by Yunfeng Li, Zhenwei Shi, Yunyun Zhao, Zhengli Tan, Hongxia Guo and Zhaoxuan Lu in The Journal of Vascular Access</p

    sj-pdf-2-jva-10.1177_11297298221115003 – Supplemental material for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis

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    Supplemental material, sj-pdf-2-jva-10.1177_11297298221115003 for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis by Yunfeng Li, Zhenwei Shi, Yunyun Zhao, Zhengli Tan, Hongxia Guo and Zhaoxuan Lu in The Journal of Vascular Access</p

    sj-pdf-3-jva-10.1177_11297298221115003 – Supplemental material for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis

    No full text
    Supplemental material, sj-pdf-3-jva-10.1177_11297298221115003 for Comparative effectiveness and safety among different tip-design hemodialysis long-term catheters: A meta-analysis by Yunfeng Li, Zhenwei Shi, Yunyun Zhao, Zhengli Tan, Hongxia Guo and Zhaoxuan Lu in The Journal of Vascular Access</p

    Downregulation of survivin by RNAi inhibits the growth of esophageal carcinoma cells.

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    Esophageal squamous cell carcinoma ranks among one of the most frequent cause of cancer death in the world. Understanding of the molecular mechanisms involved in the pathogenesis of esophageal cancer becomes critical to develop more effective treatments. Elevated expression of survivin in esophageal carcinoma has been reported before and suppression of survivin expression leads to many tumor cells growth inhibition. We hypothesized that downregulation of survivin would inhibit the growth of human esophageal cancer cells. RNA interference directed against survivin was introduced into a human esophageal squamous cell carcinoma cell line KYSE510. Stable clones were selected and western blot analysis was performed to detect the protein level of survivin. Tumor cell growth in vitro and in vivo was assessed by trypan blue exclusion and nude mice experiments. Annexin V/propidium iodide staining followed by flow cytometric analysis and TUNEL assay were used to detect apoptosis in cell culture and in nude mice. We found that RNA interference could efficiently and stably suppress survivin expression in KYSE510 cells. Downregulation of survivin resulted in significantly inhibition of tumor growth in vitro and in vivo. The mechanism appears to be increased induction of apoptosis. Our results suggest a potential role for the targeting of survivin in the treatments of esophageal carcinoma

    Asynchronous fracture of hierarchical microstructures in hard domain of thermoplastic polyurethane elastomer: Effect of chain extender

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    Four chain extenders, 1,3-propanediol (PDO), 2-methyl-1,3-propanediol (MPO), 2,2-dimethyl-1,3-propanediol (NPG) and 2,2,4,4-tetramethyl-1,3-cyclobutanedio (CBDO) are chosen to synthesize model polyurethanes, respectively. Although with similar oxygen distance between the two hydroxyl groups, their volumes increase gradually according to computer simulation. As expected, the degree of microphase separation decreases with the increasing chain extender volume. Except for CBDO based polyurethane, the other three samples show systematic variations in mechanical properties. Various techniques including single-molecule force spectroscopy (SMFS), small-angle X-ray scattering (SAXS) and Fourier transform infrared spectroscopy (FTIR) are employed to investigate the structural changes after tensile break in different length scales. A picture of asynchronous fracture of microstructures during the tensile break of thermoplastic polyurethane elastomers can be obtained by the combination of different analytical methods. It is interesting to note that the macroscopic break may not affect the state of hydrogen bonding or the hard phase network. Sometimes, the hydrogen bonding state changes a lot while the phase network keeps almost the same, or vice versa. (C) 2018 Elsevier Ltd. All rights reserved

    Accumulation of cytoplasmic beta-catenin correlates with reduced expression of E-cadherin, but not with phosphorylated Akt in esophageal squamous cell carcinoma: immunohistochemical study

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    Accumulation of β-catenin in cytoplasm occurs frequently during the pathogenesis of esophageal squamous cell carcinoma (ESCC). The mechanism leading to this alteration, however, is largely unknown. In the present study, immunohistochemistry was performed for β-catenin, E-cadherin and Ser473 phosphorylated Akt (P-Akt) in 44 tissue samples of ESCC and corresponding normal esophageal epithelium. Exon 3 of the β-catenin gene was analyzed by using single-strand conformation polymorphism and direct sequencing. In addition to the reduced expression of E-cadherin and membranous β-catenin observed in 65.9% and 68% of ESCC tested, respectively, cytoplasmic accumulation of β-catenin was also detected in 68% (30/44) cases. However, only two cases were found to have the same β-catenin gene mutation. The data showed that cytoplasmic accumulation of β-catenin was significantly associated with reduced expression of E-cadherin (P &lt; 0.05) and that of membranous β-catenin (P &lt; 0.05). Furthermore, cytoplasmic β-catenin was correlated significantly with lymph node metastasis (P &lt; 0.05). In contrast, although strong staining of P-Akt occurred in 14 of 44 cases (32%), there was no significant correlation between the positive staining of P-Akt and cytoplasmic β-catenin. Taken together these results suggest that the lost membranous β-catenin might translocate to cytoplasm depending on reduced expression of E-cadherin, while Akt seems unlikely to play a role in this process

    Krüppel-like factor 4 represses transcription of the survivin gene in esophageal cancer cell lines

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    Aberrant expression of survivin has been shown to be regulated at the transcription level in cancer cells. In this study, we demonstrate that there are six putative binding sites of Krüppel-like factor 4 (KLF4) within the 2000-bp region upstream of the transcription start site of the human survivin gene. Luciferase reporter gene assays revealed that survivin promoter activity is repressed upon overexpression of KLF4 in EC9706 cells. A chromatin immunoprecipitation assay indicated that KLF4 indeed binds the survivin promoter in vivo. It specifically binds the site located at position -40 among the six binding sites as determined by electrophoretic mobility shift assay. Ectopic expression of KLF4 decreases the mRNA and protein levels of survivin. Furthermore, overexpression of survivin partially reverses KLF4-induced cell apoptosis. These results indicate that KLF4 is a transcriptional repressor of the human survivin gene in esophageal squamous cancer cells

    ?-Catenin/TCF pathway upregulates STAT3 expression in human esophageal squamous cell carcinoma

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    Precise roles of ?-catenin/TCF pathway involved in esophageal tumorigenesis remain elusive. Here we found STAT3 overexpression in esophageal cancer cells and tissues, and its overexpression in esophageal squamous cell carcinoma (ESCC) tissues correlated with ?-catenin cytoplasmic/nuclear accumulation. A functional TCF binding element was detected in STAT3 promoter which specifically bound to TCF4. Transfected ?-catenin induced STAT3 transcriptional activity dose-dependently, and also enhanced STAT3 mRNA and protein levels. These inductions were specifically abolished by dominant-negative TCF4. These results suggest that STAT3 is a target of ?-catenin/TCF pathway and might participate in esophageal tumorigenesis
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