SUMMARY:An electroactive material with remarkable solubility, processibility as well as mechanical properties has been developed by complexation (thermal doping) of polyaniline (PANi) emeraldine base with dodecylbenzenesulfonic acid (DBSA) in the solid state. Isothermal treatment of such a mixture was found to promote the complex formation. Optimum conditions of complexation were established with respect to the formation of layered structure, electrical conductivity and solubility. The optimal temperature for the doping process was found to be in a range of 100-120°C while the best ratio of DBSA to PANi was between 3 : 1 and 4 : 1 by weight, a nearly stoichiometric equivalence of aniline repeat units and DBSA molecules. The time of isothermal treatment should be controlled within 30 min. Thermal doping induced orientation to polymer chains in a layered structure, whereby the hydrophobic tails of the surfactants function as spacers between parallel stacks of the main chains. This anisotropy was achieved by the self-assembly during the thermal doping rather than ordinary drawing or stretching of the polymers. A unique liquid crystalline mesophase with a smectic-like optical texture was observed for the soluble portions of some specimens. The excess DBSA in the samples is considered to function as a solvent and to give rise to the liquid crystalline fluidity of the phase. The scanning tunneling microscopy (STM) image 5000 x 5000 A on a submicrometer scale obtained from a P+Ni/DBSA thin film exhibit! a surface morphology with a granular size of 200-300 A. The image of 150 x 150 A on a molecular scale obtained from multilayer PANiIDBSA deposited on a highly oriented pyrolytic graphite (HOPG) surface provides a direct observation of a self-assembled structure and close layer packing of the polymer backbone with dimensions in accord with the results found by X-ray diffraction. Our results indicate that the thermal doping process of polyaniline by DBSA offers new possibilities to obtain optimal structures through a self-assembly.

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Background: Renal cell carcinoma (RCC) that originates from the proximal renal tubules is the most common cancer of the human kidney. Increasing circRNA/miRNA/mRNA networks have been found in RCC regulation. This study will explore the regulatory relation of circular RNA (circRNA) circ_0035483, microRNA-31-5p (miR-31-5p) and high mobility group A1 (HMGA1). Methods: The levels of circ_0035483, miR-31-5p and HMGA1 were measured by real-time polymerase chain reaction (qRT-PCR) or Western blot. Cell proliferation was determined using Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell migration and invasion were assessed by transwell assay. HMGA1 and epithelial-mesenchymal transition (EMT)-related protein levels were quantified using Western blot. Glycolytic metabolism was evaluated by glucose consumption and lactate production. The interaction between targets was confirmed via dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays. In vivo experiment was performed through the establishment of xenograft models in mice. Results: Circ_0035483 expression was upregulated in RCC tissues and cells. The inhibitory effects on RCC cell proliferation, migration, invasion, EMT and glycolysis were induced after circ_0035483 was downregulated. MiR-31-5p was identified as a target of circ_0035483 and miR-31-5p upregulation was related to the function of circ_0035483 knockdown in RCC cells. Additionally, miR-31-5p targeted HMGA1 and inhibited the malignant behaviors of RCC cells by negatively regulating HMGA1. Moreover, HMGA1 expression was regulated by circ_0035483 via targeting miR-31-5p. Circ_0035483 also affected tumor growth in vivo by relying on the miR-31-5p/HMGA1 axis. Conclusion:These findings clarified that the tumor-promoting function of circ_0035483 in RCC was partly achieved by regulating the miR-31-5p/HMGA1 axis.

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The aim of this study was to clarify the combined effects and dose-effect relationships of rhGH on tumor growth, nutrition status, and immune function in MKN-45 xenograft mice. In this study, animal models were induced in nude mice using the subcutaneous transplantation of MKN-45 cells, and rhGH was injected daily for 14 days. Three rhGH treatment dosages were set with reference to the equivalent dosage converted from human clinical dosage, including 2 IU (0.67 mg), 10 IU (3.35 mg) and 50 IU (16.75 mg) per kg body weight. The tumor volume, body weight and food intake were measured every two or three days. After 14 days of rhGH treatment, the tumors were isolated and weighed. The expression levels of Ki-67, vascular endothelial growth factor (VEGF) and CD31in tumor tissues were detected by immunohistochemistry (IHC). The protein expression levels of pJAK2, JAK2, pSTAT3, STAT3, pAKT, AKT, pERK and ERK were measured by western blotting. The percentage of active NK cells in peripheral blood mononuclear cells (PBMCs) was detected by fluorescence-activated cell sorting (FACS). The results showed that rhGH had improved the food intake, increased the body weight and strengthened the immune function of MKN-45 xenograft mice but had not promote tumor growth. MKN-45 xenograft mice treated with rhGH at a higher dosage gained more weight, while those treated with rhGH at a lower dosage showed stronger immune function and smaller tumor volume.