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Dental implanted materials require excellent mechanical properties, biocompatibility as well as integration with bone tissue and gingival tissue to achieve early loading and long-term stability. In this study, cubic shape sodium tantalite (ST) submicro-particles with the size of around 180 nm were synthesized by a hydrothermal method, and ST/polyetheretherketone (PEEK) composites (TPC) with ST content of 20 w% (TPC20) and 40 w% (TPC40) were prepared by melting blend. The results showed that the compressive strength, thermal properties, surface roughness, hydrophilicity and surface energy as well as adsorption of proteins on TPC40 were also significantly enhanced compared with TPC20 and PEEK. Moreover, the responses (adhesion and proliferation as well as differentiation) of rat bone marrow mesenchymal stem cells (rBMSCs), and responses (adhesion, and proliferation) of human gingival epithelial (HGE-1) cells to TPC40 were significantly promoted compared with TPC20 and PEEK. The results demonstrated that ST content in TPC had remarkable effects on the surface properties, which played key roles in stimulating the responses of both rBMSCs and HGE-1 cells. TPC40 with increased surface properties and excellent cytocompatibility might have great potential as an implanted material for dental application.

A novel poly(1,2,3-triazole) (PTA) resin was prepared from a diazide and a multialkyne. The thermal stability and degradation kinetics of the cured PTA resin were investigated with the aid of the thermogravimetric analysis (TGA) technique. The degradation temperature of the cured PTA resin reaches 360 °C (Td5). Apparent kinetic parameters of the degradation of the cured resin is obtained by using Ozawa's method. The average apparent degradation activation energies of the PTA resin are about 190 kJ/mol under nitrogen and 160 kJ/mol under air. The cured PTA resin was pyrolyzed at 400 and 570 °C separately and the pyrolysis fragments were determined by using the Py/GC/MS combined technique. The results show that the degradation of the cured PTA resin initiates at CH2 N bonds. Nitrogen and related compounds which result from the cleavage of C N and N N bonds of 1,2,3-triazole ring were found in the pyrolysis products at 570 °C but no at 400 °C. Finally, a degradation mechanism of the cured polytriazole resin was proposed.

Benzocyclobutene-terminated imides were prepared and fully characterized with 1H NMR, MS, and FT-IR. The thermal degradation of polymers was investigated by using thermogravimetric analyzer (TGA) and high-resolution pyrolysis-gas chromatography–mass spectrometry (HR-Py-GC–MS). TGA showed that thermal degradation of the polymer was a single-stage process in N2, whereas a three-stage degradation in air atmosphere. The major involved products were found to be CO2, naphthalene and naphthalene derivatives. Degradation mechanism of the polymer was suggested and the relationship between structures of the polymer and degradation products was also discussed.

Stimulation of transfected HepG2 cells (TFG2) with the alpha(1)-adrenergic agonist phenylephrine (PE) significantly activated p21(waf1/cip1) gene expression without affecting p53 gene expression. Northern blotting and reporter assay demonstrated that this induction was due to PE stimulation of p21(waf1/cip1) mRNA stability. To further define the underlying mechanism, we prepared a chloramphenicol acetyltransferase (CAT)-p21(waf1/cip1) 3'-untranslated region (3'-UTR) hybrid construct by inserting the 3'-UTR of p21(waf1/cip1) mRNA just downstream from the CAT coding sequence and transfected it into TFG2 cells. PE treatment enhanced the activity of this construct by 6-fold. Deletion analyses indicated that an AU-rich element (AURE) located between 553 to 625 within the p21(waf1/cip1) 3'-UTR was required for this induction. RNA gel shift assays demonstrated that this AURE bound an RNA-binding protein. This protein has been purified 5000-fold from PE-treated TFG2 cells by heparin-Sepharose and RNA affinity chromatography. SDS-polyacrylamide gel electrophoresis, UV cross-linking, and Northwestern analyses indicated the molecular mass of this protein as 24 and 52 kDa. Finally, PE treatment markedly enhanced this RNA-protein binding by a p42/44 mitogen-activated protein kinase-dependent mechanism. These data suggest that the AURE located between 553 and 625 within the p21(waf1/cip1) mRNA 3'-UTR, which binds an RNA-binding protein, is responsible for PE-induced p21(waf1/cip1) mRNA stability.