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The volatile content in nitrile rubber was measured by halogen moisture meter and compared with the results obtained by the hot-roll method. The influence of different measurement conditions on the measured results of the halogen moisture meter was investigated. The results showed that using the halogen moisture meter, the volatile content in nitrile rubber raw rubber could be measured by both the preset drying time method and preset mass loss method. Under suitable conditions such as sample mass of 3 g, drying temperature of 110 ℃, preset heating time of 8 min, or preset mass loss of 1/140 mg/s, the measured results were consistent with the hot-roll method. This method reduced measure time, was easy to operate, and could be used to guide quickly actual production.

In the title one-dimensional coordination polymer, {[Eu(C9H4N2O4)(C9H5N2O4)(H2O)3]·2H2O}n, one of the 1H-benzimidazole-5,6-dicarboxylate (Hbdc) ligands is protonated at the imidazole group (H2bdc). The EuIII ion is eight-coordinated by two O atoms from two Hbdc ligands, three O atoms from two H2bdc ligands and three water molecules, showing a distorted square-antiprismatic geometry. The EuIII ions are bridged by the carboxylate groups of the Hbdc and H2bdc ligands, forming a chain along [110], with an Eu...Eu separation of 5.4594 (3) Å. These chains are further connected by intermolecular O—H...O, N—H...O and N—H...N hydrogen bonds, as well as π–π interactions between the imidazole and benzene rings [centroid–centroid distances = 3.558 (3), 3.906 (2), 3.397 (3), 3.796 (2) and 3.898 (2) Å], into a three-dimensional supramolecular network.

In the title coordination polymer, [Ag(C14H8NO2)]n, the AgI cation is coordinated by two O atoms and one N atom from two symmetry-related acridine-9-carboxylate ligands in a distorted trigonal-planar geometry. The metal atoms are connected by the ligands to form chains running parallel to the b axis. π–π stacking interactions [centroid-to-centroid distances 3.757 (2)–3.820 (2) Å] and weak Ag...O interactions further link the chains to form a layer network parallel to the ab plane. The AgI cation is disordered over two positions, with refined site-occupancy factors of 0.73 (3):0.27 (3).

Abstract Objectives This study explored the response of nasopharyngeal carcinoma cells to TGF-β1-induced growth suppression and investigated the roles of the TGF-β/Smad signaling pathway in nasopharyngeal carcinoma cells. Methods The cells of nasopharyngeal carcinoma cell line CNE2 were treated with TGF-β1. The growth responses of CNE2 cells were analyzed by MTT assay. The mRNA expression and protein subcellular localization of the TGF-β/Smad signaling components in the CNE2 were determined by real time RT-PCR and immunocytochemical analysis. Results We found that the growth of CNE2 cells was not suppressed by TGF-β1. The signaling proteins TβRII, Smad 7 were expressed normally, while Smad2, Smad3, and Smad4 increased significantly at the mRNA level. TGF-β type II receptor and Smad7 had no change compared to the normal nasopharyngeal epithelial cells. In addition, Smad2 was phosphorylated to pSmad2, and the activated pSmad2 translocated into the nucleus from the cytoplasm, while the inhibitory Smad-Smad7 translocated from the nucleus to the cytoplasm after TGF-β1 stimulation. Conclusion The results suggested that CNE2 cells are not sensitive to growth suppression by TGF-β1, but the TGF-β/Smad signaling transduction is functional. Further work is needed to address a more detailed spectrum of the TGF-β/Smad signaling pathway in CNE2 cells.

Glucocorticoid (GC) inhibits testosterone production in adult Leydig cells by the glucocorticoid receptor (GR). However, whether GC affects the development of Leydig cells is unclear. The goal of the present study is to investigate the effects of GC on steroidogenesis of rat progenitor Leydig cells (PLCs) in vitro. Dexamethasone (DEX) inhibited androsterone (AO) production in PLCs. The GR antagonist RU38486 reversed the DEX-induced inhibition of AO, whereas the mineralocorticoid receptor antagonist RU28318 did not. RU38486 also reversed DEX-induced reductions in steady-state mRNA levels of steroidogenic acute regulatory protein (Star) and 3β-hydroxysteroid dehydrogenase 1 (Hsd3b1). Steroidogenic acute regulatory protein (StAR) protein expression and 3β-hydroxysteroid dehydrogenase (3βHSD) enzyme activity were affected similarly. These results show that GCs inhibit steroidogenesis of PLCs by suppression of StAR and 3βHSD via a GR-mediated mechanism.

Objectives: This study explored the response of nasopharyngeal carcinoma cells to TGF-beta1-induced growth suppression and investigated the roles of the TGF-beta/Smad signaling pathway in nasopharyngeal carcinoma cells., Methods: The cells of nasopharyngeal carcinoma cell line CNE2 were treated with TGF-beta1. The growth responses of CNE2 cells were analyzed by MTT assay. The mRNA expression and protein subcellular localization of the TGF-beta/Smad signaling components in the CNE2 were determined by real time RT-PCR and immunocytochemical analysis., Results: We found that the growth of CNE2 cells was not suppressed by TGF-beta1. The signaling proteins TbetaRII, Smad 7 were expressed normally, while Smad2, Smad3, and Smad4 increased significantly at the mRNA level. TGF-beta type II receptor and Smad7 had no change compared to the normal nasopharyngeal epithelial cells. In addition, Smad2 was phosphorylated to pSmad2, and the activated pSmad2 translocated into the nucleus from the cytoplasm, while the inhibitory Smad-Smad7 translocated from the nucleus to the cytoplasm after TGF-beta1 stimulation., Conclusion: The results suggested that CNE2 cells are not sensitive to growth suppression by TGF-beta1, but the TGF-beta/Smad signaling transduction is functional. Further work is needed to address a more detailed spectrum of the TGF-beta/Smad signaling pathway in CNE2 cells.