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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.

Both fibroblast growth factor 2 (FGF2) and luteinizing hormone (LH) have been reported to regulate androgen production in Leydig cells in progenitor Leydig cells. The objective of the present study is to examine the regulation of androgen production in rat immature Leydig cells (ILCs). ILCs were isolated from 35-day-old rat testes and cultured in DMEM/F12 medium with LH (1 ng/ml) or FGF2 (10 ng/ml). 5α-Androstane-3α, 17β-diol (3α-DIOL), the primary androgen in ILCs, and testosterone (T) were measured by Radioimmuno assay. The results showed the LH stimulated androgen production in ILCs, and FGF2 did not. However, FGF2 decreased the LH-stimulated androgen production. Real-time PCR and enzyme assay showed that FGF2 decreased levels of several steroidogenic enzymes, inhibited the expressions of steroidogenic acute regulatory (StAR) protein and steroidogenic factor 1 ( Nr5a1) in LH-stimulated ILCs. FGF2-mediated inhibition of Nr5a1gene expression may be the mechanism through which FGF2 inhibits LH-stimulated androgen production. [ABSTRACT FROM AUTHOR]

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.

Androgen deprivation is commonly used in the treatment of metastatic prostate cancer. The (-)-gossypol enantiomer has been demonstrated as an effective inhibitor of Bcl-2 in the treatment of prostate cancer. However, the mechanism of gossypol as an inhibitor of androgen biosynthesis is not clear. The present study compared (+)- and (-)-gossypols in the inhibition of 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-HSD isoform 3 (17beta-HSD3) in human and rat testes. Gossypol enantiomers were more potent inhibitors of rat 3beta-HSD with IC(50)s of approximately 0.2microM compared to 3-5microM in human testes. However, human 17beta-HSD3 was more sensitive to inhibition by gossypol enantiomers, with IC(50)s of 0.36+/-0.09 and 1.13+/-0.12 for (-)- and (+)-gossypols, respectively, compared to 3.43+/-0.46 and 10.93+/-2.27 in rat testes. There were species- and enantiomer-specific differences in the sensitivity of the inhibition of 17beta-HSD3. Gossypol enantiomers competitively inhibited both 3beta-HSD and 17beta-HSD3 by competing for the cofactor binding sites of these enzymes. Gossypol enantiomers, fed orally to rats (20mg/kg), inhibited 3beta-HSD but not 17beta-HSD3. This finding was consistent with the in vitro data, in which rat 3beta-HSD was more sensitive to gossypol inhibition than rat 17beta-HSD3. As the reverse was true for the human enzymes, gossypol might be useful for treating metastatic prostate cancer.