The present work investigated the effects of annealing on corrosion behavior, Ni2+ release, cytocompatibility, and antibacterial ability of nickel-titanium-oxygen (Ni-Ti-O) nanopores (NPs) anodically grown on nearly equiatomic NiTi alloy, aiming at optimizing annealing process to yield favorable comprehensive performance. The morphology and crystal structure of the NPs were characterized by scanning electron microscopy and X-ray diffraction respectively. It was found that when the annealing temperature was < 600 degrees C, the NP layer could be well preserved on the substrate surface, and annealed at 400 degrees C led to the transformation of amorphous phase to anatase. Annealing at 200 degrees C significantly enhanced the corrosion resistance and at 400 degrees C drastically reduced Ni2+ release of the NiTi alloy, but their cytocompatibility had no appreciable difference, indicating the release level of Ni2+ is well tolerated by osteoblasts. Although the release amount of Ni2+ is reduced after annealing especially the sample annealed at 400 degrees C, their antibacterial ability is even better when compared with that of the unannealed sample. These results suggest the NPs annealed as at 200-400 degrees C are promising as coatings of biomedical NiTi alloy.

Eaf factors play a crucial role in tumor suppression and embryogenesis. To investigate the potential mechanism of Eaf activity, we performed loss-and gain-of-function assays in zebrafish using morpholino and mRNA injections, respectively. We found that eaf1 and eaf2 inhibit Wnt/beta-catenin signaling, thereby modulating mesodermal and neural patterning in the embryo. Moreover, ectopic expression of eaf1 and eaf2 in embryos and cultured cells blocked beta-catenin reporter activity. By immunoprecipitation, we also observed that Eaf1 and Eaf2 bound to the Armadillo repeat region and C-terminus of beta-catenin, as well as to other beta-catenin transcription complex proteins, such as c-Jun, Tcf and Axin, suggesting the formation of a novel complex. In addition, the N-terminus of Eaf1 and Eaf2 bound to beta-catenin and exhibited dominant-negative activity, whereas the C-terminus appeared to either harbor a suppression domain or to recruit a repressor. Both the N- and C-terminus must be intact for Eaf1 and Eaf2 suppressive activity. Lastly, we demonstrate a conservation of biological activities for Eaf family proteins across species. In summary, our evidence points to a novel role for Eaf1 and Eaf2 in inhibiting canonical Wnt/beta-catenin signaling, which might form the mechanistic basis for Eaf1 and Eaf2 tumor suppressor activity.

A simple and sensitive liquid chromatographic method coupled with electrogenerated chemiluminescence (ECL) was described for the separation and quantification of naproxen in human urine. The method was based on the ECL of naproxen in basic NaNO3 Solution with a dual-electrode system. Factors affected the ECL emission were investigated. Under the optimal conditions, the ECL intensity has a linear relationship with the concentration of naproxen in the range of 4.0 x 10(-8) g mL(-1) to 2.0 x 10(-6) g mL(-1) and the detection limit was 1.6 x 10(-8) g mL(-1) (S/N=3). Application of the method to the analyses of naproxen in human urine proved feasible. (C) 2009 Elsevier B.V. All rights reserved.

Biocompatibility is crucial for implants. In recent years, numerous researches were conducted aiming to modify titanium alloys, which are the most extensively used materials in orthopedic fields. The application of zirconia in the biomedical field has recently been explored. In this study, the biological ZrO2 coating was synthesized on titaniumalloy (Ti6Al4V) substrates by a duplex-treatment technique combining magnetron sputtering with micro-arc oxidation (MAO) in order to further improve the corrosion resistance and biocompatibility of Ti6Al4V alloys. The microstructures and phase constituents of the coatings were characterized by scanning electron microscope (SEM) equipped with energy dispersive spectroscopy (EDS) and X-ray diffraction (XRD), the surface wettability was evaluated by contact angle measurements. The results show that ZrO2 coatings are porous with pore sizes less than 2 mu m and consist predominantly of the tetragonal ZrO2 (t-ZrO2) and cubic ZrO2(c-ZrO2) phase. Electrochemical tests indicate that the corrosion rate of Ti6Al4V substrates is appreciably reduced after surface treatment in the phosphate buffer saline (PBS). In addition, significantly improved cell adhesion and growth were observed from the ZrO2/Zr surface. Therefore, the hybrid approach of magnetron sputtering and MAO provides a surface modification for Ti6Al4V to achieve acceptable corrosion resistance and biocompatibility.

BRD4 is a member of the BET (bromodomain and extraterminal domain) family proteins that can bind acetylated histones and influence transcription, which are considered as potential therapeutic targets in many distinct diseases. And the BET inhibitor JQ1 has been proven to be effective in suppressing multiple inflammatory and autoimmune diseases. This study aimed to examine the therapeutic potential of JQ1 on a lupus model, MRL-Ipr mice. Ten-week-old MRL-Ipr mice were treated with JQ1 (oral administration of 200 mg/kg) or vehicle for 8 weeks. The proteinuria, nephritic damage, serum biochemistry, autoantibodies and cytokines were examined. Splenocytes of MRL-Ipr mice were isolated for in vitro experiments. Treatment with JQ1 significantly attenuated the progression of proteinuria and nephritis. The serum concentrations of anti-dsDNA antibody as well as B-cell activating factor (BAFF), interleukin (IL)-1 beta, IL-6, IL-17 and INF-gamma, were inhibited, and IL-10 augmented by JQ1. Importantly, JQ1 improved the survival of lupus mice. In vitro, BAFF, IL-1 beta, IL-6, IL-17 and INF-gamma were inhibited, and IL-10 augmented by JQ1 (500 nM) in the cultures of splenocytes from diseased MRL-Ipr mice, which was further supported by a significant reduction in immune complex-mediated activation of human monocytes in vitro by JQ1. Taken together, JQ1 effectively alleviates lupus in MRL-Ipr mice by suppressing BAFF, pro-inflammatory cytokines and autoimmunity, supporting the therapeutic value JQ1 in lupus disease. (C) 2015 Elsevier B.V. All rights reserved.

Captopril exhibit electrogenerated chemiluminescence (ECL) in NaNO3 solution when constant current is exerted. Based on this observation, a direct ECL method coupled with high-performance liquid chromatography (HPLC) separation is developed for determination of captopril in human serum. Factors affected the ECL emission are investigated. Under the optimal conditions, the ECL intensity has a linear relationship with the concentration of captopril in the range of 4.0 x 10(-6)-2.0 x 10(-3) g mL(-1) and the detection limit is 2 x 10(-6) g mL(-1) (S/N = 3). Compared with the common electrogenerated chemiluminescence experiments, the developed method need no any other fluorescence additives. (C) 2012 Elsevier B.V. All rights reserved.

After liver injury, regeneration manifests as either (1) hepatocytes proliferating to restore the lost hepatocyte mass or (2) if hepatocyte proliferation is compromised, biliary epithelial cells (BECs) dedifferentiating into liver progenitor cells (LPCs), which subsequently differentiate into hepatocytes. Following pharmacogenetic ablation of hepatocytes in Tg(fabp10a:CFP-NTR) zebrafish, resulting in severe liver injury, signal transducer and activator of transcription 3 (Stat3) and its target gene and negative regulator, socs3a, were upregulated in regenerating livers. Using either Stat3 inhibitors, JSI-124 and S3I-201, or stat3 zebrafish mutants, we investigated the role of Stat3 in LPC-driven liver regeneration. Although Stat3 suppression reduced the size of regenerating livers, BEC dedifferentiation into LPCs was unaffected. However, regenerating livers displayed a delay in LPC-to-hepatocyte differentiation and a significant reduction in the number of BECs. While no difference in cell death was detected, Stat3 inhibition significantly reduced LPC proliferation. Notably, stat3 mutants phenocopied the effects of Stat3 chemical inhibitors, although the mutant phenotype was incompletely penetrant. Intriguingly, a subset of socs3a mutants also displayed a lower number of BECs in regenerating livers. We conclude that the Stat3/Socs3a pathway is necessary for the proper timing of LPC-to-hepatocyte differentiation and establishing the proper number of BECs during LPC-driven liver regeneration.=20