The more absorbed light will lead to more charges and therefore increasing the I sc. The reason for the increase in FF can be attributed to the increased R sh as discussed above

compared to the cells without CdS. For the ITO/nc-TiO2/CdS(n)/P3HT:PCBM/Ag cells, however, with the increase of CdS LGX818 in vitro cycle number n from 5 to 15, the V oc decreased from 0.6 to 0.33 V. The I sc decreased from 5.81 to 4.9 mA/cm2 and the FF decreased from 0.50 to about 0.36. These results might be caused by the increased roughness of the ITO/nc-TiO2/CdS(n)/P3HT:PCBM/Ag cells with the increase in cycle number n. On one hand, the CdS nanocrystalline film can prevent the charge transfer back from TiO2 to the P3HT:PCBM film. On the other hand, the increased absorption selleck compound amount of CdS will increase the roughness of the ITO/nc-TiO2/CdS films as shown in Figure 2, which might lead to form small CdS nanoparticle islands instead of a uniform film. Some of these islands may not be fully covered by the P3HT:PCBM film, which leads to increased leakage current in the cells and therefore decreasing the V oc and I sc. The decrease in FF may be due to the reduced R sh, which decreased from about 67 to about 21 Ω/cm2 with the increase of n from 5 to 10 (Figure 5). Finally, the PCE of the ITO/nc-TiO2/CdS(n)/P3HT:PCBM/Ag

cells decreased from 1.57% to 0.61% (Table 1), which is still higher than that (0.15%) of the ITO/nc-TiO2/P3HT:PCBM/Ag cell. Nonetheless, our results clearly show that the PCE of the ITO/nc-TiO2/CdS(n)/P3HT:PCBM/Ag

cells increased significantly by depositing CdS on TiO2. The best PCE of 1.57% for the ITO/nc-TiO2/CdS(5)/P3HT:PCBM/Ag cell is achieved, which is about ten times that (0.15%) of the ITO/nc-TiO2/P3HT:PCBM/Ag cell. To sum up, the three main reasons for the improved efficiency of the ITO/nc-TiO2/CdS/P3HT:PCBM/Ag cells are as follows: first, the absorbance of the spectra of the ITO/nc-TiO2/CdS/P3HT:PCBM film increased significantly due to the deposited CdS QDs; second, the deposited CdS layer between the nc-TiO2 and active layer (P3HT:PCBM) can reduce the charge recombination as an energy barrier Cyclin-dependent kinase 3 layer; and third, the interfacial area increased due to the increased roughness of the ITO/nc-TiO2/CdS film compared to the ITO/nc-TiO2 without CdS QDs, which makes more excitons click here dissociate into free electrons and holes at the P3HT/CdS and P3HT/TiO2 interfaces. According to the above results, it should be expected that the efficiency of the ITO/nc-TiO2/CdS/P3HT:PCBM/Ag cell can be further improved by inserting interfacial layer materials such as PEDOT:PSS between the P3HT/PCBM layer and the anode (Ag). As an example, the I-V characteristics of the best ITO/nc-TiO2/P3HT:PCBM/PEDOT:PSS/Ag and ITO/nc-TiO2/CdS(5)/P3HT:PCBM/PEDOT:PSS/Ag devices under an AM 1.5G (100 mW/cm2) condition and in the dark are shown in Figure 6.

Appl Phys Lett 2006,17(88):172107–172107.CrossRef 32. Souza D, Kiewra JPE, Sun Y, Callegari A, Sadana DK, Shahidi G, Webb DJ: Inversion mode n-channel GaAs field effect transistor with high- k /metal gate. Appl Phys Lett 2008,15(92):153508–153508.CrossRef KPT 330 33. Adamopoulos G, Thomas S, Bradley DD, McLachlan MA, Anthopoulos TD: Low-voltage ZnO thin-film transistors based on Y 2 O 3 and Al 2 O 3 high- k dielectrics deposited by

spray pyrolysis in air. Appl Phys Lett 2011, 98:123503.CrossRef 34. Yan L, Lu HB, Tan GT, Chen F, Zhou YL, Yang GZ, Liu W, Chen ZH: High quality, high- k gate dielectric: amorphous LaAlO 3 thin films grown on Si (100) without Si interfacial layer. Fedratinib Applied Physics A 2003,5(77):721–724.CrossRef 35. Lu XB, Liu ZG, Zhang

X, Huang R, Zhou HW, Wang XP, Nguyen BY: Investigation of high-quality ultra-thin selleck kinase inhibitor LaAlO 3 films as high- k gate dielectrics. J Phys D Appl Phys 2003,36(23):3047.CrossRef 36. Gougousi T, Kelly MJ, Terry DB, Parsons GN: Properties of La-silicate high- k dielectric films formed by oxidation of La on silicon. J Appl Phys 2003,3(93):1691–1696.CrossRef 37. Mahata CM, Bera K, Das T, Mallik S, Hota MK, Majhi B, Verma S, Bose PK, Maiti CK: Charge trapping and reliability characteristics of sputtered Y 2 O 3 high- k dielectrics on N- and S-passivated germanium. Semicond Sci Technol 2009,8(24):085006.CrossRef 38. Pan TM, Lei TF, Chao U0126 molecular weight TS, Chang KL, Hsieh KC: High quality ultrathin

CoTiO 3 high- k gate dielectrics. Electrochem Solid-State Lett 2000,9(3):433–434. 39. Kim SK, Kim KM, Kwon OS, Lee SW, Jeon CB, Park WY, Hwang CS, Jeong J: Structurally and electrically uniform deposition of high- k TiO 2 thin films on a Ru electrode in three-dimensional contact holes using atomic layer deposition. Electrochem Solid-State Lett 2005,12(8):F59-F62.CrossRef 40. Abermann S, Pozzovivo G, Kuzmik J, Strasser G, Pogany D, Carlin JF, Grandjean N, Bertagnolli E: MOCVD of HfO 2 and ZrO 2 high- k gate dielectrics for InAlN/AlN/GaN MOS-HEMTs. Semicond Sci Technol 2007,12(22):1272.CrossRef 41. Adamopoulos G, Thomas S, Wöbkenberg PH, Bradley DD, McLachlan MA, Anthopoulos TD: High-mobility low-voltage ZnO and Li-doped ZnO transistors based on ZrO 2 high- k dielectric grown by spray pyrolysis in ambient air. Adv Mater 2011,16(23):1894–1898.CrossRef 42. Gaskell JM, Jones AC, Aspinall HC, Taylor S, Taechakumput P, Chalker PR, Heys PN, Odedra R: Deposition of lanthanum zirconium oxide high- k films by liquid injection atomic layer deposition. Appl Phys Lett 2007,11(91):112912–112912.CrossRef 43. Gaskell JM, Jones AC, Chalker PR, Werner M, Aspinall HC, Taylor S, Taechakumput P, Heys PN: Deposition of lanthanum zirconium oxide high- k films by liquid injection ALD and MOCVD. Chem Vap Depos 2007,12(13):684–690.CrossRef 44.

Tumor animal models Male athymic nude mice (6-8 wk old, 18-22 g) were housed in a pathogen-free mouse colony and provided with sterilized #CHIR98014 mw randurls[1|1|,|CHEM1|]# pellet chow and sterilized water. All experiments were performed in accordance with the guidelines of the Animal Care Committee of the hospital. SMMC-7721 cells were treated with trypsin when near confluence and harvested. Cells were pelleted by centrifugation at 1200 rpm for 5 min and resuspended in sterile culture medium, then

implanted subcutaneously into the flank of the mice (2 × 106 cells per animal). The mice were subjected to optical imaging studies when the tumor volume reached 0.5~1.8 cm in diameter. Immunocytochemical and immunohistochemical analysis To investigate the expression of Sp17 in the SMMC-7721 and HO8910 cell lines, cells were cultured on a coverglass and then fixed with cooled acetone. Anti-Sp17 monoclonal antibody was then added at a concentration of 2 μg/ml and incubated overnight at 4°C. The primary antibody was detected with anti-mouse IgG labeled with horseradish peroxidase (DAKO). Diaminobenzidine (DAB) substrate was added for 7 min followed by washing with deionized water and hematoxylin was applied for

1 min to counterstain the cell on slices. DNA Damage inhibitor Then the cell slices were dehydrated via graded ethanols followed by xylene and coverslips were attached with permount. why The immunocytochemical reaction turned brown and was observed using a light microscope. Tumor tissue sections (3 μm) from mouse model were placed on glass slides, heated at 60°C for 20 min, and then

deparaffinized with xylene and ethanol. For antigen retrieval, tumor specimens mounted on glass slides were immersed in preheated antigen retrieval solution (DAKO high pH solution; DAKO) for 20 min and cooled for 20 min at room temperature. After the inactivation of endogenous peroxidase, the tissue slices were treated with anti-Sp17 monoclonal antibody and unrelated monoclonal antibody (mose anti-Candida enolase) with the same protocol as immunocytochemistry. Synthesis of anti-Sp17-ICG-Der-02 The synthesis of the anti-Sp17-ICG-Der-02 complex was conducted in three consecutive steps: First, the dye (1 mg, 0.001 mmol) was dissolved in H2O (0.5 ml) and mixed with the catalysts EDC (2.90 mg, 0.015 mmol) and NHS (1.73 mg, 0.015 mmol) (GL Biochem Co. Ltd, Shanghai, China) for the activation of the carboxylic acid functional group for about 4 h at room temperature. Next, the active ICG-Der-02 solution was added dropwise to 50 μl (200 μg) anti-Sp17 solution and then stirred at 4°C for 10 h in the dark. The reaction was quenched by adding 200 μl of 5% acetic acid (HOAc). Finally, the mixture was dialyzed (molecular weight cutoff 10 kDa) against 0.1 mol/L phosphate buffer solutions (pH = 8.3) until no free dye dialyzed out.

% of Si, respectively. Figure 4e shows results of thermal emission quenching at 488-nm excitation wavelength for a sample with 39 at.% Ruboxistaurin of Si. It can be seen that the Er3+-related emission is also characterized by two quenching energies equal to about 20 and 60 meV. These values are almost the same as for 266-nm excitation and very similar to VIS emission where values of 15 and 70 meV have been obtained. This indicates that in this case also, we deal with indirect excitation of Er3+ ions. Since 488 nm corresponds also to direct excitation of Er3+ ions, most probably, we deal with both kinds of excitation simultaneously. We believe, however, that indirect excitation is in this

case dominant. Nevertheless, the results obtained at this excitation wavelength for 37 at.% of Si are not so obvious. In this case, two statistically equal

fits with one (20 meV) and two energies (20 and 6 meV) were possible to achieve. The higher MRT67307 cost energy is clear and has the same origin as in the previous cases. One explanation of this fact would be the excitation spectrum for this sample where its edge is much shifted to blue as compared to samples with 39 at.% of Si. Thus, in this case, we can indeed observe a major contribution from a direct excitation of Er3+ ions rather than via intermediate states. Conclusions The existence of efficient excitation transfer from silicon nanoclusters to Er3+ ions has been shown for SRSO thin films deposited by ECR-PECVD

by means of PL, TRPL, PLE and temperature-dependent MM-102 concentration PL experiments. However, it has been shown that for our samples, this energy transfer is most efficient at high excitation energies. Epothilone B (EPO906, Patupilone) Much less efficient energy transfer has been observed at 488-nm excitation. In this case, depending on Si nanocluster size, we deal with dominant contribution to Er3+ excitation from indirect excitation channel (big nanoclusters) or from direct excitation of Er3+ ions (small nanoclusters). Moreover, it has been shown that a wide emission band in the VIS spectral range is a superposition of three emission sub-bands coming from spatially resolved objects with very different kinetics: a band at around 450 nm, with 20-ns decay, which is not changing with Si content and is related with optically active defect states and STE in SRSO matrix; a band at approximately 600 nm related to aSi-NCs with hundred-microsecond emission decay and strong dependence on Si content following the predictions of quantum confinement model; and a third band at around 800 nm (1.54 eV) (Si-NCs, defects) with either very fast (<3 ns) or very slow (>100 μs) emission kinetics, also depending on Si content. Additionally, it has been shown that two Er3+ sites are present in our samples: isolated ions and clustered ions with emission decay times of approximately 3 and <1 ms, respectively. Acknowledgments AP would like to acknowledge the financial support from the Iuventus Plus program (no. IP2011 042971).

PubMed 53. Pfaffl MW: A new mathematical model for relative quantification in real-time RT-PCR. Nucleic Acids Res 2001, 29:e45.PubMedCrossRef Authors’ contributions RFT and ECM performed and designed experiments, and interpreted data. TFK designed experiments and interpreted the data. PWOT designed experiments, analyzed data and co-wrote the manuscript. JCC conceived the study, designed the experiments, interpreted the data and co-wrote the manuscript. All authors read and approved the final manuscript.”
“Background

Gram-negative proteobacteria deploy various types of protein secretion systems for exporting selected sets of proteins to the cell surface, the extracellular space or into host cells [1, 2]. Type III Secretion Systems (T3SS) are directly related to pathogenicity click here or to symbiosis with higher organisms and constitute essential mediators of the interactions between gram-negative bacterial cells

and eukaryotic ones [3–8] as the T3SS efficiently translocates bacterial proteins (effectors) directly into the host cell cytoplasm when fully developed. The T3SS apparatus comprises three distinct parts: a) the basal body, which forms a cylindrical base that penetrates the two bacterial membranes and the periplasmic space; b) the extracellular part with the needle or the pilus as its main feature which is formed through the polymerization of specialized protein subunits that are T3SS substrates themselves; and c) the cytoplasmic GW-572016 cost part, which forms the export gate for

secretion control. This apparatus is built by specific core proteins encoded by a conserved subset of genes tightly organized in gene clusters with counterparts in the bacterial flagellum [6, 7]. PhyloSelleckchem AR-13324 genetic analyses of 3-oxoacyl-(acyl-carrier-protein) reductase the core T3SS proteins revealed that the T3S systems evolved into seven distinct families that spread between bacteria by horizontal gene transfer. (1) The Ysc-T3SS family, named after the archetypal Yersinia system, is present in α-, β-, γ-, and δ- proteobacteria. At least in α-proteobacteria the system confers resistance to phagocytosis and triggers macrophage apoptosis. (2) The Ssa-Esc-T3SS family is named after the archetypal T3SS of enteropathogenic and enterohemorrhagic E.coli. (3) The Inv-Mxi-Spa-T3SS family named after the Inv-Spa system of Salmonella enterica and the Inv-Mxi T3S system of Shigella spp. The family members trigger bacterial uptake by nonphagocytic cells.(4) The Hrc-Hrp1- and (5) the Hrc-Hrp2-T3SS families are present in plant pathogenic bacteria of the genus Pseudomonas, Erwinia, Ralstonia and Xanthomonas. The two families are differentiated on the basis of their genetic loci organization and regulatory systems. (6) The Rhizobiales-T3SS family (hereafter referred to as Rhc-T3SS) is dedicated to the intimate endosymbiosis serving nitrogen fixation in the roots of leguminous plants. (7) Finally the Chlamydiales-T3SS is present only in these strictly intracellular nonproteobacteria pathogens [8, 9].

Node

supports are shown by posterior probabilities from Bayesian inferences. Figure S3. SMART outputs representing the number of ANK motifs found in Pk1 translated sequences. Figure S4. SMART outputs representing the number of ANK motifs found in Pk2 translated sequences. Table S1. List of primers used in this study for sequencing (PCR), for expression analyses (RT-PCR), or for Southern blots (SB). Expected PCR product size in base pair (bp) was calculated relative to the wVulC reference sequences. BI 10773 Table S2. List of pk1 and pk2 sequences used for Figure 1, Additional file 1 : Figure S3 and Additional file 1 : Figure S4. Accession numbers from this study are in bold. (DOC 2 MB) References 1. Baldo L, Dunning Hotopp JC, Jolley KA, et al.: Multilocus sequence typing system for the endosymbiont Wolbachia pipientis. Appl Environ Microbiol 2006, 72:7098–7110.PubMedCrossRef 2. Bouchon D, Cordaux R, Grève P: Feminizing Wolbachia and the evolution of sex determination in isopods. In Insect Symbiosis. Edited by: Bourtzis K, Miller TA. Taylor & Francis Group, Boca Raton; 2008:273–294.CrossRef 3. Hilgenboecker K, Hammerstein P, Schlattmann P, Telschow A, Werren JH: How many species are infected with Wolbachia? A statistical analysis AG-881 in vitro of current data. FEMS Microbiol Lett 2008, 281:215–220.PubMedCrossRef 4.

Taylor MJ, Bandi C, Hoerauf A: Wolbachia bacterial endosymbionts of filarial nematodes. Adv Parasitol 2005, 60:245–284.PubMedCrossRef 5. Bourtzis K: Miller TA: Insect Symbiosis. Taylor & Francis Group, Boca Raton; 2003.CrossRef 6. Werren JH: Biology of Wolbachia. Annu Rev Entomol 1997, 42:587–609.PubMedCrossRef 7. Foster J, Ganatra M, Kamal I, et al.: The Wolbachia LY3039478 in vivo Genome of Brugia malayi: endosymbiont evolution within a human pathogenic nematode. PLoS Biol 2005, 3:e121.PubMedCrossRef 8. Klasson L, Walker T, Sebaihia M, et al.: Genome evolution of Wolbachia

strain wPip from the Carnitine palmitoyltransferase II Culex pipiens group. Mol Biol Evol 2008, 25:1877–1887.PubMedCrossRef 9. Klasson L, Westberg J, Sapountzis P, et al.: The mosaic genome structure of the Wolbachia wRi strain infecting Drosophila simulans. Proc Natl Acad Sci USA 2009, 106:5725–5730.PubMedCrossRef 10. Salzberg SL, Dunning Hotopp JC, Delcher AL, et al.: Serendipitous discovery of Wolbachia genomes in multiple Drosophila species. Genome Biol 2005, 6:R23.PubMedCrossRef 11. Wu M, Sun LV, Vamathevan J, et al.: Phylogenomics of the reproductive parasite Wolbachia pipientis wMel: a streamlined genome overrun by mobile genetic elements. PLoS Biol 2004, 2:e69.PubMedCrossRef 12. Bork P: Hundreds of ankyrin-like repeats in functionally diverse proteins: mobile modules that cross phyla horizontally? Proteins 1993, 17:363–374.PubMedCrossRef 13. Li J, Mahajan A, Tsai M-D: Ankyrin repeat: a unique motif mediating protein-protein interactions. Biochemistry 2006, 45:15168–15178.PubMedCrossRef 14.

PubMedCrossRef 41. Douillard JY, Rosell R, De Lena M, Riggi M, Hurteloup P, Mahe MA: Impact of postoperative radiation therapy on survival in patients with complete resection and stage I, II, or IIIA non-small-cell lung cancer treated with this website Adjuvant chemotherapy: the adjuvant Navelbine International Trialist Association (ANITA) Randomized Trial. Int J Radiat Oncol Biol Phys 2008, 72:695–701.PubMedCrossRef 42. Lally BE, Detterbeck FC, Geiger AM, Thomas CR Jr, Machtay M, Miller AA, Wilson LD, Oaks TE, Petty WJ, Robbins ME, Blackstock AW: The risk of death from heart disease in patients with nonsmall cell lung

cancer who receive postoperative radiotherapy: analysis of the Surveillance, Epidemiology, and End Results database. Cancer 2007, 110:911–917.PubMedCrossRef 43. Matsuguma H, Nakahara R, Ishikawa Y, Suzuki H, Inoue K, Katano S, Yokoi K: Postoperative radiotherapy for patients with completely resected pathological stage IIIA-N2 non-small cell lung BAY 1895344 ic50 cancer: focusing on an effect of the number of mediastinal lymph node stations involved. Interact Cardiovasc Thorac Surg 2008, 7:573–577.PubMedCrossRef 44. Sawyer TE, Bonner JA, Gould PM, Foote RL, Deschamps C, Trastek VF, Pairolero PC, Allen MS, Lange CM, Li H: Effectiveness of postoperative irradiation in stage IIIA non-small cell lung cancer according to regression tree analyses of recurrence risks. Ann Thorac Surg 1997, 64:1402–1407.

discussion 1407–1408PubMedCrossRef 45. Pepe C, Hasan B, selleck screening library Winton TL, Olopatadine Seymour L, Graham B, Livingston RB, Johnson DH, Rigas JR, Ding K, Shepherd FA: Adjuvant vinorelbine and cisplatin in elderly patients: National Cancer Institute of Canada and Intergroup Study JBR.10. J Clin Oncol 2007, 25:1553–1561.PubMedCrossRef 46. Fruh M, Rolland E,

Pignon JP, Seymour L, Ding K, Tribodet H, Winton T, Le Chevalier T, Scagliotti GV, Douillard JY, et al.: Pooled analysis of the effect of age on adjuvant cisplatin-based chemotherapy for completely resected non-small-cell lung cancer. J Clin Oncol 2008, 26:3573–3581.PubMedCrossRef 47. Fervers B: Chemotherapy in elderly patients with resected stage II-IIIA lung cancer. BMJ 343:d4104. 48. Alam N, Shepherd FA, Winton T, Graham B, Johnson D, Livingston R, Rigas J, Whitehead M, Ding K, Seymour L: Compliance with post-operative adjuvant chemotherapy in non-small cell lung cancer. An analysis of National Cancer Institute of Canada and intergroup trial JBR.10 and a review of the literature. Lung Cancer 2005, 47:385–394.PubMedCrossRef 49. Strauss GM, Herndon JE, Maddaus MA, Johnstone DW, Johnson EA, Watson DM, Sugarbaker DJ, Schilsky RA, Vokes EE, Green MR, The Calgb RTOG: Adjuvant chemotherapy in stage IB non-small cell lung cancer (NSCLC): Update of Cancer and Leukemia Group B (CALGB) protocol 9633. ASCO Meeting Abstracts 2006, 24:7007. 50. Besse B, Le Chevalier T: Adjuvant chemotherapy for non-small-cell lung cancer: a fading effect? J Clin Oncol 2008, 26:5014–5017.PubMedCrossRef 51.

To date, single-walled carbon nanotubes (SWNTs) were fully investigated for photoacoustic imaging [30]. For example, for cell imaging, Avti et al. adopted photoacoustic microscopy to detect, map, and quantify the trace amount of SWNTs in different histological C59 wnt datasheet tissue specimens. The results showed that noise-equivalent detection sensitivity was as low as about 7 pg [31]. For in vivo PA imaging, Wu et al. adopted RGD-conjugated SWNTs as a PA contrast agent, and strong PA signals could be observed from the tumor in the SWNT-RGD-injected group [32]. With

the aim of enhancing the sensitivity of the PA signal of SWNTs, Kim et al. developed one kind of gold nanoparticle-coated SWNT by depositing a thin layer of gold nanoparticles MK-8776 in vivo around check details the SWNTs for photoacoustic imaging in vivo and obtained enhanced NIR PA imaging contrast (approximately 102-fold) [33–35]. However, to date, few reports are closely associated with the use of multiwalled carbon nanotubes (MWNTs) as a PA contrast agent. Therefore, it is very necessary to investigate the feasibility and effects of the use of MWNTs and gold nanorod-coated MWNTs as PA contrast agents. In addition, CNT-based in vivo applications have to consider their toxicity [36]. How to decrease

or eliminate their cytotoxicity has become a great challenge. How to develop one kind of safe and effective NIR absorption enhancer MWNT has become our concern. Gold nanorods (GNRs), because of their small size, strong light-enhanced absorption in the NIR, and plasmon resonance-enhanced properties, have become attractive noble nanomaterials for their potential in applications such as photothermal therapy [37], biosensing [38], PA imaging [39], and gene delivery [40] for cancer treatment. However, the toxicity derived from a large amount of the surfactant cetyltrimethylammonium bromide (CTAB) during GNR synthesis severely ioxilan limits their biomedical applications. Therefore,

removal of CTAB molecules on the surface of GNRs is an important step to avoid irreversible aggregation of GNRs and enhance their biocompatibility. In our previous work, we used a dendrimer to replace the CTAB on the surface of GNRs, markedly decreasing the toxicity of GNRs, and realized the targeted imaging and photothermal therapy [41]. We also used folic acid-conjugated silica-modified GNRs to realize X-ray/CT imaging-guided dual-mode radiation and photothermal therapy. Silica-modified GNRs can markedly enhance the biocompatibility of GNRs [42–44]. In recent years, molecular imaging has made great advancement. Especially, the system molecular imaging concept has emerged [45], which can exhibit the complexity, diversity, and in vivo biological behavior and the development and progress of disease in an organism qualitatively and quantitatively at a system level.

Statistical analysis All quantitative data were expressed as mean ± SD and analyzed find more using a one-way analysis of variance (ANOVA). All statistical analyses were carried out using the SPSS statistical software package (version 11.0, SPSS Inc. Chicago, USA). P < 0.05 was considered statistically significant. Results Activation

of AhR pathway by DIM To test whether the AhR signal pathway could be activated by DIM, we treated the gastric cancer cell line SGC7901 with DIM. RT-PCR and Western blot analysis showed that after DIM treatment, AhR protein in the total cell lysates gradually decreased (Figure 1). CYP1A1, a classic target gene of AhR, was utilized as an indicator of AhR signal pathway activation. The baseline level of CYP1A1 expression was not observed in SGC7901 cells, but both CYP1A1 mRNA and protein expression were increased in a dose- and time-dependent manner following DIM treatment (Figure 1). To further confirm the DIM-induced CYP1A1 expression was AhR-dependent, we treated SGC7901 cells with a specific AhR antagonist, resveratrol [16, 17]. cells were treated with DIM (30 μmol/L)

only or DIM (30 μmol/L) plus different concentrations of resveratrol (0, 1, 5, 10, 20 μmol/L), respectively for 6 h (Figure 2). In concordance with previous results, treatment of SGC7901 cells with 30 μmol/L DIM caused Staurosporine a Aurora Kinase inhibitor remarkable increase in CYP1A1 expression. However, this DIM-induced CYP1A1 expression was partially reversed by resveratrol in a dose-dependent manner (Figure 2A and B). Figure 1 AhR and CYP1A1 expression in SGC7901 cells after DIM treatment. A and B: RT-PCR; C and D: Western blotting. Treatment of SGC7901 cells with AhR modulator DIM resulted in a time – (A and C) and concentration -dependent (B and D) induction of CYP1A1 expression. The results shown are representative of three independent experiments. Figure 2 Inhibition of DIM -induced CYP1A1 mRNA and protein expression by resveratrol. enough A: CYP1A1 mRNA was detected by RT-PCR; B: CYP1A1 protein was detected by Western

blotting. RSV: resveratrol . The results shown are representative of three independent experiments. Treatment of SGC7901 cells with 30 μmol/L DIM caused a remarkable increase in CYP1A1 expression. This DIM-induced CYP1A1 expression was partially reversed by resveratrol in a concentration-dependent manner. Effect of DIM on cellur proliferation Proliferation of SGC7901 cells was determined by MTT assay after 6–72 h of treatment with increasing concentrations of DIM (0–50 μmol/L). Results showed that DIM inhibited SGC7901 cellular proliferation in a concentration- and time-dependent manner, Resveratrol (10 μmol/L) could partially reverse the inhibition effects of DIM (30 μmol/L) on cellur proliferation at the time points: 6 h and 12 h (Figure 3), but we did not find the reversal effects at other time points (24 h, 48 h and 72 h, data were not shown). Figure 3 Viability of SGC7901 cells after DIM treatment was assessed by MTT assay.

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