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phase III study of gemcitabine in combination with radiation therapy versus gemcitabine alone in patients with localized, unresectable pancreatic cancer: E4201 [abstract]. J Clin Oncol 2008, 26:a4506. 16. Ioka T, Nakamura S, Nishiyama K: A randomized phase II study of gemcitabine 1000 mg/msq and concurrent radiotherapy comparing gemcitabine alone for unresectable locally advanced pancreatic adenocarcinoma [abstract]. Int J Radiat Oncol Biol Phys 2010, 78:S102.CrossRef 17. Hoyer M, Roed H, Sengelov L, Traberg A, Ohlhuis L, Pedersen J, Nellemann H, Berthelsen BGB324 cost A, Eberholst F, Engelholm SA, von der Maase H: Phase-II study Selleckchem Luminespib on stereotactic radiotherapy of locally advanced pancreatic carcinoma. Radiother Oncol 2005, 76:48–53.PubMedCrossRef 18. Mahadevan A, Jain S, Goldstein M, Miksad R, Pleskow D, Sawhney M, Brennan D, Callery M, Vollmer C: Stereotactic body radiotherapy and gemcitabine for locally advanced pancreatic cancer. Int J Radiat Oncol Biol Phys 2010, 78:735–742.PubMedCrossRef 19. Schellenberg D, Kim J, Christman-Skieller C, Chun CL, Columbo

LA, Ford JM, Fisher GA, Kunz PL, Van Dam J, Quon A, Desser TS, Norton J, Hsu A, Maxim PG, Xing L, Goodman KA, Chang DT, Koong AC: Single-fraction stereotactic body radiation therapy and sequential gemcitabine for the treatment of locally advanced pancreatic cancer. Int J Radiat Oncol Biol Phys 2011, 81:181–188.PubMedCrossRef 20. Polistina F, Costantin G, Casamassima F, Francescon P, Guglielmi R, Panizzoni G, Febbraro A, Ambrosino G: Unresectable DOCK10 locally advanced pancreatic cancer: a multimodal treatment using neoadjuvant chemoradiotherapy (gemcitabine plus stereotactic radiosurgery) and subsequent surgical exploration. Ann Surg Oncol 2010, 17:2092–2101.PubMedCrossRef 21. Nagai S, Fujii T,

Kodera Y, Kanda M, Sahin TT, Kanzaki A, Yamada S, Sugimoto H, Nomoto S, Takeda S, Morita S, Nakao A: Prognostic implications of intraoperative radiotherapy for unresectable pancreatic cancer. Pancreatology 2011, 11:68–75.PubMedCrossRef 22. Ogawa K, Karasawa K, Ito Y, Ogawa Y, Jingu K, Onishi H, Aoki S, Wada H, Kokubo M, Ogo E, Etoh H, Kazumoto T, Takayama M, Nemoto K, Nishimura Y: Intraoperative radiotherapy for unresectable pancreatic cancer: a multi-institutional retrospective analysis of 144 patients. Int J Radiat Oncol Biol Phys 2011, 80:111–118.PubMedCrossRef 23. Pfreundner L, Baier K, Schwab F, Willner J, Bratengeier K, Flentje M, Feustel H, Fuchs KH: 3D-Ct-planned interstitial HDR brachytherapy + percutaneous irradiation and chemotherapy in inoperable pancreatic carcinoma. Methods and clinical outcome. Strahlenther Onkol 1998, 174:133–141.PubMedCrossRef 24.

5×105 cells/well. Total RNA was extracted from CCA cell lines using

TRIzol® reagent following the manufacturer’s instructions (Invitrogen). Total RNA was isolated using a previously described method [20]. Total RNA (1 μg) was reverse transcribed in a 20 μL reaction mixture, containing 0.5 μg of oligo(dT)15 primer, 20 U of RNasin® ribonuclease inhibitor, and 200 U of ImProm-II™ reverse transcriptase in learn more 1× PCR buffer, 3 mmol/L MgCl2, and 1 mmol/L dNTPs. The first-strand cDNA was synthesized at conditions of 42°C for 60 min. The reverse transcription products served as templates for real-time PCR. PCR amplification was performed using specific primers for the NQO1, wild type p53 and the internal control using β-actin. The primer sequences were as follows: 1) NQO1 (NM_000903.2): forward primer 5’-GGCAGAAGAGCACTGATCGTA-3’ and reverse primer 5’-TGATGGGATTGAAGTTCATGGC-3’;

2) wild type p53 (NM_005256778.1) [25]: forward primer 5’-ATGGAGGAGCCGCAGTCAGATCC-3’ and reverse primer 5’-TTCTGTCTTCCCGGACTGAGTCTGACT-3’; 3) β-actin: forward primer 5’-TGCCATCCTAAAAGCCAC-3’ and reverse primer 5’-TCAACTGGTCTCAAGTCAGTG-3’. The real-time fluorescence PCR, based on EvaGreen® dye, was carried out in a final volume of 20 μL containing 1x SsoFast™ EvaGreen® supermix (#172-5200; Bio-Rad, CA, USA), 0.5 μmol/L Obeticholic Acid mouse of each NQO1 or wild type p53, and 0.25 μmol/L of β-actin primer. Thermal cycling was performed for each gene in duplicate on cDNA samples in 96-well reaction plates using the ABI 7500 Sequence Detection system (Applied Biosystems). Methane monooxygenase A negative control was also included in the experimental

runs. The negative control was set up by substituting the template with DI water. Real-time PCR was conducted with the following cycling conditions: 95°C for 3 min, followed by 40 cycles of 95°C for 15 s and 60°C for 31 s. To verify the purity of the products, a melting curve analysis was performed after each run. Upon completion of 40 PCR amplification cycles, there was a dissociation step of ramping temperature from 60°C to 95°C steadily for 20 min, while the fluorescence signal was continually monitored for melting curve analysis. The concentration of PCR product was calculated on the basis of established standard curve derived from serial dilutions of the positive control for NQO1, wild type p53 and β-actin in the CCA cell lines. Western blot analysis After treatment with chemotherapeutic agents, CCA cells were washed with PBS, collected, and lysed at 4°C with 1x cell lysis buffer with 1 mmol/L dithiothreitol and 0.1 mmol/L phenylmethylsulfonyl fluoride (PMSF) with vigorous shaking. After centrifugation at 12,000 g for 30 min, supernatant was collected and stored at -80°C until use. Thirty microgram of the protein samples were mixed with 5x loading-dye buffer, heated at 90°C for 10 min, and proteins were then separated by electrophoresis in 10% SDS-polyacrylamide gel.

Objective = 40×. Table 3 Immunoreactivity of VEGF, and the number of patients Category Number of patients (%) alive/dead Percentage of positive     tumour cells learn more (P)        <1% 2 (3.6%) 2/0    1-25% 25 (44.6%) 17/8    26-50% 18 (32.1%) 10/8    51-75% 7 (12.5%) 4/3    76-100% 4 (7.1%) 2/2 Staining intensity (I)        Negative 2 (3.6%) 2/0    Weak 11 (19.6%) 10/1    Moderate 24 (42.9%) 12/12    Strong

19 (33.9%) 11/8 Expression score (P+I)        Low (0-2) 12 (21.4%) 12/0    High (3-7) 44 (78.6%) 23/21 Correlation of VEGF expression with clinicopathological characteristics and survival VEGF expression and clinicopathological characteristics are detailed in Table 4. Fisher’s exact test was performed. We did not observe significant correlation between VEGF expression (high/low) and gender (P = 0.7477), age >18 months/≤ 18 months old (P = 0.2701), or histology (favourable/unfavourable) (P = 0.27). Also, there was no significant difference in VEGF expression between the transplant and non-transplant patients (P = 0.7378). Table 4 VEGF expression and other clinicopathologic factors Characteristics VEGF score   Low High  

No. patients Total number 12 44 Gender        Male 7 28    Female 5 16 Age        >18 months old 4 32    ≤ 18 months old 8 12 Histologic subtype        Stroma-rich     Well differentiated 1 2 Intermixed 3 7 Focal nodular 1 2    Stroma-poor     Undifferentiated 6 24 Differentiating 1 9 Histology        Favourable 5 18    Unfavourable BMS-777607 chemical structure 7 26 Stage        1 1 2    2 7 8    3 3 17    4 0 17    4s 1 0 Transplant        No 9 30    Yes 3 14 Survival        Alive 12 23    Dead 0 21 There was significant association between advanced disease stage and high VEGF expression as determined by Fisher exact test (P = 0.0014), and significant

correlation between high VEGF expression score and high tumour stage as determined by Spearman’s coefficient of rank, (rho = 0.453, P = 0.0005). The VEGF expression score was significantly higher in the group Depsipeptide purchase of non-survival patients compared to the group of patients that survived more than 5 years, as determined by Mann Whitney test (P < 0.0001). Also, significant correlation between VEGF expression and survival was determined by Spearman's coefficient of rank (rho = -0.472, P = 0.0002). All patients with low VEGF expression score survived. Interestingly, in the group of patients ≤ 18 months old we did not observe any correlation between VEGF expression and tumour stage (Spearman's coefficient of rank rho = 0.17, P = 0.46), opposite to the patients > 18 months old (rho = 0.635, P < 0.0001). In the same group of patients (≤ 18 months old), we also did not observe any correlation between VEGF expression score and survival (Spearman’s coefficient of rank rho = 0.19, P = 0.42; Fisher’s exact test P = 1.

The best results were obtained using a fivefold molar excess of benzimidazole with respect to quinobenzothiazinium salts 2. It may be assumed that the other reaction product are benzimidazolium salts 5, the structure of which can be stabilized via delocalization

Ulixertinib of positive charge among the benzimidazole nitrogen atoms. Scheme. 3 Synthesis of compounds 4 Benzimidazolium salts 5 were neither isolated from the reaction mixture nor identified in the course of this study, as the primary objective here was to obtain quinobenzothiazine 4 derivatives as free quinoline bases. Excess benzimidazole and benzimidazolium salts 5 that form during the reaction were separated from quinobenzothiazines 4 by pouring post-reaction mixtures into water. Both benzimidazole and salts 5 are well-soluble in water, whereas

compounds 4 fall out of solution as solids. In order to obtain quinobenzothiazine derivatives 7 containing aminoalkyl substituents at the thiazine nitrogen atom, compounds 4 were transformed, in the presence of sodium hydroxide, Adriamycin purchase into salts 6, which were then alkylated using aminoalkyl chlorides (Scheme 4). The reaction occurred as N-alkylation at the thiazine nitrogen atom and led to compounds 7. The structure of compounds 7 was confirmed with 1H NMR spectroscopy by performing NOE 1H–1H homonuclear experiment. By irradiating methylene group protons at the thiazine nitrogen atom an enhancement of H1 and H11 proton signals from compounds 7 was obtained (Scheme 5). Scheme. 4 Synthesis of compounds 7 Scheme. 5 NOE 1H–1H homonuclear experiment for compound 7a Antiproliferative activity The activity of the obtained compounds 4 and 7 was investigated in vitro using cultured SNB-19 and C-32 cell lines and cisplatin as a reference. The examined quinobenzothiazines 4 had various substituents (CH3, F, Cl, Br) introduced into 9- and 11-positions of the quinobenzothiazine ring. In Inositol monophosphatase 1 addition, they also contain a nitrogen atom in the 8-position

of the quinobenzothiazine ring. Compounds 7 contains aminoalkyl substituents: 2-(N-piperidyl)ethyl (compounds 7(a–d)) and 3-(N,N-dimethylamino)propyl (compound 7e) at the thiazine nitrogen atom. One of the mechanisms involved in antiproliferative effects of chemotherapeutics is DNA intercalation. This mode of action is typical for antiproliferative anthracycline antibiotics (e.g., doxorubicin) that feature planar tetracyclic (aromatic or heteroaromatic) fused rings. This mode of action, affecting cancer cells’ DNA, has been indeed suggested in reports concerning antiproliferative properties of phenothiazine and benzo[a]phenothiazine derivatives (Motohashi et al., 2000; Hossain et al., 2008; Hossain and Kumar, 2009). Structurally, compounds 4 and 7 studied herein are their analogs. The experiments demonstrated that the majority of the investigated compounds 4 and 7 showed antiproliferative activity toward examined cell lines within the 5.6–12.

(1998).

Also we indicate the reddening direction based on Cohen et al. (1981). The diagram is consistent in indicating that these sources are 1-Myr old PMS stars with masses less than ∼3 solar masses. The vast majority of these sources measured in this study are cluster members (Jones and Walker 1988; Sirolimus nmr Getman et al. 2005; Hillenbrand 1997; Lucas et al. 2001). The proper motions and radial velocities of ONC members show a dispersion of a few km s−1 (Jones and Walker 1988; Fűrész et al. 2008), implying that these stars will move within about 1 pc, in 1 Myr. In Fig. 2, the measured degree of CP for each source is generally small. We conclude that none of the detected point sources clearly show significant integrated circular polarizations (>than 1.5 % both in

K s and H bands in the same handedness); one source does have a CP > 1.5%, both in the K s and H bands, but is embedded in the western Bioactive Compound Library ic50 high CP region and hence substantially contaminated. OMC-1S shows aperture circular polarimetry of about 0.3% in K s band. These results are consistent with previous observations (Clayton et al. 2005). Fig. 2 Histograms of circular polarization degree (%) of 353 point-like sources. a in the K s band (2.14 μm); b in the H band (1.63 μm). The histograms are constructed using a bin width of 0.2% Fig. 3 Color-magnitude mafosfamide diagram for 353 point-like sources used in Fig. 2, using their J-band (1.25 μm) and H-band (1.63 μm) data in the same observation. The vertical axis shows J magnitude, and the horizontal axis shows J-H magnitude. Our observational data are plotted with crosses. The filled circles denote the loci of 1 Myr old PMS stars at 460 pc, according to the stellar evolution model by Testi et al. (1998). The assumed masses are 0.1, 0.2, 0.4, 0.6, 0.8, 1, 1.2, 1.5, 2, 2.5, 3, and 3.5 solar masses, from bottom to top (the second point from the top for 3.5 solar

masses), connected by the solid line. The dashed line identifies the reddening law through the loci of the 2.5 solar masses (Cohen et al. 1981) CP in Massive Star-forming Regions: Possible Implications for the Origins of Homochirality We will now discuss the implications of these results for the origin of biomolecular homochirality. Bailey (2001) discusses how CPL in star-forming regions might be important in producing EEs and ultimately seeding homochirality on terrestrial planets. Imaging circular polarimetry of several YSOs (Gledhill et al. 1996; Chrysostomou et al. 1997; Bailey et al. 1998; Chrysostomou et al. 2000; Clark et al. 2000; Ménard et al. 2000; Chrysostomou et al. 2007; Fukue et al. 2009; Clayton et al. 2005) and numerical simulations (Fischer et al. 1996; Wolf et al. 2002; Whitney and Wolff 2002; Lucas et al. 2004; Lucas et al. 2005; Chrysostomou et al.

Neurol Res 2003, 25: 729–738.PubMedCrossRef 12. Friedrich MG, Toma MI, Petri S, Cheng JC, Hammerer P, Erbersdobler A, Huland H: Expression of maspin in non-muscle invasive bladder carcinoma; correlation Selleck PD0325901 with tumor angiogenesis and prognosis. Eur Urol 2004, 45: 737–743.PubMedCrossRef 13. Bolat F, Gumurdulu D, Erkanli S, Kayaselcuk F, Zeren H, Ali Vardar M, Kuscu E: Maspin overexpression correlates with increased expression of vascular endothelial growth factors A, C, and D in human ovarian carcinoma. Pathol Res Pract 2008, 204: 379–387.PubMedCrossRef 14. Gynecologic oncology group, Secord AA, Lee PS, Darcy KM,

Havrilesky LJ, Grace LA, Marks JR, Berchuck A: Maspin expression in epithelial ovarian cancer and associations with poor prognosis: a gynecologic oncology group study. Gynecol Oncol 2006, 101: 390–397.PubMedCrossRef 15. Davidson B: Anatomic site-related expression of cancer-associated molecules in ovarian carcinoma. Curr cancer drug targets 2007, 7: 109–120.PubMedCrossRef 16. McCarty KS Jr, Miller LS, Cox EB, Konrath J, McCarty KS Sr: Estrogen receptor analyses. Correlation of biochemical and immunohistochemical methods using monoclonal antireceptor antibodies. Arch Pathol Lab Med 1985, 109: 716–721.PubMed 17. Hata

K, Udagawa J, Fujiwaki R, Nakayama K, Otani H, Miyazaki K: Expression of angiopoietin-1, angiopoietin-2, and Tie2 genes in normal ovary with corpus luteum and in ovarian cancer. Oncology 2002, 62: 340–348.PubMedCrossRef 18. LBH589 chemical structure Hashiya N, Jo N, Aoki M, Matsumoto K, Nakmura T, Sato Y, Ogata N, Ogihara T, Kaneda Y, Morishita R: In Vivo evidence of angiogenesis induced by transcription factor Ets-1: Ets-1 is located upstream of angiogenesis cascade. Circulation 2004, 109: 3035–3041.PubMedCrossRef 19. Takai N, Miyazaki T, Nishida M, Nasu K, Miyakawa I: c-Ets-1 is a promising marker in epithelial ovarian cancer. Int J Mol Med 2002, 9: 287–292.PubMed 20. Sternlicht

MD, Kedeshian P, Shao ZM, Safarians S, Barsky SH: The human myoepithelial cell Progesterone is a natural tumor suppressor. Clin Cancer Res 1997, 3: 1949–1958.PubMed 21. Hendrix MJ: De-mystifying the mechanism of maspin. Nat Med 2000, 6: 374–376.PubMedCrossRef 22. Zhang M, Maass N, Magit D, Sager R: Transactivation through Ets and Ap1 Transcription sites determines the expression of the tumor-suppressing gene maspin. Cell growth differ 1997, 8: 179–186.PubMed 23. Sood AK, Fletcher MS, Gruman LM, Coffin JE, Jabbari S, Khalkhali-Ellis Z, Arbour N, Seftor EA, Hendrix MJ: The paradoxical expression of maspin in ovarian carcinoma. Clin Cancer Res 2002, 8: 2924–2932.PubMed Competing interests The authors declare that they have no competing interests.

Differences between trials could possibly be attributed to the use of carboplatin; however, this seems unlikely because carboplatin is associated

with lower rates of nausea, vomiting, and nephrotoxicity, but a higher rate of thrombocytopenia, relative EGFR inhibitor to cisplatin [5, 6]. In this exploratory analysis, defining ≥65 years as ‘elderly’ allowed for sufficient patient numbers to be included in the main subgroup. Further analysis of ≥70-year-old patients showed efficacy and safety similar to those in ≥65-year-old patients, but the former was limited by a small population size, yielding more variable results. Our study underscores that NSCLC patients, regardless of age, benefit from appropriate treatment [13], and supports the idea that treatment selection in the elderly should not be based solely on chronological age. This exploratory analysis suggests that the outcomes of elderly patients with

nonsquamous NSCLC are consistent with those in the <70-year age group and the Q-ITT population with respect to dose intensity, efficacy, and tolerability. Therefore, with few limitations, elderly patients with advanced nonsquamous NSCLC and good performance status should be treated similarly to younger patients. We and others have shown that platinum-based SCH727965 cost doublet therapy is a tolerable, viable option for elderly advanced NSCLC patients [11, 12, 14]. However, our conclusions are hypothesis generating, as this retrospective analysis had a small sample size and unbalanced between-arm patient characteristics. The limitations of retrospective elderly patient studies include potential differences between chronological age and medical fitness, elderly population heterogeneity, arbitrary age cut-offs, and age-associated co-morbidities. Our selection criteria

of fit elderly patients may not have been applicable to the general elderly population. Therefore, a prospective clinical trial involving a carefully controlled group of elderly patients is warranted. Acknowledgments This work was supported by Eli Lilly and Company. The sponsor was responsible for the design and conduct of the trial, as well as the collection, analysis, and interpretation of data. The manuscript was prepared with input from all authors; all authors approved the final version for submission Racecadotril to the journal. Rebecca Cheng and Mauro Orlando are employees of Eli Lilly and Company and own stock in the company. Helen Barraclough is an employee of Eli Lilly and Company. Joo-Hang Kim’s institution received a grant from Eli Lilly and Company for this clinical trial. José Rodrigues-Pereira has no relevant conflicts of interest to report. The authors wish to thank the patients, their families, and the study personnel who participated in this clinical trial. We also thank Shu Bin Liu and Wei Shan Shi for assistance with statistical analyses.

However, L. reuteri CF48-3A and ATCC 55730 did not suppress TNF production GS-1101 price by LPS-activated cells, while PTA 6475 and ATCC PTA 5289 inhibited production of TNF by 76% and 77% respectively, when compared to the media control (ANOVA,

p < 0.001). Figure 4 L. reuteri strains proficient in biofilm formation suppress TNF production. Cell-free supernatants from L. reuteri biofilms cultured in 24-well plates (A) or flow cells (B) were added to human monocytoid cells in the presence of E. coli-derived LPS. Quantitative ELISAs measured the amounts of human TNF produced by THP-1 cells. As biofilms, TNF inhibitory strains (ATCC PTA 6475 and ATCC PTA 5289) retained their ability to suppress TNF produced by LPS-activated human monocytoid cells. L. reuteri ATCC PTA 6475 and ATCC PTA 5289 biofilms cultured in 24-well plates (A) inhibited TNF by 60% and 50% respectively, (ANOVA, p < 0.02). Supernatants of L. reuteri ATCC PTA 5289 cultured in a flow cell (B) inhibited TNF by 73% when compared to the media control (ANOVA, p < 0.0001). L. reuteri selleck inhibitor cultured as planktonic cells and biofilms produced the antimicrobial factor, reuterin Antimicrobial activities of

L. reuteri were assessed by examining supernatants of planktonic and biofilm cultures for reuterin. Planktonic cells and biofilms of L. reuteri produced reuterin, although differences in reuterin production were evident among strains. Planktonic cultures of

ATCC PTA 6475, ATCC PTA 5289, ATTC 55730 and CF48-3A produced 51.2, 45.2, 225.9, and 230.3 mM of reuterin, respectively. When reuterin quantities were normalized to initial CFU/mL, planktonic cultures of ATCC PTA 6475 and ATCC PTA 5289 produced 2.32 and 2.3 mmol reuterin/1012 cells, respectively, and ATCC 55730 and CF48-3A produced 31.89 and 36.24 mmol reuterin/1012 cells, respectively (Fig. 5). For biofilms cultured in multiwell plates, the four wild type L. reuteri strains ATCC PTA 6475, ATCC PTA 5289, ATTC 55730 and CF48-3A produced 26.8, 16.5, 19.1, and 22.1 mM of reuterin, respectively. After normalization of reuterin quantities to bacterial cell counts, ATCC PTA 6475, ATCC PTA 5289, CF48-3A, and ATCC 55730 produced 6.61, 5.41, 43.4, however and 53.94 mmol of reuterin/1012 cells, respectively, when cultured as biofilms in multiwell plates (Fig. 6). Trends in reuterin production were consistent with planktonic and biofilm cultures of ATCC PTA 6475 and ATCC 5289 producing lower quantities of reuterin than strains ATCC 55730 and CF48-3A. Interestingly, the relative abilities of L. reuteri strains to produce reuterin were inversely correlated with relative abilities to aggregate and adhere to polystyrene (Fig. 1A). Figure 5 L. reuteri strains cultured as planktonic cells produce the antimicrobial compound, reuterin. Stationary phase planktonic cultures of L. reuteri were incubated anaerobically in a glycerol solution.

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21. Nguyen A, Chang AC, Reddel RR: Stanniocalcin-1 acts in a negative feedback loop in the prosurvival ERK1/2 signaling pathway selleck chemicals during oxidative stress. Oncogene 2009, 28:1982–1992.PubMedCrossRef 22. He LF, Wang TT, Gao QY, Zhao GF, Huang YH, Yu LK, Hou YY: Stanniocalcin-1 promotes tumor angiogenesis through up-regulation of VEGF in gastric cancer cells. J Biomed Sci 2011, 18:39.PubMedCrossRef 23. Chang AC, Jellinek DA, Reddel RR: Mammalian stanniocalcins and cancer. Endocr Relat Cancer 2003, 10:359–373.PubMedCrossRef 24. Okabe H, Satoh S, Kato T, Kitahara O, Yanagawa R, Yamaoka Y, Tsunoda T, Furukawa Y, Nakamura Y: Genome-wide analysis of gene expression in human hepatocellular carcinomas using cDNA microarray: identification of genes involved in Cyclin-dependent kinase 3 viral carcinogenesis and tumor progression. Cancer Res 2001, 61:2129–2137.PubMed 25. Fujiwara Y, Sugita Y, Nakamori S, Miyamoto A, Shiozaki K, Nagano H, Sakon M, Monden M: Assessment of Stanniocalcin-1

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Variations in mechanical properties for BFO thin films deposited under different conditions are discussed in conjunction with the crystalline structure, grain size, and surface morphology of the resultant films. Methods The BFO thin films investigated in this study were deposited on Pt/Ti/SiO2/Si(100) substrates at the deposition temperatures of 350°C, 400°C, and 450°C, respectively. The deposition process was conducted in a radio frequency magnetron sputtering system, and a

commercially available Bi1.1FeO3 pellet was used as the target. The base pressure of the sputtering chamber was better than 1 × 10−7 Torr. During deposition, a mixed gas of Ar/O2 = 4:1 with a total pressure was introduced, and the input power was maintained at 80 W. All of the BFO thin films are about 200 nm thick. The composition of the film was identified by an energy-dispersive X-ray analysis and double checked by X-ray MK0683 mw fluorescence analysis. The crystal structure of BFO thin films was analyzed by X-ray diffraction (X’Pert XRD, PANalytical B.V., Almelo, The Netherlands; CuKα, λ = 1.5406 Å). The selleckchem surface features were examined by atomic force microscopy (AFM; Topometrix-Accures-II, Topometrix Corporation, Santa Clara, CA, USA). The root mean square of the surface roughness, R RMS, was calculated by the

following equation [16]: (1) Here N is the number of data and r n is the surface height of the nth datum. Nanoindentation experiments were preformed on a MTS Nano Indenter® XP system (MTS Nano Instruments, Knoxville, TN, USA) with a three-sided pyramidal

Berkovich indenter tip by using the CSM technique [15]. This technique is accomplished by imposing a small, sinusoidal varying force on top of the applied linear force that drives the motion of the indenter. The displacement response of the indenter at the excitation frequency and the phase angle between the force and displacement are measured continuously as a function of the penetration depth. Solving for the in-phase and out-of-phase portions of the displacement response gives rise to the determination of the Casein kinase 1 contact stiffness as a continuous function of depth. As such, the mechanical properties changing with respect to the indentation depth can be obtained. The nanoindentation measurements were carried out as follows: First, prior to applying loading on BFO thin films, nanoindentation was conducted on the standard fused silica sample to obtain the reasonable range (Young’s modulus of fused silica is 68~72 GPa). Then, a constant strain rate of 0.05 s−1 was maintained during the increment of load until the indenter reached a depth of 60 nm into the surface. The load was then held at the maximum value of loading for 10 s in order to avoid the creep which might significantly affect the unloading behavior.