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CrossRef 14. Popat KC, Eltgroth M, LaTempa TJ, Grimes CA, Desai TA: Titania nanotubes: a novel platform for drug-eluting coatings for medical implants. Small 2007, 3:1878–1881.CrossRef 15. Das K, Bose S, Bandyopadhyay A, Karandikar B, Gibbins BL: Surface coatings for improvement of bone cell materials and antimicrobial activities of Ti implants. J Biomed Mater Res B 2008, 87:455–460. 16. Chun AL, Vactosertib ic50 Moralez JG, Webster TJ, Fenniri H: Helical rosette nanotubes: a biomimetic coating for orthopedics. Biomaterials 2005, 26:7304–7309.CrossRef 17. Popat KC, Leoni L, Grimes CA, Desai TA: Influence of engineered titania nanotubular surfaces on bone cells. Biomaterials 2007, 28:3188–3197.CrossRef 18.

Bauer S, Park J, von der Mark K, Schmuki P: Improved attachment of mesenchymal stem cells on super-hydrophobic TiO 2 nanotubes. Acta Biomater 2008, 4:1576–1582.CrossRef 19. Park J, Bauer S, von der Mark K, Schmuki P: Nanosize and vitality: TiO 2 nanotube diameter directs cell fate.

Nano Lett 2007, 7:1686–1691.CrossRef 20. Bauer S, Park J, Faltenbacher J, Berger S, von der Mark K, Schmuki P: Size selective behavior of mesenchymal stem cells on ZrO 2 and TiO 2 nanotube array. Integr Biol 2009, 1:525–532.CrossRef 21. McCool B, Tripp CP: Inaccessible hydroxyl groups on silica are accessible in supercritical CO 2 . J Phys Chem B 2005, 109:8914–8919.CrossRef 22. Tsai PJ, Yang CH, Hsu WC, Tsai WT, Chang PLX-4720 JK: Enhancing hydrogen storage on carbon nanotubes via hybrid chemical etching and Pt decoration employing supercritical carbon dioxide fluid. Int J Hydrogen Energ 2012, 37:6714–6720.CrossRef 23. Reverchon E, Porta GD, Adami R: Medical device sterilization using

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81 to OR = 1 42) Table 4 Effects of adjustment for work-related

81 to OR = 1.42). Table 4 Effects of adjustment for work-related factors, health, and lifestyle-related factors on the association between educational level and sick leave   1–9 days sick leave† 10 or more days sick leave† Low education‡ Intermediate education‡ Low education‡ Intermediate education‡ OR 95 % CI OR 95 % CI OR 95 % CI OR 95 % CI Model 1: sex, age, and ethnicity 1.06 0.76–1.48 1.29 0.98–1.70 1.81* 1.15–2.85 1.85* 1.21–2.82 Model 2: model 1 + reduced perceived general health 1.07 0.77–1.50 1.30 0.99–1.72

1.77* 1.12–2.81 selleck compound 1.81* 1.18–2.79 Model 3: model 1 + work-related factorsa 1.00 0.71–1.41 1.20 0.91–1.58 1.62* 1.01–2.61 1.69* 1.09–2.62 Model 4: model 1 + lifestyle-related factorsb 1.04 0.74–1.47 1.29 0.97–1.71 1.69* 1.05–2.75 1.77* 1.14–2.77 Model 5: model 1 + work-related factors + health 1.04 0.74–1.47 1.22 0.92–1.62 1.59 0.99–2.55 1.65* 1.05–2.59 Model 6: model 1 + work-related factors + health + lifestyle-related factors 0.98 0.69–1.40 1.18 0.88–1.58 1.42 0.86–2.34 1.58 0.98–2.54 †Reference category: no Sepantronium cell line sick leave ‡Reference

category: high educational level aWork-related factors: awkward postures, low job control, low skill discretion, poor relation with colleagues bLifestyle-related factors: overweight/obesity * p < 0.05 Discussion In the current study, it was aimed to identify whether working conditions as well as lifestyle-related factors and health play a role Farnesyltransferase in the causal pathway of educational inequalities in productivity loss at work and sick leave. Educational differences were found for productivity loss at work and sick leave. These educational differences in productivity loss at work and sick leave were particularly apparent in the more severe categories of productivity

loss at work and sick leave. Unhealthy lifestyle-related factors, a poor general health, and unfavorable work conditions were also more prevalent among lower educated employees, but did not influence the association between education and productivity loss at work. Work-related factors and obesity did have an influence on educational differences in sick leave. Previous research found educational differences in sick leave (Beemsterboer et al. 2009; Duijts et al. 2007). In our study, these findings were corroborated, especially for 10 or more days with sick leave. We also found educational differences in productivity loss at work. Employees with a low educational level had a higher risk of productivity loss at work. Although productivity loss at work and sick leave were not associated, educational level was associated with both outcomes. The results of this study imply that both work-related and lifestyle-related factors do play a role in the mechanisms through which socioeconomic position affects sick leave. Unhealthy lifestyle behaviors and a decreased perceived general health were more prevalent among lower educated persons (see also Kamphuis et al.

NGS 454   ERR315664 51 11 2 Corby already published/closest to ce

NGS 454   ERR315664 51 11 2 Corby already published/closest to centroid uncommon but well characterised – virulent in animal model and protozoa GenBank (NC_009494.2)   [34] 454 11 2 H091960011 second of cluster unique environmental strain (from Roman baths in Bath) NGS mate paired Illumina 268 ERR315665 Trichostatin A chemical structure 578 11 2 Alcoy already published responsible for a very big outbreak in Spain GenBank (NC_014125.1)   [35] 59 12 25 H070840415 closest to centroid quite common environmental strain – a few cases of LD. NGS mate paired Illumina 246 ERR315666 188 12 25 H075160080 second of cluster no particular data NGS paired end Illumina 298 ERR315667

36 13 9 Philadelphia already published/closest to this website centroid the type strain – well characterised caused the Philadelphia outbreak. GenBank (NC_002942.5)   [36] 37 13 9 H034680035 internationally significant in top six strains that cause disease NGS 454   ERR315668 186 13 9 H044500045 second of cluster unique clinical isolate NGS paired end Illumina 375 ERR315669 34 14 34 RR08000134 closest available

to centroid no particular significance NGS paired end Illumina 301 ERR315670 68 14 34 H074360710 second of cluster no particular significance NGS mate paired Illumina 179 ERR315671 707* 15 71 H091960009 only one in cluster unique environmental strain (from Roman baths in Bath) NGS paired end Illumina and mate paired Illumina Paired end 136 Mate paired 50 ERR315672 Asterisks designate strains that are likely to have plasmids based on the analysis described in the methods section of this manuscript. GBA3 The sequence data described can be obtained using the European Nucleotide Archive accession number listed in the table. De novo assembly The reads were assembled de novo into scaffolds. The genomic content of these scaffolds was assessed using BLAST Ring Image Generator [37] where the scaffolds were the query sequences and the reference sequence was the genome from the Corby strain (Figure  5). Corby was chosen since it is known to be virulent in both humans and

animal models and has extra mobile genetic elements not seen to date in the other sequenced legionella genomes [34, 38]. Regions showing a high level of variability compared to the Corby genome were investigated further by looking at the gene content of those regions (Additional file 1: Table S1). Figure 5 BRIG blast analysis of the Legionella genomes using the genome of Corby as a reference. The strains and figure colours used were from centre to outside ST152 (CST1 mauve), ST5 (CST1 light blue), ST611 (CST124 dark blue), ST454(CST2 medium blue), ST47(CST16 leaf green), ST376 (CST17 dark green), ST46(CST45 light green), ST59 (CST25 pink), ST42(CST14 red), ST84 (CST15 purple), ST337 (CST130 mauve), ST23 (CST19 light blue), ST37 (CST9 dark blue), ST68 (CST34 medium blue), ST154 (CST12 leaf green) and ST707 (CST71 dark green).

Regardless of environmental temperature, these data should not be

Regardless of environmental temperature, these data should not be interpreted as reason to avoid ingesting carbohydrate

during exercise. Carbohydrate delivery during exercise bouts of >1 hr is well known to increase performance [49–51]. However, a growing body of evidence may also suggest that carbohydrate availability during training bouts can alter the metabolic response and perhaps result in increased reliance on fat stores when carbohydrate availability is low [2, 7, 8, 52]. The concept of a ‘periodized diet’ to control and maximize fuel oxidation and the adaptations to specific blocks of training for both endurance and resistance exercise is an exciting new area of applied sport nutrition research. Acknowledgments The authors wish to thank BMS-907351 purchase the subjects for their investment in time and energy. References 1. Holloszy JO: Biochemical adaptations in muscle. Effects of exercise on mitochondrial oxygen uptake and respiratory enzyme activity in skeletal muscle. J Biol Chem 1967, 242:2278–2282.PubMed 2. Cameron-Smith D, Burke LM, Angus DJ, Tunstall RJ, Cox GR, Bonen A, Hawley JA, Hargreaves M: A short-term, high-fat diet up-regulates lipid metabolism

and gene expression in human skeletal muscle. Am J Clin Nutr 2003, 77:313–318.PubMed 3. Baur JA, Pearson KJ, Price NL, Jamieson HA, Lerin C, Kalra A, Prabhu VV, Allard JS, Lopez-Lluch G, Lewis K, et al.: Resveratrol improves selleck health and survival of mice on a high-calorie diet. Nature 2006, 444:337–342.PubMedCrossRef 4. Davis JM, Murphy EA, Carmichael MD, Davis B: Quercetin increases brain and muscle mitochondrial biogenesis and exercise tolerance. Am J Physiol Regul Integr Comp Physiol 2009, 296:R1071–1077.PubMedCrossRef 5. McConell GK, Lee-Young RS, Chen ZP, Stepto NK, Huynh NN, Stephens TJ, Canny Fenbendazole BJ, Kemp BE: Short-term exercise training in humans reduces AMPK signalling during prolonged exercise independent of muscle glycogen. J Physiol 2005, 568:665–676.PubMedCrossRef 6. Dumke CL, Mark Davis J, Angela Murphy E, Nieman DC, Carmichael MD, Quindry JC, Travis Triplett N, Utter AC, Gross Gowin SJ, Henson DA, et al.: Successive bouts of cycling stimulates

genes associated with mitochondrial biogenesis. Eur J Appl Physiol 2009, 107:419–427.PubMedCrossRef 7. Hansen AK, Fischer CP, Plomgaard P, Andersen JL, Saltin B, Pedersen BK: Skeletal muscle adaptation: training twice every second day vs. training once daily. J Appl Physiol 2005, 98:93–99.PubMedCrossRef 8. Slivka DR, Dumke CL, Hailes WS, Cuddy JS, Ruby BC: Substrate use and biochemical response to a 3,211-km bicycle tour in trained cyclists. Eur J Appl Physiol 112:1621–1630. 9. Azad MA, Kikusato M, Maekawa T, Shirakawa H, Toyomizu M: Metabolic characteristics and oxidative damage to skeletal muscle in broiler chickens exposed to chronic heat stress. Comp Biochem Physiol A Mol Integr Physiol 2010, 155:401–406.PubMedCrossRef 10.

The shape of bright spots from both Ni and Ag maps is the same wh

The shape of bright spots from both Ni and Ag maps is the same which indicates that both Ag and Ni are present in particles with alloyed structure. Figure 2 EFTEM maps of Ag 0.9 -Ni 0.1 NPs. (a) Zero-loss image, (b) Ni map, and (c) Ag map [48]. If the ionic PI3K Inhibitor high throughput screening precursors are multivalent and both metals have some probabilities to be reduced by hydrated electrons and radiolytic radicals, the less noble metal ions (M’+) will act as electron donors to the more noble metal ions (M+). Thus, at the first step, monometallic clusters of noble metal (Mn) will be formed. Then, when concentration of M+ ions decreases, M’+ ions

are reduced afterwards at the surface of Mn. The final result is a core-shell cluster where the more noble metal M is coated by the other one M’ [24]. For example, the Cu(core)/Al2O3(shell) nanoparticles were formed when mixed CuCl2 and AlCl3 solution in the presence of PVP was gamma-irradiated [49]. Copper ions have a higher possibility to selleck compound be reduced (higher redox potential, E0(V) = +0.34) than aluminum ions ( E0(V) = -1.66), so the rate of reaction of hydrated electrons in the solution with Cu ions was higher than with Al ions. Thus, when bivalent Cu ions

were irradiated, the reduction occurred until Cu zero-valent content increased. Then in a further step, when Cu2+ ions were depleted, the reduction of Al3+ increased which occurred exclusively at the surface of the Cu particles to form core-shell structure. The core/shell structure of the clusters, as analysed by transmission electron microscopy (TEM; Figure 3), electron diffraction, and XRD, was clearly confirmed [49]. The boundary between the core and shell

was not sharp, since the shells are CuAlO2 and Al2O3 instead of pure Al. Figure 3 TEM images of Cu Adenosine and [email protected] 2 -Al 2 O 3 nanoparticles. (a) pure Cu nanoparticles and (b) [email protected] nanoparticles in core-shell structure [49]. Under proper conditions, individual nucleation and growth of two kinds of metal atoms can occur separately to form heterostructure. For example, when FePt nanoparticles reacted with AuCl-(PPh3) in the presence of 1,2-dichlorobenzene containing 1-hexadecylamine, the successive growth of Au on to the FePt seeds was observed which resulted in the formation of heterodimers of FePt-Au (Figure 4) [50]. Figure 4 TEM and HRTEM images of FePt-Au heterostructured nanoparticles. (a) TEM image, and (b) HRTEM image of FePt-Au heterodimer nanoparticles reported by Choi et al. [50]. Effects of synthesis parameters The synthesis of metallic nanoparticles by irradiation is governed by a number of experimental parameters such as the choice of solvent and stabilizer, the precursor to stabilizer ratio, pH value during synthesis, and absorbed dose. All of these parameters determine the final ordering, particle size and distribution, and surface area of resultant nanoparticles.

The surface core-level shifts (SCLSs) of the Ga 3d state for

The surface core-level shifts (SCLSs) of the Ga 3d state for SIS3 purchase the S1′, S2′, and S3′ components relative to the bulk at 19.58 eV are −0.302, +0.251, and +0.613 eV, respectively. The Gaussian widths of the bulk and surface are 0.33 and 0.45 eV, respectively. For the As 3d state, the S1, S2, and S3 components relative to the bulk located at 40.43 eV (the 3d 5/2 state) were found to be +0.159, −0.249, and −0.599 eV, respectively. A ‘+’ or ‘−‘

sign indicates a shift towards a higher or lower binding energy, respectively. The Gaussian width is about 0.31 eV. The lifetime is 0.22 eV. In Figure 2b,d, the change in intensity of the components at 60° emission angle is displayed, clearly identifying the surface components. The smallest As component, S3, is most likely associated with the As in the tilted As-Ga dimers in the defaulted terrace. The shifted magnitude of component S3 is the greatest among those reported in the literature, suggesting that the tilted

angle of the dimer is great so as to cause a large charge transfer. Figure 2 Analysis of the core-level spectra for the clean Ga-rich GaAs(001)-4 × 6 surface. (a) As 3d state, θ e = 0°, (b) As 3d state, θ e = 60°, (c) Ga 3d state, θ e = 0°, and (d) Ga 3d state, θ e = 60°. check details Figure 3 displays a fit to the TMA-exposed surface prior to exposure to H2O. As shown in Figure 3a, two Al 2p states are well resolved with an energy separation of 0.650 eV. The one with lower binding energy is associated

with a charge transfer from As to Al. This is possible when a methyl ligand is replaced by a direct bond to an As atom. Considering that the GaAs(001)-4 × 6 surface is ‘As-terminated’ and component S3 shows a negative SCLS, we assumed that dimethylaluminum (DMA) bonds with the dangling bond of the As in the As-Ga dimer. Figure 3 Analysis of the core-level spectra influenced by 1 cycle of TMA-only exposure. (a) Al 2p, (b) As 3d, and (c) Ga 3d states. Because the high-binding-energy Al 2p state remains in the same position and with similar line width after the subsequent water purge, the TMA precursor must have maintained the Al in the molecular charge state while residing on the surface. That indicates that this TMA does not form a bond tuclazepam with a surface atom. That is in agreement with the absence of a new surface As level and leads to the conclusion that the TMA is physisorbed on the S1 As atoms. For the As 3d core-level spectrum, the TMA-exposed surface reveals only minor changes from the clean surface. First, the widths of both top-surface S1 and S3 components are 15% to 20% broader than the subsurface S2 component. Second, the SCLS of the S1 component becomes 0.056 eV without changing the strength. Third, the intensity of the S3 component slightly decreases concurrently with a slight increase of the S2 intensity. Because the Al in DMA bonds with S3 As atom, this As underneath the Al behaves as a subsurface atom.

In order to further enhance therapeutic efficacy, we inserted a c

In order to further enhance therapeutic efficacy, we inserted a constitutive expression HSV-TK gene into this vector to develop a novel armed oncolytic adenovirus (Ad.hTERT-E1A-TK). We subsequently evaluated whether Ad.hTERT-E1A-TK could preferentially replicate in NSCLC and HSV-TK/GCV system could effectively kill NSCLC both in vitro and in vivo. Materials and methods Cells and cell culture HEK293 (human embryonic kidney 293) cells were purchased from

Invitrogen (San Diego, CA, USA). NCIH460 (human large cell lung cancer), A549 (human lung adenocarcinoma), SW1990 (human pancreas cancer), Hela (human cervical carcinoma), and SMMC-7721 (human hepatoma) were obtained from the Cells Bank of the Chinese Academy of Science (Shanghai, China). Primary human dermal fibroblasts were provided by our laboratory, and which Selleck Nutlin 3 was derived from bioptic tissue for dermatoplasty (a written informed consent was obtained from patients). Cells were cultured in DMEM or RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS).All of the tumor cells had activated telomerase activities,

while primary human dermal fibroblasts showed lower telomerase activity according to our previous study. Adenoviral vectors Ad.hTERT-E1A-TK is an oncolytic adenoviral vector that is able to replicate in hTERT activated tumor cells and carries a constitutive expression HSV-TK-HAtag cassette. The construction of Ad.hTERT-E1A-TK has been described previously [11]. Ad.GFP is a replication-defective Ad that this website lacks adenoviral E1A gene and expresses the green fluorescent protein gene (GFP). Ad.null is also a replication-defective not Ad but expresses no extraneous gene. The dl309 is a wild-type Ad that contains intact adenoviral E1 gene. Ad.hTERT-E1A and Ad.hTERT-E1A-CD had similar structure with Ad.hTERT-E1A-TK and were used as positive control

for oncolytic adenovirus. The former contains no therapeutic gene while the later has Escherichia colicytosine deaminase gene (E coli CD) instead of Herpes Simplex Virus Thymidine Kinase (HSV-TK). Purified, high titer viral stocks were generated according to the protocol described by Huang et al [12]. The schematic diagram of Ad.hTERT-E1A-CD or Ad.hTERT-E1A-TK was shown in Additional file 1. Western blot analysis The adenoviral HSV-TK and E1A expression was confirmed by Western blot as described below. The cells were plated in 6-well plates and infected with the Ad.hTERT-E1A-TK at a multiplicity of infection (MOI) of 10 plaque forming units (PFU) per cell. Cells were harvested and lysed 48 h later after infection in SDS sample buffer (containing 10 mM β-mercaptoethanol, 100 mM Tris-CL [pH 6.8], 2% SDS, and 0.1% bromophenol blue).

J Hepatol 2008,48(Suppl 1):S104–112 PubMedCrossRef 13 Lotito SB,

J Hepatol 2008,48(Suppl 1):S104–112.PubMedCrossRef 13. Lotito SB, Actis-Goretta L, Renart ML, Caligiuri M, Rein D, Schmitz HH, Steinberg FM, Keen CL, Fraga CG: Influence of oligomer chain length on the antioxidant activity of procyanidins. Biochem Biophys

Res Commun 2000, 276:945–951.PubMedCrossRef 14. Matsui N, Ito R, Nishimura E, Yoshikawa M, Kato M, Kamei M, Shibata H, Matsumoto I, Abe K, Hashizume S: Ingested cocoa can prevent high-fat diet-induced obesity by regulating the expression ATM Kinase Inhibitor of genes for fatty acid metabolism. Nutrition 2005, 21:594–601.PubMedCrossRef 15. Grassi D, Necozione S, Lippi C, Croce G, Valeri L, Pasqualetti P, Desideri G, Blumberg JB, Ferri C: Cocoa reduces blood pressure and insulin resistance and improves endothelium-dependent vasodilation in hypertensives. Hypertension 2005, 46:398–405.PubMedCrossRef 16. McKim SE, Konno A, Gabele E, Uesugi T, Froh M, Sies H, Thurman RG, Arteel GE: Cocoa extract protects against early alcohol-induced liver injury in the rat. Arch Biochem Biophys 2002, 406:40–46.PubMedCrossRef 17. Kleiner DE, Brunt EM, Van Natta M, Behling C, Contos MJ, Cummings OW, Ferrell LD, Liu YC, Torbenson MS, Unalp-Arida A, et al.: Design and validation of a histological scoring system for nonalcoholic fatty liver disease. Hepatology 2005, 41:1313–1321.PubMedCrossRef 18. Pastore A, Federici G, Bertini E, Piemonte F: Analysis of glutathione: implication

in redox and detoxification. Clinica chimica acta 2003, 333:19–39.CrossRef 19. Serrander L, Cartier L, Bedard K, Banfi B, Lardy B, Plastre O, Sienkiewicz A, Forro L, selleck compound Schlegel W, Krause Verteporfin cost KH: NOX4 activity is determined by mRNA levels and reveals a unique pattern of ROS generation. Biochem J 2007, 406:105–114.PubMedCrossRef 20. Schmittgen TD, Zakrajsek BA, Mills AG, Gorn V, Singer MJ, Reed MW: Quantitative reverse transcription-polymerase chain reaction to study mRNA decay: comparison of endpoint and real-time methods. Anal Biochem 2000, 285:194–204.PubMedCrossRef

21. Nan YM, Wu WJ, Fu N, Liang BL, Wang RQ, Li LX, Zhao SX, Zhao JM, Yu J: Antioxidants vitamin E and 1-aminobenzotriazole prevent experimental non-alcoholic steatohepatitis in mice. Scand J Gastroenterol 2009, 44:1121–1131.PubMedCrossRef 22. Martin GG, Atshaves BP, Huang H, McIntosh AL, Williams BJ, Pai PJ, Russell DH, Kier AB, Schroeder F: Hepatic phenotype of liver fatty acid binding protein gene-ablated mice. Am J Physiol Gastrointest Liver Physiol 2009, 297:G1053–1065.PubMedCrossRef 23. Rajaraman G, Wang GQ, Yan J, Jiang P, Gong Y, Burczynski FJ: Role of cytosolic liver fatty acid binding protein in hepatocellular oxidative stress: effect of dexamethasone and clofibrate treatment. Mol Cell Biochem 2007, 295:27–34.PubMedCrossRef 24. Musso G, Gambino R, Cassader M: Non-alcoholic fatty liver disease from pathogenesis to management: an update. Obes Rev 2010, 11:430–445.PubMedCrossRef 25.

The ZnO seed layer was formed by spin coating the colloid solutio

The ZnO seed layer was formed by spin coating the colloid solution at 3,000 rpm followed by annealing in a furnace at 400°C for 1 h. The following hydrothermal growth was carried out at 90°C for 6 h in a Teflon bottle by placing the seeded substrates vertically in aqueous growth solutions, which contain 20 mM zinc nitrate, 20 mM hexamethylenetetramine, and 125 mM 1,3-diaminopropane. Then the FTO glass with ZnO nanoneedle arrays was rinsed with deionized water

thoroughly and annealed at 500°C for 1 h to remove any residual organics and to improve the crystalline structure. Assembly of the solid-liquid heterojunction-based UV detector The solid-liquid heterojunction-based UV detector was assembled in the same structure as that of a dye-sensitized solar cell, except that no dye molecules were adsorbed and the electrolyte used in this case was deionized C646 manufacturer water, as discussed in our previous work URMC-099 [32]. Figure  1 shows the schematic structure of the nanocrystalline ZnO/H2O solid-liquid heterojunction-based UV detector. For device manipulation, FTO glass with vertically aligned ZnO nanoneedle arrays was used as the active electrode. A 20-nm-thick Pt film deposited on FTO glass by magnetron sputtering formed the counter electrode.

Afterwards, the work electrode (ZnO/FTO) and the counter electrode (Pt/FTO) were adhered together face to face with a 60-μm-thick sealing material (SX-1170-60, Solaronix SA, Aubonne, Switzerland). Finally, deionized water was injected into the space between the top and counter electrode. A ZnO/H2O solid-liquid heterojunction-based UV detector was fabricated with an active

area for UV irradiation of about 0.196 cm2. Figure 1 Schematic device structure of the ZnO nanoneedle array/water solid-liquid heterojunction-based ultraviolet photodetector. Characterization of ZnO nanoneedle arrays and the UV photodetector The crystal structure of the ZnO nanoneedle arrays Thymidine kinase was analyzed by XRD (XD-3, PG Instruments Ltd., Beijing, China) with Cu Kα line radiation (λ = 0.15406 nm). The surface morphology was characterized using a scanning electron microscope (Hitachi S-4800, Hitachi, Ltd., Chiyoda, Tokyo, Japan). The optical transmittance was measured using a UV-visible dual-beam spectrophotometer (TU-1900, PG Instruments, Ltd., Beijing, China). The photoresponse characteristics of the UV detector under illumination were recorded with a programmable voltage-current sourcemeter (2400, Keithley Instruments Inc., Cleveland, OH, USA). A 500-W xenon lamp (7ILX500, 7Star Optical Instruments Co., Beijing, China) equipped with a monochromator (7ISW30, 7Star Optical Instruments Co.) was used as the light source. For the photoresponse switching behavior measurement, photocurrent was measured by an electrochemical workstation (RST5200, Zhengzhou Shirusi Instrument Technology Co. Ltd, Zhengzhou, China).

N Engl J Med 354:669–683PubMedCrossRef 2 Wactawski-Wende J, Kotc

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and the risk of colorectal cancer. N Engl J Med 354:684–696PubMedCrossRef 3. Chlebowski RT, Johnson KC, Kooperberg C, Pettinger M, Wactawski-Wende J, Rohan T, Rossouw J, Lane D, O’Sullivan MJ, Yasmeen S, Hiatt RA, Shikany JM, Vitolins M, Khandekar J, Hubbell FA, Investigators W’s H I (2008) Calcium and vitamin D supplementation and the risk of breast cancer. J Natl Cancer Inst 100:1581–1591PubMedCrossRef 4. Brunner RL, Selleck Bafilomycin A1 Wactawski-Wende J, Caan BJ, Cochrane BB, Chlebowski RT, Gass ML, Jacobs ET, LaCroix AZ, Lane D, Larson J, Margolis KL, Millen AE, Sarto GE, Vitolins MZ, Wallace RB (2011) The effect of calcium plus vitamin D on risk for invasive cancer: results of the Women’s Health Initiative (WHI) calcium plus vitamin D randomized clinical trial. Nutr triclocarban Cancer 63:827–841PubMedCrossRef 5. Hsia J, Heiss G, Ren H, Allison M, Dolan NC, Greenland P, Heckbert SR, Johnson KC, Manson JE, Sidney S, Trevisan M, for the Women’s Health Initiative Investigators (2007) Calcium/vitamin D supplementation and cardiovascular

disease in women. Circulation 115:846–854PubMedCrossRef 6. LaCroix AZ, Kotchen J, Anderson G, Brzyski R, Cauley JA, Cummings SR, Gass M, Johnson KC, Ko M, Larson J, Manson JE, Stefanick ML, Wactawski-Wende J (2009) Calcium plus vitamin D supplementation and mortality in postmenopausal women: the Women’s Health Initiative calcium-vitamin D randomized controlled trial. J Gerontol A Biol Sci Med Sci 64:559–567PubMedCrossRef 7. Wallace RB, Wactawski-Wende J, O’Sullivan MJ, Larson JC, Cochrane B, Gass M, Masaki K (2011) Urinary tract stone occurrence in the Women’s Health Initiative randomized controlled trial of calcium and vitamin D supplements. Am J Clin Nutr 94:270–277PubMedCrossRef 8.