Bench press 1RM was significantly increased after caffeine ingestion, but lower body strength and power (Wingate) were not changed. Although caffeine may have ergogenic effects on upper body strength and Gilteritinib molecular weight during activities more aerobic in nature, it is unlikely that the caffeine content of the active supplement in the current study had any effect on the LPM variable. Despite this finding, caffeine likely played a role in the improvement of %BF. Supplemental caffeine is often used to

increase lipolysis during exercise [38] and spare glycogen [39], a benefit that could potentially be seen if the supplement used in the present study was taken for a longer period of time. In one study, overweight participants consumed buy VX-765 a dietary supplement containing 240 mg/day of caffeine for eight weeks and AZD6244 molecular weight achieved a significant (p < 0.006) amount of weight loss and fat mass loss in addition to a decrease in hip girth measurements [40]. It is also plausible that the increased

LPM was due to the actual combination of ingredients rather than one single ingredient in particular. A similar pre-workout supplement, when ingested for a period of three weeks, significantly increased leg press strength in recreationally-trained males [41]. The particular multi-ingredient supplement used in Spradley and associates’ research contained 300mg of caffeine as well as beta-alanine, creatine, and BCAAs included in the supplement [41]. Multi-ingredient pre-workout drinks containing a combination of caffeine, creatine, amino acids, and beta-alanine, commonly demonstrating a delay in fatigue and improved peak and mean power measures after acute supplementation [42-44]. One such supplemental drink was consumed by 15 trained males before each workout for eight weeks and results revealed significant improvements in strength for the experimental group [44]. This study conducted Rucaparib by Kudrna and colleagues demonstrates the possibility for improvements through pre-exercise supplement drinks with an adequate training

and supplementation period [44]. Increased training volume (attributable to delayed onset of fatigue) was seen after trained individuals consumed 18g of a multi-ingredient ergogenic supplement drink before high intensity interval training (HIIT) sessions for three weeks [4] Ingredients in the active supplement were similar to those in the current study (BCAAs, caffeine, creatine) and although group by time interactions were not significant in Smith’s study, 95% confidence intervals suggested that the supplement was beneficial on measures of aerobic performance [4]. Considering the short duration of supplementation, comparable conclusions can be drawn, suggesting potential training benefits related to the supplement if doses of ingredients and supplementation duration are adequate.

This study was approved by the Institutional Review Board of Japanese Association for the Promotion of State of Art in Medicine. Discussion Impressively high al-BMD around the BRONJ lesion is summarized in Table 1.

Highly statistically significant difference was found in individual cases as well as the whole series. It was especially noteworthy that BRONJ occurred only near the site with high PS-341 concentration al-BMD despite two similar dental extractions. The computerized alveolar bone densitometry using dental X-ray film appears to be handy and useful to detect rises of local alveolar bone density with reference to the occurrence of BRONJ, as suggested by the six cases presented. In addition to the increase of jaw bone cortical thickness and suppression of bone turnover, local increases of alveolar bone density appears

to contribute to BRONJ possibly through compromised circulation and physicochemical overload. Fall of the level of bone turnover may suppress defense reaction against external stimuli. Restricted angiogenesis may also occur along with osteosclerosis, leading to ischemia and poor nutritional supply interfering with wound healing process. On the other hand, the increase of density may selleck chemicals llc suggest a response to nearby necrotic process already started to be aggravated, completing the necrosis in the response to the invasive procedure. Radiation therapy also increases al-BMD. A 54-year-old male (reference case) underwent radiation therapy

for cancer of the tongue on March 2, 2004 BAY 63-2521 manufacturer and given 20 courses of irradiation over a period of 2 months. Surgery for the cancer was performed in May 2005. Osteonecrosis Atorvastatin of the jaw appeared on extraction of first molar of the right mandible on February 2007 at another dental clinic, with persistent bone exposure. On May 18, 2007, alveolar bone density was measured on dental and panorama X-ray film. High bone density of 171 to 191 brightness was noted throughout this period. Al-BMD at corresponding site in this case was as high as in case 1, probably indicating a local risk for osteonecrosis of the jaw regardless of the cause (Fig. 4). Fig. 4 Reference case, a 54-year-old male with osteonecrosis of the jaw following radiation and tooth extraction exhibited high al-BMD values of 159–207 including the site around extraction and development of osteonecrosis of the jaw BRONJ is apparently a multi-factorial disease caused by systemic and local factors. As is evident from the discussion above, the present method using dental X-ray film with aluminum step wedge pasted makes it possible to measure alveolar bone mineral density at selected sites of the alveolar bone quantitatively with a higher sensitivity and reproducibility, unlike observation of panoramic X-ray film of the whole series of teeth only providing an overview or general impression.

To understand the effects of cobalt precursor on electrochemical performance of the corresponding Selleck Nepicastat Co-PPy-TsOH/C catalysts, many physicochemical techniques have been employed in this work. Figure 4 presents XRD patterns of the Co-PPy-TsOH/C catalysts prepared from various precursors, the standard data for CoO and α-Co are also shown for comparison. Four apparent characteristic peaks can be clearly observed at 2θ of 24.5°, 44.2°,

51.5°, and 75.8° in all of the synthesized catalysts, which could be assigned to C(002), Co(111), Co(200), and Co(220) plane. This suggests that cobalt in the Co-PPy-TsOH/C catalysts exists mainly as metallic α-Co with face-centered cubic (fcc) structure. The Co(111) and Co(200) peaks become sharper and sharper with the order of cobalt acetate, cobalt nitrate, cobalt chloride and cobalt oxalate, implying a growth in the crystallite size of metallic cobalt. Generally, an average crystallite size, d, can be estimated with the Shcherrer equation [27, 28]: (4) where λ is the wavelength of incident X-ray, θ is the incident angle of X-ray for a

specific mirror, and B is the half-peak width. In order to avoid the interference of CoO on the Co(111) plane, the Co(200) plane was adopted in this study to calculate the crystallite size of metallic cobalt. The calculated specific values are listed in Table 1. It can be inferred that the relativity of the crystallite size of metallic cobalt in the catalysts is exactly opposite to the trend of ORR performance. Vistusertib mw In addition, Sclareol two weak diffraction peaks observed at 2θ of 36.5° and 42.2° indicate the co-existence of a very small amount of CoO (PDF 43–1004) in the catalysts. Therefore, it could be figured out that the crystallite size of metallic cobalt in the catalysts has essential influence on the catalytic performance towards ORR, the smaller the crystallite size, the better the performance. A small-amount co-existence of CoO in the catalysts does not have an adverse effect on the performance. But on the contrary, it is probably that the synergetic effect between metallic cobalt and the oxide may effectively enhance

the catalytic performance as presented by previous researches [29, 30]. Figure 4 XRD patterns of Co-PPy-TsOH/C catalysts prepared from various cobalt precursors. Table 1 Crystallite size of metallic cobalt in Co-PPy-TsOH/C catalysts prepared from various cobalt precursors Cobalt precursor Crystallite size of metallic co/nm Cobalt acetate 0.4253 Cobalt Selonsertib nitrate 0.4947 Cobalt oxalate 0.6432 Cobalt chloride 0.6099 Figure 5 displays TEM images of the Co-PPy-TsOH/C catalysts prepared from various precursors. Small and uniformly distributed metallic cobalt particles can be clearly seen in the catalyst with cobalt acetate as precursor. Yet, when cobalt nitrate is used as the precursor, serious agglomeration of the catalyst particles can be found, the particle size even reaches as large as 50 nm.

PubMedCrossRef 7. Zaborina O, Holbrook C, Chen Y, Long J, Zaborin A, Morozova I, Fernandez H, Wang Y, Turner JR, Alverdy JC: Structure-function aspects of PstS in multi-drug-resistant CP690550 Pseudomonas aeruginosa. PLoS Pathog 2008,4(2):e43.PubMedCrossRef 8. Long J, Zaborina O, Holbrook C, Zaborin A, Alverdy J: Depletion of intestinal phosphate after operative injury activates the virulence of P aeruginosa causing lethal gut-derived sepsis. Surgery 2008,144(2):189–197.PubMedCrossRef 9. Zaborin

A, Romanowski K, Gerdes S, Holbrook C, Lepine F, Long J, Poroyko V, Diggle SP, Wilke A, Righetti K, et al.: Red death in Caenorhabditis elegans caused by Pseudomonas aeruginosa PAO1. Proc Natl Acad Sci USA 2009,106(15):6327–6332.PubMedCrossRef 10. Zaborina O, Zaborin A, Romanowski K, Babrowski T, Alverdy J: Host Stress and Virulence Expression in Intestinal Pathogens: Development of Therapeutic Strategies using Mice and C. elegans. Curr Pharm Des 2011,17(13):1254–1260.PubMed 11. Nugent SG, Kumar D, Rampton

DS, Evans DF: Intestinal luminal pH in inflammatory bowel disease: possible determinants and implications for therapy with aminosalicylates and other drugs. Gut 2001,48(4):571–577.PubMedCrossRef 12. Bown RL, Gibson JA, Sladen GE, Hicks B, Dawson AM: Effects of lactulose and other laxatives on ileal and colonic pH as measured by a radiotelemetry device. Gut 1974,15(12):999–1004.PubMedCrossRef 13. Ewe K, Schwartz S, Petersen S, Press AG: Inflammation does not decrease intraluminal pH in chronic inflammatory bowel disease. Dig Dis Sci 1999,44(7):1434–1439.PubMedCrossRef TH-302 molecular weight 14. Press AG, Hauptmann IA, Hauptmann L, Fuchs B, Fuchs M, Ewe K, Ramadori G: SHP099 order gastrointestinal pH profiles in patients with inflammatory Metformin supplier bowel disease. Aliment Pharmacol Ther 1998,12(7):673–678.PubMedCrossRef 15. Evans DF, Pye G, Bramley R, Clark AG, Dyson TJ, Hardcastle JD: Measurement of gastrointestinal pH profiles in normal ambulant human subjects. Gut 1988,29(8):1035–1041.PubMedCrossRef 16. Alverdy J, Holbrook C, Rocha F, Seiden L, Wu RL, Musch M, Chang E, Ohman D, Suh S: Gut-derived sepsis occurs when the right pathogen with the right virulence genes meets the right host:

evidence for in vivo virulence expression in Pseudomonas aeruginosa. Ann Surg 2000,232(4):480–489.PubMedCrossRef 17. Wagner T, Soong G, Sokol S, Saiman L, Prince A: Effects of azithromycin on clinical isolates of Pseudomonas aeruginosa from cystic fibrosis patients. Chest 2005,128(2):912–919.PubMedCrossRef 18. Laughlin RS, Musch MW, Hollbrook CJ, Rocha FM, Chang EB, Alverdy JC: The key role of Pseudomonas aeruginosa PA-I lectin on experimental gut-derived sepsis. Ann Surg 2000,232(1):133–142.PubMedCrossRef 19. Stintzi A, Evans K, Meyer JM, Poole K: Quorum-sensing and siderophore biosynthesis in Pseudomonas aeruginosa: lasR/lasI mutants exhibit reduced pyoverdine biosynthesis. FEMS Microbiol Lett 1998,166(2):341–345.PubMedCrossRef 20.

For the NB-Seas subset, STs that occurred multiple times were either recovered from North Sea isolates (ST758, ST760 and ST764) or Baltic Sea isolates (ST481) but not from both (Figure 2E). Two STs were found in the retail samples too: ST394 was found in a sample taken from Sri Lankan prawn farms

and in a German retail sample find more originating from the Indian Ocean; ST540 isolates were recovered from Ecuadorian Nutlin-3a in vitro prawn farms as well as from a German retail sample originating from Ecuador. Phylogenetic analysis Global dataset The UPGMA analysis based on the concatenated sequences revealed a high genetic diversity among the analyzed strains (Figure 3). However, groups of isolates were identified by clustering of STs. These clusters contain strains with > 99% similarity. The two main clusters (marked by I and II) of the UPGMA showed a different composition in terms of geographic origin of strains. A higher proportion of South American (54%) and European STs (65%) was located in cluster I, whereas a higher proportion of Asian STs (60%) was located in cluster II. Nine of the 20 clusters (marked www.selleckchem.com/products/pci-32765.html by boxes) largely consisted of strains originating from the same continent (Figure 3A). The CCs that were identified by goeBURST clustered together and the DLVs and TLVs were closely related in the UPGMA too (Figure 3A). Figure 3 UPGMA tree constructed from the concatenated nucleotide (A) and peptide (B) sequences

of 130 isolates. Squares next to the tree are colored regarding geographical origin (Asia-red, South America-green, Europe-blue and diverse origin-black). A STs of strains are shown and asterisks (*) mark STs found in more than one isolate originating from the same continent. Boxes mark cluster of isolates with more than 99% similarity. Coloring of boxes indicates the origin of majority of strains, while light grey boxes are indicative of clusters of diverse origins. Smaller dark grey boxes indicate doublets AMP deaminase and CCs. Main clusters are indicated by Roman numerals. B pSTs of strains are shown and asterisks (*) mark pSTs representing more than one ST. Boxes mark clusters

of pSTs with more than 99.95% similarity. All pSTs except pST79 and pST164 belong to a single CC. In contrast, the pSTs were grouped into one major cluster, except for pST79 and pST164 from Ecuador that were DLV and TLV, respectively (Figure 3B). The AA-UPGMA revealed no clustering depending on the geographic origin of strains. The pSTs that were more common and belonged to different STs did not originate from the same continent as indicated by the black squares. Therefore neither geographic dependency of pST affiliation nor clustering depending of origin was present. Comparing the results obtained by UPGMA analysis of MLST and AA-MLST data, clusters on nucleotide level were not always found on peptide level (Figures 3A and B). All STs that form a CC or doublet were characterized by the same pST (CC410 and doublet ST246-ST56 were pST1; doublet ST760-ST412 was pST6).

Fourthly, an “Asian Center

for Corporate Social Responsibility at AIT” (ACCSR) has been recently launched, which is a joint venture partnership between the AIT and CSR Asia. Its learn more mission is to advance the development and implementation of effective sustainability solutions both for and by business, and to facilitate development of the supportive framework conditions for corporate social responsibility and sustainable development. The ACCSR will provide a platform for dialog and innovation for the representatives of the private sector in seeking creative solutions for the challenging issues of sustainable development. The pathway to enhancing sustainable development, considering not only the three pillars of economy, environment, and society, but a cross-cutting theme, namely, the human dimension (self), is not easy. The formulation and implementation of sustainable development policies at international, national, and local levels require a new breed of: Policymakers and planners, who can prepare and execute sustainable development policies; and Technical experts working in various sectors, who can develop and disseminate environmentally and socio-economically sustainable MK-4827 in vivo technologies. During the last few years, it is becoming increasingly important for institutions of higher learning

to start considering sustainable development efforts and initiatives from a significantly longer term perspective or horizon considering sustainable development in a more comprehensive manner. The ADB’s long-term strategy looks at a 2020 period, while the OECD projects 2030 scenarios as to how higher education could evolve, with the aim of informing and facilitating strategic change to be made by government decision makers and other key stakeholders in higher education. While traditionally it may have been the role of a university to take a didactic role

in development, telling society Sitaxentan what is right and what is wrong, and providing science and technology based upon research done within the ivory tower, that role is changing. Society, with its ever increasing number of knowledge centers, has begun to talk back. PCI-32765 concentration Therefore, higher education needs to undergo, and is undergoing, fundamental changes. More and more, universities are becoming neutral platforms on which to build collaboration between the public and private sectors and between those who conduct research and those who use it. Universities are becoming the facilitators of dialog and technology transfer. Therefore, we need to forge forward-looking curricula that tear down the walls of traditional disciplines. Institutions of higher learning should be able to train graduates who could address these emerging issues.

In vitro studies demonstrate that ceftaroline is not a substrate for Selleck EPZ5676 the cytochrome P450 system and it does not inhibit or induce the major cytochrome P450 isoenzymes. Therefore, there is minimal potential for drug–drug interactions between ceftaroline and drugs that are cytochrome P450 substrates, inhibitors, or inducers [5]. Clinical Efficacy The FOCUS Trials The FOCUS (ceFtarOline Community-acquired pneUmonia trial vS ceftriaxone in hospitalized patients) 1 and 2 studies (NCT00621504 and NCT00509106, respectively) were multinational, multicenter, phase 3, double-masked, randomized, active comparator-controlled trials,

designed to evaluate the safety and efficacy of ceftaroline fosamil 600 mg IV every 12 h compared with ceftriaxone 1 g IV every 24 h for 5–7 days for the treatment of typical CABP in patients requiring hospital admission [12, 13, 44, 45]. Renal dose adjustments were based on creatinine clearance. For subjects enrolled in FOCUS 1 (which included North American check details participants), clarithromycin was administered during the first 24 h based on established practice guidelines advocating empiric macrolide use [46]. The primary objective of the studies

was to determine whether the clinical cure rate of ceftaroline fosamil was non-inferior to that of ceftriaxone in the co-primary modified intent-to-treat efficacy (MITTE) and clinically evaluable (CE) populations at the test-of-cure (TOC) visit (8–15 days after completion of therapy). The non-inferiority margin was set at −10%. The MITTE population included all participants in the pneumonia risk category (PORT) III or IV who received any amount of study drug according to their randomized treatment group. The CE selleck chemicals llc population included participants in the MITTE population who demonstrated sufficient adherence to the protocol. Baseline characteristics and demographics were comparable between the two study

arms and between the two studies. The majority of participants were Caucasian males over the age of 50 years recruited from Eastern and Western Europe. The most common pathogens isolated were S. pneumoniae (41.7%) and S. aureus (16.5%), followed by Gram-negative organisms, of which H. influenzae was the most frequent [44]. Clinical cure rates favored ceftaroline in a priori-defined integrated CB-839 chemical structure analysis of the MITTE and CE populations (Table 3) [12–15, 44, 47]. Planned secondary analysis of the CE subjects with at least one typical pathogen identified at baseline showed clinical cure in 85.1% of participants compared with 75.5% of participants in the ceftaroline and ceftriaxone groups, respectively [difference 9.7%, 95% confidence interval (CI) 0.7–18.8%] [44]. Cure rates against S. pneumoniae, MDRSP and S. aureus favored ceftaroline, and were similar to ceftriaxone for Gram-negative pathogens [44].

Furthermore, three additional T3SEs that are present in phylogroup 2 Pav are inferred to have been lost completely in Pav BP631 since it’s divergence from Pmp and Pan. This striking pattern suggests that phylogroup 1 Pav BP631 was under strong selective pressure to lose T3SEs deployed by the other Pav lineage. The only putatively functional selleck chemicals T3SEs that are

common among the three Pav strains are HopAA1 and HopAZ1. HopAA1 is encoded in the CEL and descended from the common ancestor of P. syringae. It has been shown to play a role in the suppression of innate immunity in Arabidopsis [35]. Pav BP631 also carries a paralogous copy (in-paralog) of hopAA1 in addition to the one in the CEL. This paralogous hopAA1 allele is also learn more present in the two strong Arabidopsis pathogens Pto DC3000 and Pma ES4326. One of the most interesting findings is that hopAZ1 was independently acquired in all three Pav strains, which points to HopAZ1 as a promising candidate for modulating hazelnut host specificity. Unfortunately, this T3SE has not been functionally characterized and has no conserved domains. HopAZ1 alleles are present in twelve of the 29 P. syringae strains with SAHA HDAC mw sequenced genomes and dispersed among four of five phylogroups. A genealogical analysis of the hopAZ1 family shows strong discordance

from the evolutionary history of the core genome, indicating frequent horizontal transmission of this T3SE family (Additional file 3: Figure S3). Conclusions Our comparative genomic analysis of three Pav

isolates has further confirmed convergent evolution of two independent lineages onto hazelnut, and that this convergence is not due to genetic exchange between lineages. Furthermore, the divergence in T3SE complements suggests that the molecular mechanisms of defense evasion are distinct in each lineage. There has been particularly extensive remodeling of its T3SE repertoire in the more recently emerged lineage possibly in response to recognition by host factors that have coevolved with the T3SEs deployed by the other lineage. However, both lineages have been diversifying as hazelnut pathogens since long before the initial hazelnut decline outbreak this website was first documented in 1976. This suggests that changes in agricultural practice such as the propagation of new cultivars in Greece in the 1960s and 70s and the expansion of hazelnut cultivation into marginal habitats in Italy may have provided suitable conditions for the epidemic emergence of previously cryptic pathogens. While this scenario is clearly conjecture, we now have a number of strong candidate loci to pursue. Functional characterization of these loci in the future may reveal the key steps that these two distinct lineages took in order to subvert the hazelnut immune system. Methods Sequencing and genome assembly followed the methods described in [36].

Medium was then removed, DMSO (200 μl) was added, and the absorbance maxima at test and reference wavelengths of 490 Epoxomicin datasheet and 630 nm, respectively, were recorded. The proliferation inhibitory rate (%) was calculated as: [1-(absorbance of baicalin GW786034 treated group/absorbance of control group)] × 100. Colony-forming assay CA46 cells were seeded at a density of 4 × 102/well in 24-well flat bottom plates and then cultured with baicalin at different concentrations in RPMI-1640 medium with 10% FBS and 0.7% methylcellulose at 37°C for 10 days. Colony formation was observed

using phase contrast inverse microscopy. The resulting cell colonies (>50 cells/colony) were counted, and colony formation rate (%) was calculated as: (formed colonies/seeded cells) × 100. Measurements of cells in early and late apoptosis The ability of baicalin to induce apoptosis in CA46 cells was examined by Annexin V-FITC/PI double-staining and flow cytometry. Preparations were treated with baicalin at varying concentrations for 48 h. Cells were then

harvested, resuspended to 5 × 105 /ml in binding buffer (HEPES, 10 mM, pH 7.4, 150 mM NaCl, 5 mM KCl, 1 mM MgCl2, 1.8 mM CaCl2), and doubly stained with Annexin V-Fluorescein Isothiocyanate ARN-509 (FITC)/Propidium Iodide (PI) (BD, Franklin, NJ, USA) according to the manufacturer’s instructions. The percentages of viable, early apoptotic, late apoptotic, and necrotic cells were determined using a CPICX XL flow cytometer (Beckman Coulter, Fullerton, CA, USA). DNA fragmentation assay After 48 h exposure to baicalin at varying concentrations, CA46 cells were collected by centrifugation and washed twice with PBS. Cell pellets were resuspended in 40 μl of lysis buffer (0.1 M EDTA, 0.1 M Tris–HCl pH 8.0, 0.8% SDS) and subsequently treated with 10 μl RNase A (50 μg/ml) at 37°C for 1 h and with 10 μl proteinase K (20 μg/ml) at 50°C overnight. Extracted cellular DNA was subjected to agarose gel (2.0%) chromatography at 35 V for 3 h. Gels were photographed after staining with 0.5 μg/ml ethidium bromide. Western blot analyses Western

blotting was performed as described Arachidonate 15-lipoxygenase previously [8]. CA46 cells were treated with 40 μM baicalin for 0–72 h prior to lysis. Protein Detector LumiGLO Western Blot Kits were purchased from KPL (Gaithersburg, MD, USA). Antibodies to the following proteins were used for these analyses: β-actin (NeoMarkers, Fremont, CA, USA); Akt, p-Akt (Ser473), mammalian target of rapamycin (mTOR), p-mTOR (Ser2448), IκB, p-IκB (Ser 32), PARP, cleaved caspase-9 (Asp330), and cleaved caspase-3 (Asp175) (Cell Signaling, Danvers, MA, USA); NF-κB p65 (eBioscience, San Diego, CA, USA). The density of β-actin served as an internal loading control. Statistical analysis Experimental findings are expressed as means ± standard deviation. Comparisons involving different baicalin concentrations or incubation times were conducted using analysis of variance (ANOVA).

84 at 397.8 eV, and the ratio of the azobenzene peak (N2) was 0.16 at 400.1 eV, for a 3,600-L aniline sample on the GOx surface [19, 20]. These N 1 s peaks indicated that aniline had oxidized to azobenzene in the presence of the oxygen groups on the GOx surface, which suggested that the GOx surface acted as a reaction reagent at 300 K. The oxidation reaction efficiency under ZD1839 molecular weight a 365-nm UV light exposure was measured as the aniline coverage was increased from 3,600 L to 14,400 L. Figure 3 HRPES measurements indicating oxidation from aniline to azobenzene on GOx surfaces prepared using benzoic acid. N 1 s core level spectra of (a) 3,600 L aniline on EG at 300 K, (b) 3,600

L aniline on a GOx surface prepared using benzoic acid at 300 K. The N1 and N2 peaks corresponded to the aniline and azobenzene nitrogen peaks. (c) and (d) show the plots of the intensity ratio between the N1 and N2 features as a function of the aniline coverage

on the EG and GOx surfaces, respectively. The plots of the coverage-dependent intensity of the aniline peaks (N1) and the azobenzene peaks (N2) on the EG and GOx surfaces are displayed in Figure  3c,d. Figure  3c shows that the intensity ratio remained unchanged, although the exposure of aniline was increased to 14,400 L. Thus, we concluded that Selleckchem IACS-010759 the EG surface did not promote the oxidation reaction process because oxygen groups were not present. Figure  3d, on the other hand, clearly revealed that the PS-341 chemical structure Relative intensity ratio between aniline and azobenzene increased with increasing aniline coverage on the GOx surface. As the aniline coverage increased from 3,600 L to 14,400 L aniline, the azobenzene (N2) peak increased significantly from 0.16 to 0.71 whereas the aniline (N1) peak

decreased from 0.84 to 0.29. These results suggested that the high concentration of aniline enhanced the occurrence of azobenzene due to the Le Chatelier’s principle on the GOx surface. It can be clearly explained that as the aniline coverage increased, the oxidation reaction involving the oxygen carriers on the GOx surface proceeded with greater efficiency because the high aniline coverage TCL increased the possibility of the oxidation reaction. Table  1 summarizes the aniline and azobenzene intensity measurements as a function of the aniline surface coverage. Table 1 Intensity measurements indicating relative aniline and azobenzene coverage Aniline exposure (L) Relative intensity of aniline (N1) Relative intensity of azobenzene (N2) 3,600 0.84 0.16 4,800 0.45 0.55 7,200 0.40 0.60 9,000 0.35 0.65 10,800 0.31 0.69 14,400 0.29 0.71 A function of aniline surface coverage at 300 K. The work function was measured as the center position of the low kinetic energy cut-off for each sample, as shown in Figure  4a. The monolayer EG spectrum (the black spectrum in Figure  4a) yielded a work function of 4.31 eV [20, 21].