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83. Seaton K, Ahn SJ, Sagstetter AM, Burne RA: A transcriptional regulator and ABC transporters link stress tolerance, (p)ppGpp, and genetic competence in Streptococcus mutans. J Bacteriol 2011,193(4):862–874.PubMedCrossRef

84. Trieu-Cuot P, Carlier C, Poyart-Salmeron C, Courvalin P: A pair of mobilizable shuttle vectors conferring resistance to spectinomycin SAR302503 solubility dmso for molecular cloning in Escherichia coli and in gram-positive bacteria. Nucleic Acids Res 1990,18(14):4296.PubMedCrossRef 85. Que YA, Haefliger JA, Francioli P, Moreillon P: Expression of Staphylococcus aureus clumping factor A in Lactococcus lactis subsp. cremoris using a new shuttle vector. Infect Immun 2000,68(6):3516–3522.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions SJA carried out the RNA microarray experiments and associated

data analysis, performed all real-time PCR studies, participated in the conception and design of the study, and helped draft the manuscript. MDQ carried out all of the RNA isolations for comparing the effects of glucose and oxygenation on lrgAB Astemizole expression. ER optimized and carried out all of the quantitative competence assays. RAB participated in the design and coordination of the study, and helped draft the manuscript. KCR participated in the conception and design of the study, performed the H2O2 assays, intracellular ROS measurements, and drafted the manuscript. All authors read and approved the final manuscript.”
“Background The Deepwater Horizon oil spill of 2010 in Gulf of Mexico serves as a reminder of the potential adverse impacts of petroleum compounds to the environment [1, 2]. Petroleum is a complex mixture of saturated and aromatic hydrocarbons, polar compounds, resins and asphaltenes. Saturates are proportionally the most significant fraction by mass while the most toxic and persistent compounds are the polar and aromatic hydrocarbons [3]. Such compounds can be responsible for massive wildlife death soon after oil spills and, as well as over the medium and long-term [1]. Unfortunately, accidents resulting in oil spills happen routinely, and due to tidal activity spilled oil is commonly transported to coastal regions.

diphtheriae. Immuno-fluorescence microscopy carried out for control verified that observation (Figure 1). 17DMAG nmr Additionally, this approach showed an uneven, speckled staining of the mutants, indication an altered surface structure compared to the wild-type strains. Figure 1 Immuno-fluorescence microscopy of C. diphtheriae wild-type and mutant strains.

An antiserum directed against the surface proteome of C. diphtheriae was used as primary antibody; Pitavastatin Alexa Fluor 488 goat anti-rabbit was used as secondary antibody. A: ISS3319, B: Lilo1, C: ISS4060, D: Lilo2. To analyse, if all bacteria within the observed chains of mutants were still viable or if changes were correlated with detrimental effects on survival of bacteria, we carried out LIVE/DEAD staining. No significant differences were observed between wild-type and mutants in respect to viability, in all cases the majority of bacteria were fully viable and

exclusively stained by SYTO9 green and not by propidium iodide (Figure 2). During manipulation of bacteria (washing steps, resuspension of pellets), we observed that chains of mutants were occasionally broken down to smaller units. Using LIVE/DEAD staining, we could show that disruption of chains by vigorous vortexing (5 min) was not detrimental to the bacteria (Figure 2C and 2F), indicating that mutant strains have a fully functional and rigid peptidoglycan layer. Figure 2 LIVE/DEAD staining of C. diphtheriae wild-type and mutant strains. Green fluorescent bacteria have a functional Ruboxistaurin research buy cytoplasmic membrane and are stained green, red propidium iodide staining indicates non-viable

cells. A: ISS3319, B-C: Lilo1, D: ISS4060, E-F: Lilo2, C and F: cells subjected to 5 min of vigorous vortexing. For all strains, ISS3319, ISS4060, Lilo1 and Lilo2, identical doubling times of about 70 min were observed. Interestingly, with a final optical Alanine-glyoxylate transaminase density (OD600) of approx. 13, the mutants reached a more than fourfold higher OD600 compared to the corresponding wild-type strains, which reached final optical densities between 2.5 and 3. This observation corresponds nicely with the increased colony size of the mutants (data not shown) and suggests that the altered bacterial size and form has no severe impact on light scattering and consequently OD measurement. Analysis of surface proteins Since we assumed that the altered shape of the mutants might be correlated with an altered cell surface, especially in the light of the immuno-fluorescence microscopy approach (Figure 1), which showed a different antibody binding compared to the wild-type, we isolated the surface proteins of wild-type and mutant strains. When these were subjected to SDS-PAGE and silver staining, significant differences in protein patterns were observed (Figure 3A).

Figure 2 Effect of RpfF Bc on AHL synthase gene cepI expression. (A) The β-galactosidase activity of a cepI-lacZ transcriptional fusion in H111 wild-type (■), ∆rpfFBc (▲) and ∆rpfFBc supplemented with BDSF signal (◆). BTK inhibitor nmr (B) Western blotting assay of CepI protein level. The data presented are the means of three replicates and error bars represents the standard deviation. BDSF system controls AHL signal production through its receptor RpfR Previous studies showed that two BDSF sensors, BCAM0227 and RpfR (BCAM0580), are involved in the BDSF-mediated QS. Among them, BCAM0227, which was originally characterized in B.

cenocepacia strain J2315, controls only a subset of the BDSF-regulated phenotypes and target genes [19], whereas RpfR was shown to be

a major receptor of BDSF as null mutation of RpfR results in similar mutant phenotypes as the BDSF-minus mutants [14]. These results suggest that two BDSF Angiogenesis inhibitor signaling pathways may be operating in B. cenocepacia, which motivated us to investigate which BDSF signaling pathway plays a role in regulation of the cepI expression. Significantly, deletion of the BDSF receptor gene rpfR caused a similar reduction in AHL signal production as the deletion mutant of rpfF Bc that encodes a BDSF synthase (Figure 3A). Analysis MRT67307 order of the cepI expression profile using its promoter fused with the lacZ reporter gene showed that RpfR controlled the cepI expression at the transcriptional level (Figure 3B). Importantly, in contrast to the deletion mutant of rpfF Bc , which could be rescued by addition of BDSF (Figure 2A), addition of BDSF to the

rpfR mutant had no effect on the cepI expression (Figure 3B). The data are consistent with the idea that BDSF modulates AHL signal production through its cognate receptor RpfR. Agreeable with our recent finding that BCAM0227 has a negligible role in BDSF signaling [14], deletion of this gene Carnitine palmitoyltransferase II did not reveal any effect on cepI expression in B. cenocepacia H111 (Additional file 1: Figure S1). Figure 3 Effect of RpfR on AHL system. (A) AHL signal production was quantified with the aid of AHL reporter strain CF11 to test the β-galactosidase activity. (B) The β-galactosidase activity of a cepI-lacZ transcriptional fusion in H111 wild-type (■), ∆rpfR (▲) and ∆rpfR supplemented with BDSF signal (◆). For convenient comparison, the AHL signal production of wild-type strain was defined as 100% and used to normalize the AHL signal production of other strains. The data presented are the means of three replicates and error bars represents the standard deviation. BDSF system controls AHL signal production and biological functions through regulation of intracellular c-di-GMP level RpfR is a modular protein with PAS-GGDEF-EAL domains. Among these domains, PAS is the domain interacting with BDSF, and GGDEF and EAL domains are associated with c-di-GMP metabolism [14].

Erlich HA: Molecular biology of rifomycin MSS Information Corp 1973. 34. Tanaka click here K, Tamaki M, Watanabe S: Effect of furanomycin on the synthesis of isoleucyl-tRNA. Biochim Biophys Acta 1969, 195:244–5.PubMed 35. Hughes J, Mellows G: Inhibition of isoleucyl-transfer ribonucleic acid synthetase in Escherichia coli by pseudomonic acid.

Biochem J 1978, 176:305–18.PubMed 36. Kim S, Lee SW, Choi EC, Choi SY: Aminoacyl-tRNA synthetases and their inhibitors as a novel family of antibiotics. Appl Microbiol Biotechnol 2003,61(4):278–88.PubMed 37. Dumler JS, Barbet AF, Bekker CP, Dasch GA, Palmer GH, Ray SC, Rikihisa Y, Rurangirwa FR: Reorganization of genera in the families Rickettsiaceae and Anaplasmataceae in the order Rickettsiales : unification of some species of Ehrlichia with Anaplasma, Cowdria with Ehrlichia and Ehrlichia with Neorickettsia, descriptions of six new species combinations and designation of Ehrlichia equi and ‘HGE agent’ as subjective synonyms of Ehrlichia

phagocytophila. Int J Syst Evol Microbiol 2001,51(Pt 6):2145–65.PubMed 38. Li L, Stoeckert CJ, Roos DS: OrthoMCL: identification of ortholog groups for eukaryotic genomes. Genome research 2003,13(9):2178–89.CrossRefPubMed 39. Raverdy S, Foster JM, Roopenian E, Carlow CKS: The Wolbachia endosymbiont of Brugia malayi has an MDV3100 solubility dmso active buy PP2 pyruvate phosphate dikinase. Mol Biochem Parasitol 2008,160(2):163–6.CrossRefPubMed 40. Hasan S, Daugelat S, Rao PSS, Schreiber M: Prioritizing genomic drug targets in pathogens: application to Mycobacterium tuberculosis. PLoS Comput Biol 2006,2(6):e61.CrossRefPubMed 41. Russ AP, Lampel S: The Org 27569 druggable genome: an update. Drug Discov Today 2005,10(23–24):1607–10.CrossRefPubMed

42. Hopkins AL, Groom CR: The druggable genome. Nat Rev Drug Discov 2002,1(9):727–30.CrossRefPubMed 43. Wishart DS, Knox C, Guo AC, Cheng D, Shrivastava S, Tzur D, Gautam B, Hassanali M: DrugBank: a knowledgebase for drugs, drug actions and drug targets. Nucleic Acids Res 2008, (36 Database):D901–6. 44. Salama NR, Shepherd B, Falkow S: Global transposon mutagenesis and essential gene analysis of Helicobacter pylori. J Bacteriol 2004,186(23):7926–35.CrossRefPubMed 45. Altschul SF, Gish W, Miller W, Myers EW, Lipman DJ: Basic local alignment search tool. J Mol Biol 1990,215(3):403–10.PubMed 46. van Dongen S: Graph clustering by flow simulation. [http://​micans.​org/​mcl/​]PhD Thesis, Univ. of Utrecht, the Netherlands 2000. 47. Edgar RC: MUSCLE: multiple sequence alignment with high accuracy and high throughput. Nucleic Acids Res 2004,32(5):1792–7.CrossRefPubMed 48. Cormen TH, Leiserson CE, L R, Stein C: Introduction to Algorithms 2 Edition Cambridge: MIT Press 2001. Authors’ contributions AH participated in the design of the study, carried out the analyses and drafted the manuscript. PD computed minimum spanning trees and helped to draft the manuscript. JF and CC contributed to the conception of the study and helped to draft the manuscript.

Obviously, the LCs (WOBs, NOVs, Si=O states, and so on) could act as the sensitizers in the SROEr matrixes. For the investigation of the BAY 11-7082 chemical structure energy transfer from these GW3965 cell line sensitizers to Er3+, the PL spectra of Er3+ in the infrared band (4I15/2 to 4I13/2) were measured, as shown in Figure  4a. Interestingly, the PL signal from Er3+ could not be detected from the SROEr films annealed at <900°C, although the intense visible PL from the LCs (WOBs, NOVs, and Si=O states) can be observed. However, for the samples annealed above 900°C, the PL of Er3+ could be obviously resolved (its intensity increases significantly with the annealing temperatures). Therefore, the energy transfer from the NOVs could be excluded

since the NOVs selleck kinase inhibitor disappear after high-temperature annealing (1,150°C). Moreover, the sensitization of the temperature-dependent

PL of Er3+ from the WOBs could also be excluded due to their almost identical PL from the as-deposited and annealed SROEr films. Meanwhile, the evolution of the PL intensity from Er3+ is in accordance with that from the Si=O states at higher-annealing temperatures (≥900°C, the critical temperature that the Si NCs begin to precipitate in a great amount). Hence, we consider that the sensitization of Er3+ is mainly caused by the Si=O states in the SROEr matrix. According to the discussion above, the Si=O states would be induced greatly when the Si NCs precipitate in a great amount, and the energy transfer process between the Si=O states and Er3+ is

also controlled by the Si NCs in the SROEr matrix. The introduction of the Si NCs can not only enhance the luminescence of the Si=O states by facilitating the photon absorption of the Si=O states but also improve the PL of Er3+ by the energy transfer process of the Si=O states. Besides, the PL of Er3+ would also be enhanced by the activation of Er3+ in the SROEr films after high-temperature annealing (≥900°C). The PL intensity of Er3+ increased significantly when the annealing time increased from 30 to 120 min for the SROEr annealed at 1,150°C, as shown in Figure  4a. It means that further improvement of the PL property of Er3+ could be achieved by optimizing the annealing condition of the SROEr films. Figure 4 PL spectra of Er 3+ 2-hydroxyphytanoyl-CoA lyase ion and PLE spectra of both Er 3+ ion and Si=O states. (a) PL spectra of the Er3+ ions in the SROEr films with various annealing conditions. (b) Normalized PLE spectra of the Si=O states (collected at 2.2 eV) and Er3+ (collected at 0.8 eV) for the SROEr film annealed at 1,150°C for 30 min. To further determine the energy transfer mechanism in the SROEr films, the PLE spectra of the Si=O states (collected at 2.2 eV) and Er3+ (collected at 0.8 eV) for the SROEr film annealed at 1,150°C for 30 min were measured, as shown in Figure  4b, with the intensities normalized by their correspondingly maximal values.

Optimization on these three coordinates was performed using a downhill simplex algorithm in order to minimize the area of femoral neck that intersected this plane. This automated algorithm used the NN region defined above as the initial starting location of the plane. Since the algorithm started with the NN region as the initial Ilomastat guess, and this region is between the femur head and greater trochanter, convergence to the plane with the narrowest area was rapid. FNAL was measured perpendicular to this plane through its center of mass from the edge of the femoral head to where

the axis exited the femur distally. To reduce the effects of osteophytes which were prevalent and visible in the QCT dataset, the measurement was repeated eight times along line segments parallel to the neck axis. The eight measurements were buy EPZ015938 CBL0137 ic50 concentrically spaced around the neck axis. The final FNAL value was defined as the median of these eight parallel segments and the central measurement. Statistics Parameters calculated from the QCT dataset were considered the gold standard, and the parameters calculated by HSA were compared to QCT by linear regression analysis using GraphPad Prism V 5.03. If the offset (i.e.,

intercept) was not statistically different from zero (p < 0.05), the analysis was repeated with the intercept restricted to zero. In order to test the sensitivity of our results to the

placement of the NN ROI, in addition, the plane through the narrowest part of the femoral neck of the QCT dataset was also used as the basis for an alternate definition of the QCT NN ROI and compared to the HSA NN ROI. Results High linear correlations (r = 0.89–0.95) were found between HSA and QCT for CSA, CSMI, and Z at the NN and IT regions (Figs. 2 and 3). The intercepts of the linear correlation Immune system of the parameters were not statistically significant (p < 0.05) at the IT region but were statistically significant at the NN region (Table 1). The slopes of these parameters were all different from unity. Fig. 2 The correlation of HSA with QCT for the narrow neck region Fig. 3 The correlation of HSA with QCT for the trochanter region Table 1 Results of the linear correlation of HSA vs. QCT at the NN and IT regions   NN IT Cross-sectional area (cm2) r 0.95 0.93 Offset 0.32 (0.11) N.S. Slope 2.02 (0.10) 2.00 (0.02) SEE 0.13 0.31 Cross-sectional moment of inertia (cm4) r 0.94 0.93 Offset 0.30 (0.12) N.S. Slope 1.19 (0.06) 1.48 (0.03) SEE 0.22 1.40 Section modulus (cm3) r 0.93 0.89 Offset 0.19 (0.07) N.S. Slope 1.32 (0.08) 1.53 (0.03) SEE 0.10 0.50 Width (cm) r 0.95 0.95 Offset N.S. N.S. Slope 0.979 (0.004) 0.978 (0.003) SEE 0.08 0.10 Femoral neck axis length (cm) r 0.90 – Offset N.S. – Slope 1.003 (0.004) – SEE 0.22 – Numbers in parentheses are standard errors. N.S.

For high-temperature stress experiments, log-phase cells were transferred to pre-warmed 50°C tubes and incubated at 50°C for 5 min. For low pH stress experiments, log-phase cells were incubated at

37°C in TMH medium adjusted by adding 2 M HCl to pH 3.0 for 10 min. To test the effect of oxidative stress, the cells were incubated for 10 min in 220 mM H2O2. The bacterial viable count after exposure to the appropriate stresses was determined by pelleting the appropriate dilutions on the BHI agar plates, which were then selleck chemicals llc incubated at 26°C for 36 h. Macrophage infection assay J774A.1 mouse macrophage cells (6 × 105) were seeded in 24-well tissue culture plates (0.5 ml/well) and maintained in the minimum essential medium (MEM) containing the modified Eagle’s medium (Invitrogen) supplemented Quisinostat purchase with 10% heat-inactivated fetal bovine serum,

2 mM L-glutamine until confluence was achieved at 37°C under 5% CO2. WT and ΔompR were grown in TMH as described above. The cultures were collected and suspended in the MEM medium and then respectively added to cell monolayers in 24-well tissue culture plates at a multiplicity of infection generally of 20:1 (bacteria to macrophages). After incubation at 37°C for 1 h to permit phagocytosis, 6 wells of infected cell monolayers were washed thrice with 1× phosphate-buffered saline (PBS). Afterwards, the number of total macrophage cell-associated bacteria was determined. Cell-associated bacteria were determined by harvesting in 0.5 ml of 0.1% Triton X-100 in 1× PBS. After 10 min, infected cell lysates were collected serially and diluted 10-fold

in PBS; on the other hand, viable bacterial CFU was determined as described above. A second set of 6 infected monolayer wells were washed twice with 1× PBS. MEM medium supplemented with 200 μg/ml gentamicin (Invitrogen) was added to these wells for 1 h to kill extracellular bacteria. The infected monolayers were then lysed and treated as described above to determine the number of intracellular bacteria. Each experiment was repeated three or four times on different days, and each bacteria sample was used to infect at least four wells of macrophage monolayers. Results Non-polar mutation of ompR Given that the coding regions of ompR and envZ overlap in the ompB operon, a partial segment of the coding region of ompR was replaced by the kanamycin isothipendyl resistance cassette to generate the ompR mutant (ΔompR). Real-time RT-PCR was performed to assess the ompR mRNA levels in WT, ΔompR, and selleck products C-ompR (the complemented mutant). The ompR transcript was lacking in ΔompR, while it was restored in C-ompR relative to WT (data not shown), indicating successful mutation and complementation. To prove the non-polar mutation of ompR, we constructed the pRW50-harboring fusion promoter consisting of a promoter-proximal region of ompF and promoterless lacZ, and then transformed into WT, ΔompR and C-ompR, respectively (Additional file 2).

Because of the presence of carbonyl and carboxyl functional groups on its surface, the thickness

of the sheets was approximately 1 nm, slightly thicker than graphene [31]. The average size of GO sheets was in the order of several micrometers, rendering them with very large aspect ratios. Figure 2 shows the morphology of SRG/PVDF composites containing different SRG loading levels. At low filler loadings, it is rather difficult to distinguish SRG sheets from the polymer matrix, due to its low contrast to the background and monolayer nature. As the filler content increases, the SRG sheets become more distinguishable, particularly at a filler content of 1.4 vol.%. Figure 1 AFM image of GO sheets on freshly cleaved mica. The relative thickness across the horizontal line is approximately ubiquitin-Proteasome degradation 1 nm, indicating RG-7388 price the effective exfoliation of graphite oxide into monolayer GO sheets. Figure 2 SEM micrographs of PVDF nanocomposites. (a) 0.4, (b) 0.5, (c) 0.8, and (d) 1.4 vol.% SRG sheets. The percolation theory is often employed

to characterize the insulator-conductor transition of the polymer composites containing conductive fillers. Figure 3 shows the electrical conductivity versus filler content for the SRG/PVDF composites. According to the percolation theory, the static conductivity of the composites is given by [32, 33]: (1) where p c is the percolation threshold, p is the filler content, and t is the critical exponent. As shown in Table 1, the fit of electrical conductivity to Equation 1 yields a percolation threshold as low as 0.31 vol.% (Figure 3). Such a percolation threshold is lower than that of the graphene/PVDF composite prepared by direct blending chemically/thermally reduced GO sheets with polymers [34, 35]. The low p c is attributed

to the homogeneous dispersion of SRG sheets within the PVDF matrix. In this study, we found that the SRG sheets could remain stable in the PVDF solution up Adenosine triphosphate to several weeks. Without PVDF in DMF, however, black SRG precipitates appeared after 1 day. So it is considered that the PVDF molecular chains could stabilize the SRG sheets. Since the GO sheets were enclosed by the PVDF molecular chains and reduced to SRG sheets during the solvothermal process, they would not fold easily or form aggregates as often happened. This would facilitate the formation of conducting network and result in a low percolation threshold. The large aspect ratios of the SRG sheets make the percolation threshold even GDC 0068 smaller. Figure 3 Static conductivity of the SRG/PVDF composites showing percolative behavior. The red solid lines are nonlinear fits to Equation 1. The conductivity takes the average value of ten samples. Inset is the plot of log σ versus log(p−p c). Table 1 Parameters characterizing percolative behavior of SRG/PVDF composites Composite σ 0 (S/cm) p c t value SRG/PVDF 0.33 0.31 vol.% 2.64 Figure 4a shows the frequency dependency of the dielectric constant (ε r) of the SRG/PVDF composites.

Data management and analysis All questionnaires were completed at a central location and transcribed to a central JNJ-26481585 purchase database. Subjects that did not complete the questionnaires or submitted incomplete questionnaires were dropped MRT67307 in vivo from the study and not included in the study analysis (four subjects – two females from each group). Data was identified by subject number and examined for accuracy and completeness. Tabulated data was analyzed with JMP 8.0 (SAS Institute) using standard parametric paired t-tests and significance

was assessed with a two-tailed alpha level set at 0.05. Results Over the course of the 4-week supplementation period, there were no adverse events or side effects reported. There were no significant changes in body weight

or body fat percentage. At week 4, salivary cortisol exposure was significantly (p<0.05) lower (−18%) in the Relora group (Figure  1). Figure 1 Salivary Cortisol (ug/ml). Salivary cortisol was 18% lower (p<0.05) in the Relora group compared to Placebo at Week 4 (0.525+0.190 to 0.642+0.353). Significantly better (p<0.05) mood state indices were observed in the Relora group for Overall Stress (−11%) and Global Mood State (−11%) compared to Placebo (Figure  2). Mood State subscales (Figure  learn more 3) were significantly better (p<0.05) in the Relora group compared to Placebo at week 4; Tension (−13%), Depression (−20%), Anger (−42%), Fatigue (−31%), Confusion (−27%), and Vigor (+18%). Figure 2 Global Mood State (POMS) and Overall Stress (Yale Stress Survey). Global Mood State was 11% better (p<0.05) in the Relora group compared to Placebo (118+18 to 133+30) – lower score is a “better” Global Mood State (POMS). Overall Stress (Yale Stress Survey) was 11% lower (p<0.05) in the Relora group compared to Placebo (30.2+5.2 to 33.9+7.4). The global mood state was calculated based on scoring (0-4 with 0 = not at all, 2 = moderately and 4 = extremely) answers to 58 of the 65 adjectives of the POMS (a lower number

is a “better” global mood state). Global Mood State is the combined score of the 6 subscales of the POMS (McNair et al., [9]). Figure 3 Profile of Mood States (POMS). Phenylethanolamine N-methyltransferase Numerical scores for each of the 6 subscales of the POMS (McNair et al., [9]). The Relora group showed significantly improved mood state parameters compared to Placebo at Week 4 (* = p<0,05). Discussion Antidepressant drugs are the most commonly prescribed class of medications in the United States and are used by athletes and non-athletes alike [24]. More than 10% of the American population is taking one or more antidepressant drugs, which represents 27 million individuals taking more than 120 million prescriptions and spending over $80 billion per year. According to a recent survey [25], large numbers of Americans feel an antidepressant drug would be helpful for; dealing with day-to-day stresses (83%); making things easier in relations with family and friends (76%); and helping people feel better about themselves (68%).

Iron oxide nanocrystals can further enhance the adsorption capacities because of their high specific surface area [6, 10]. Another advantage of using iron oxide-based adsorbents is that they can be easily extracted from wastewater by applying an external magnetic force. Salubrinal However, few research works have reported on adsorbents with both adsorption effects. The emergence of graphene

oxide makes such combination possible due to its abundant functional moieties (hydroxyl and carboxyl groups) [11, 12], which enable possible metal oxide deposition and functional organic group grafting on its surface [13–15]. In this work, we deposited Fe3O4 nanoparticles on graphene oxide and then grafted thiol groups on the Fe3O4/graphene oxide (MGO). The thiol-functionalized MGO exhibited relatively high Hg2+ adsorption capacity. The adsorbent could be separated from the water solutions easily and reused after it was exchanged with H+. Methods Chemicals and materials Natural graphite (500 mesh), 98 wt.% H2SO4, 5 wt.% HCl aqueous solution, 30 wt.% H2O2 aqueous solution, acetone, and Na2CO3 were purchased from Sinopharm

Chemical Reagent Co., Ltd. (Shanghai, China). 1-Methyl-2-pyrrolidone click here (NMP), ferric acetylacetonate (Fe(acac)3), potassium permanganate (KMnO4), NaHCO3, 1-ethy-3-(3-dimethyllaminopropyl) carvodiimide hydrochloride (EDC), and 2-mercaptoethylamine (MEA) were purchased from Aladdin Reagent Company (Shanghai, China). Other reagents used were of analytical grades without further purification. Deionized water was used in all the processes of aqueous solution preparations. Preparation of MGO Graphene oxide (GO, 100 mg) was dispersed in 30 ml of NMP by ultrasonication at room temperature, and the mixture was heated to 190°C under an argon atmosphere. Fe(acac)3 (1.413 g, 4 mmol) was dissolved in 20 ml of NMP and added dropwise in about 1 h to the GO/NMP solution under vigorous stirring. The stirring was continued for another 4 h after the dropping was finished. After being cooled to room temperature, the mixture was washed three

times check details using acetone and water alternatively. The see more precipitate was collected by magnetic separation and was then dispersed in water by ultrasonication. The resulting black powder was collected by freeze-drying. Synthesis of thiol-functionalized MGO MGO (10 mg) was dispersed in 10 ml of deionized water by ultrasonication in an ice bath. EDC of 50 ml and a Na2CO3-NaHCO3 (1:9) buffer solution were added to adjust the pH of the system to approximately 9. After carboxyl groups on MGO were activated in 1 h, a solution containing 100 mg of MEA was added dropwise to the system. With the protection of argon, the reaction lasted for 24 h. The precipitate was collected by magnetic separation and was then dispersed in water by ultrasonication. The resulting black powder was collected by freeze-drying.