; (3) radial basis kernel: K(x, y) = exp-; (4) Sigmoid kernel:

..; (3) radial basis kernel: K(x, y) = expx-y; (4) Sigmoid kernel: K(x, y) = tanh [b(x•y)+c], where b, c and σ are parameters. Among these four types of kernel

function, radial basis kernel showed best performance according to the results from similar studies [34, 35]. The correct choice of kernel parameters is crucial for obtaining good results, so an extensive search must be conducted FK228 supplier on the parameter space before results can be trusted. Here we adopted radial basis kernel function and 5-fold cross-validation in the training set to search the best parameters for SVM-based classification in the test set. Figure 1 Classification via SVM (linear separable case). Evaluation of model performance Classification accuracy and the standard deviations of our proposed method (with prior knowledge) were compared with the original one (no prior knowledge) in the training set and test set. The framework of the above mentioned procedures is shown in Figure 2. Figure 2 Framework of our proposed method. Statistical analysis All the statistical analyses were conducted using R statistical software version 2.80 (R foundation for Statistical Computer, Vienna, Austria). Results Genes selected by PAM The number of genes selected by PAM method varied from 4 to 12 with an E7080 mw average 7.81, and the standard deviation 2.21. The combination of genes selected by PAM is shown ID-8 in Table 1. Among them,

CEACAM6, calretinin, VAC-β and TACSTD1 appeared in the results all the time. Table 1 Gene lists selected by Prediction Analysis for Microarrays Gene name GenBank access No. Location at HG_U95Av2 ERBB3 M34309 1585_at CD24 L33930 266_s_at TACSTD2 J04152 291_s_at UPK1B AB015234 32382_at HIST1H2BD M60751 38576_at TITF-1 U43203 33754_at CLDN3 AB000714 33904_at CEACAM6 M18728 36105_at PTGIS D83402 36533_at SFTPB J02761 37004_at caltrtinin X56667 37157_at VAC-β

X16662 37954_at claudin-7 AJ011497 38482_at AGR2 AF038451 38827_at TACSTD1 M93036 575_s_at Gene selection via prior biological knowledge After reviewed the full text of literature, twenty-three lung adenocarcinoma-related genes were selected. Then, Table 2 lists the eight significant genes that passed the multiple testing procedure in the training set provided by Gordon et al. The details of these genes are shown in Table 2. Table 2 Genes as prior biological knowledge Gene name GenBank access No. Location at HG_U95Av2 CXCL1 J03561 408_at IL-18 U90434 1165_at AKAP12 X97335 37680_at KLF6 U51869 37026_at AXL M76125 38433_at MMP-12 L23808 1482_g_at PKP3 Z98265 41359_at CYP2A13 U22028 1553_r_at Evaluation of model performance Our proposed method performed better after incorporating prior knowledge (Figure 3). Accuracy of the Apoptosis inhibitor modified method improved from 98.86% to 100% in training set and from 98.51% to 99.06% in test set. The standard deviation of the modified method decreased from 0.

PloS One 2013, 8:e68022 PubMedCentralPubMedCrossRef 18 Wu YC, Ch

PloS One 2013, 8:e68022.PubMedCentralPubMedCrossRef 18. Wu YC, Chang IC, Wang CL, Chen TD, Chen YT, Liu HP, Chu Y, Chiu YT, Wu TH, Chou LH, et al.: Comparison LDN-193189 clinical trial of IHC, FISH and RT-PCR methods for detection of ALK rearrangements in 312 non-small cell lung cancer patients in Taiwan. PloS One 2013, 8:e70839.PubMedCentralPubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions BW, KY and JZ carried out the DNA isolation. BW, YC, ZM, BD and YG performed real

time PCR for quantification of EGFR mutation. BW and JM performed the statistical analysis. BW and JM designed the study and drafted the manuscript. All authors read and approved the final manuscript.”
“Background Parthenolide is a sesquiterpene lactone derived from the plant feverfew. It is used to treat inflammation due to its ability of inhibiting NF-κB activity [1]. Parthenolide has also been reported to play other roles such as promoting cellular differentiation, causing cells to exit cell cycle and inducing apoptosis [2, 3]. Its pro-apoptotic effect on cancer cells is known to trigger the intrinsic apoptotic

pathway which includes elevated levels of intracellular reactive oxygen species (ROS) and alteration of BCL2 family proteins [4–6]. What’s more, recent studies have revealed that PTL could selectively eradicate acute myelogenous leukemia stem and progenitor cells [7]. It is also demonstrated that PTL could preferentially inhibit breast cancer stem-like cells [8], but the molecular mechanism was still unclear. There selleckchem are two major pathways contributing to apoptotic signaling: the extrinsic death receptor pathway and the intrinsic mitochondrial

pathway [9]. Death receptor 5 (TNFRSF10B) is a protein that belongs to tumor necrosis factor receptor (TNFR) superfamily [10]. It PD173074 manufacturer contains a cytoplasmic death domain (DD) which can recruit Fas-Associated Death Domain (FADD) and caspases to form the Death-Inducing Signal Complex (DISC) when the receptor is trimerized www.selleck.co.jp/products/sorafenib.html [11]. Subsequently, initiator caspases are activated and lead to the cleavage of downstream effectors. The activation of CASP8 can be regulated by FLICE-like inhibitor protein (CFLAR) which prevents recruitment of CASP8 to DISC [12, 13]. Development of pro-apoptotic agonists has been focused on TNFRSF10B because of its target selectivity for malignant over normal cells [14, 15]. The imbalance among the BCL2 family members which have been defined as either anti-apoptotic or pro-apoptotic is essential for the modulation of intrinsic pathway [16, 17]. The BH3-only protein PMAIP1 is a p53 transcriptional target in response to DNA damage [18]. It has been reported to be involved in chemotherapeutic agent-induced apoptosis [19].

Previous work by others has shown that culture activation of HSCs

Previous work by others has shown that culture activation of HSCs into myofibroblasts only partially reproduced the gene expression changes observed during BDL- and CCl4-induced activation [44]. Conclusion Although 4A3COOHmethyl AZD8931 molecular weight potently inhibited HSC trans-differentiation to pro-fibrogenic myofibroblasts in vitro without activating the PXR, it failed to inhibit liver fibrosis in an in vivo rat model. The cause of the disparity between in vitro and in vivo responses to 4A3COOHmethyl was most likely associated with a lack of expression

of the PGRMC1 target in liver myofibroblasts in vivo in contrast to in vitro activated myofibroblasts. This underscores the importance of animal models for testing potential anti-fibrogenics and suggests that confirming the presence of drug targets in vivo (including human diseased liver tissue) may assist in the development of effective anti-fibrotic drugs for clinical use. These data also demonstrate that the anti-fibrogenic effects of PCN in vivo are likely mediated entirely via the PXR. Methods Reagents All compounds in Additional files 1 and 2 were

purchased from Steraloids (Rhode Island, USA) except dexamethasone, betamethasone, progesterone, androstenedione and testosterone which were purchased from the Sigma Chemical Company (Poole, UK). All other reagents were from local commercial sources and were of the highest purity available. Isolation and culture of GW3965 HSCs HSCs were isolated from rats (250–300 g body weight, Harlan, UK) by sequential pronase/collagenase perfusion of the liver followed by density gradient centrifugation and elutriation as previously outlined [45]. Human HSCs were isolated by an essentially similar procedure [46] using discarded tissue from patients undergoing a hepatectomy with patient consent and ethical approval by the Grampian Regional Ethical Committee. HSCs were seeded onto plastic culture dishes and cultured in Dulbecco’s modified Eagle Medium (DMEM) containing 4.5 g/l of glucose mafosfamide and supplemented with 5% or 16% (v/v) fetal calf serum (for rat or human respectively), 80

μ/ml penicillin, 80 μg/ml streptomycin and 32 μg/ml gentamycin. Additional treatments were made by addition of compounds in an ethanol vehicle (stock solutions at 1000× final concentration). Ethanol at 0.1% (v/v) acted as control. Frequency of treatment (3 treatments per week/2 medium changes per week), as previously Ro 61-8048 described [8]. Isolation and culture of hepatocytes Rat hepatocytes were prepared by collagenase perfusion, essentially as previously described [46, 47], and cultured in William’s Medium E supplemented with 1 μg/ml bovine insulin, 10% foetal calf serum (FCS), 80 μ/ml penicillin and 80 μg/ml streptomycin on collagen type-I coated 6 well plates (BD Biosciences). After 2 hours, the medium was renewed without FCS and insulin supplementation and thereafter changed daily with renewed media additions where indicated.

In this paper we describe the development of reliable PCR-procedu

In this paper we describe the development of reliable PCR-procedures for the specific discrimination and quantification of Psv, Psn and Psf, both in vitro and in planta as epiphytes, by End Point PCR and Real-Time PCR, using two different technologies, the SYBR® Green I detection dye and three pathovar-specific TaqMan® hybridisation probes. Primers and probes specific for Psv, Psn and

Psf were designed upon the sequence data of selleckchem cloned fragments, previously amplified in Repetitive-sequence-based PCR (Rep-PCR) experiments with strains belonging to the three pathovars of P. savastanoi examined in this study using Enterobacterial Repetitive Intragenic Consensus (ERIC) primers [48]. These procedures have high sensitivity, specificity, rapidity and represent valid and innovative diagnostic tools that can suit all phytopathological laboratories, according to their equipment and skills, in order to promote and encourage the use of molecular detection methods for Psv in the frame of the certification programs for olive

propagation materials. Results Identification of P. savastanoi pathovar-specific sequences by ERIC-PCR and design of pathovar-specific primers The identities of P. savastanoi Thalidomide strains shown in Table 1 were confirmed by 16S rDNA sequencing and pathogenicity trials (data not shown). On these strains, Rep-PCR experiments buy Citarinostat with ERIC1R and ERIC2 primers were performed and the results referring to some representative strains for each P. savastanoi pathovar examined are shown in Emricasan Figure 1. The genomic ERIC-PCR profiles were highly reproducible; they consisted of bands ranging in size from 400 to

5,000 bp and were pathovar-specific. For each P. savastanoi pathovar at least a single and unique band, appearing in all the strains belonging to the same pathovar, was detected. The sizes were approximately 1,600, 830 and 1,350 bp in Psv, Psn and Psf, respectively (Figure 1). These pathovar-specific bands were then separately isolated and purified from agarose gels, cloned and analyzed for their nucleotidic sequences composition. Each band was demonstrated to consist of several fragments of the same size but having different nucleotidic sequences, which were then individually DIG-labeled and used as probes in dot blot hybridization experiments performed under high stringency with the genomic DNAs of Psv, Psn and Psf previously blotted to nylon film (data not shown).

Reduced killing of the

Reduced killing of the biofilm in comparison to planktonic cells was statistically significant (p = 0.04 and p = 0.0004 for tobramycin and ciprofloxacin, respectively). These data demonstrate that these drip-flow biofilms exhibit the antibiotic-tolerant

phenotype that is considered a hallmark of the biofilm mode of growth. When biofilm bacteria were dispersed prior to antibiotic exposure, they again became susceptible to the antibiotics. Log reductions measured for biofilm cells click here re-suspended into aerated medium and treated with tobramycin or ciprofloxacin for 12 h were 3.90 ± 0.10 and 4.40 ± 0.53, respectively. This degree of killing was the same as that measured for planktonic bacteria, indicating LDN-193189 that susceptibility was rapidly and fully restored upon dispersal of cells from the biofilm. Low buy Ilomastat oxygen concentrations in biofilms An oxygen

microelectrode was used to demonstrate the presence of oxygen concentration gradients in this system (Figure 1A). The oxygen concentration in the flowing fluid above the biofilm was approximately 6 mg l-1. Oxygen concentration decreased to 0.2 mg l-1 or less inside the biofilm. A similar profile was measured in a duplicate experiment. The oxygen concentrations shown in Figure 1A may not define the lower bound of oxygen concentration inside the biofilm because the electrode was positioned only partway into the biofilm, to avoid electrode breakage. Figure 1 Oxygen concentrations in Pseudomonas aeruginosa biofilms. Panel A shows a representative

oxygen concentration profile with depth in the biofilm. Zero on the x-axis corresponds to the biofilm-bulk fluid interface. Negative positions are located in the fluid film above the biofilm and positive positions are located inside the biomass. Panel B shows the coupling between oxygen and glucose utilization. The oxygen microelectrode was positioned at a location within the biofilm where the oxygen concentration was low. The medium flowing over the biofilm was switched between one containing glucose and ammonium ion (C, N) and a medium lacking these constituents (no C, N) as indicated by the arrows. The complete medium is present Vitamin B12 at time zero. The utilization of oxygen by bacteria is coupled to their simultaneous uptake and oxidation of a carbon source. To investigate this coupling, the oxygen microelectrode was positioned at a depth part way into the biofilm where the oxygen concentration was less than 0.5 mg l-1 (Figure 1B). The medium flowing over the biofilm was then changed from complete PBM to PBM lacking glucose and ammonium sulfate. Within a few minutes after switching to this starvation medium, the oxygen concentration in the biofilm abruptly rose to approximately 5 mg l-1. When the complete medium containing glucose and the nitrogen source was restored, the oxygen concentration quickly dropped back to its previous low level.

In order to improve the poor electronic conductivity, the bare Li

In order to improve the poor electronic conductivity, the bare Li2NiTiO4 nanoparticles are carbon-coated by simple ball milling with conductive carbon. The carbon content in the Li2NiTiO4/C composite is 19.8 wt.%. The TEM image of Figure 2b demonstrates that the Li2NiTiO4 nanoparticles are in close contact with the dispersed carbon particles. Thus, the active material particles are interconnected

by a carbon network, Tideglusib manufacturer which is favorable for fast electron transfer and lithium extraction/insertion kinetics. Figure 2 SEM image of Li 2 NiTiO 4 (a) and TEM image of Li 2 NiTiO 4 /C (b). The valence variations of Ni element in the Li2NiTiO4 electrode during cycling are analyzed by the XPS spectra and fitted in Figure 3. The characteristic binding energy located at 854.6 eV with a satellite peak at 860.5 eV in

the Ni 2p3/2 XPS spectrum for uncharged Li2NiTiO4 electrode could be assigned to Ni2+ species. The above observations are in agreement with the reported values in LiNi0.5Mn0.5O2, LiNi1/3Mn1/3Co1/3O2 and LiNi0.5Mn1.5O4[12–14]. The Ni 2p3/2 binding energy gives positive shift when the electrode is charged to 4.9 V, and the two peaks at 855.5 and 856.9 eV are corresponding to the binding energy of Ni3+ and Ni4+[15], respectively. When discharged to 2.4 V, the Ni 2p3/2 binding energy moves back to almost the original position. The best fit for the Ni 2p3/2 spectrum consists of a major peak at 854.6 eV and a less prominent one at 855.5 eV. The above BTK inhibitor purchase results ARRY-438162 purchase indicate that Ni2+ is oxidized to Ni3+ and Ni4+ during charging, Cediranib (AZD2171) and most of the high valence Ni3+/4+ is reduced to Ni2+ in the discharge process. Figure 3 XPS spectra of Ni

2p 3/2 at different charge-discharge state. Figure 4 exhibits the CV curves of the Li2NiTiO4/C nanocomposite. For the first CV curve, a sharp oxidation peak at 4.15 V corresponds to the oxidation of Ni2+ to Ni3+/Ni4+. Another oxidation peak appears around 4.79 V and almost disappears in the second and third cycles, which might be attributed to the electrolyte decomposition and the irreversible structure transitions [8, 9]. The wide reduction peak at 3.85 V is assigned to the conversion from Ni3+/Ni4+ to Ni2+. The second and third CV curves are similar, indicating a good electrochemical reversibility of the Li2NiTiO4/C electrode. Figure 4 CV curves of the Li 2 NiTiO 4 /C nanocomposite. Figure 5a shows the galvanostatic charge-discharge curves of the Li2NiTiO4/C nanocomposite at 0.05 C rate (14.5 mA g-1) under room temperature. The charge/discharge capacities in the first, second, and third cycles are 180/115 mAh g-1, 128/111 mAh g-1, and 117/109 mAh g-1, respectively, with corresponding coulombic efficiencies of 64%, 87%, and 94%. The Li2NiTiO4/C exhibits superior electrochemical reversibility after the first cycle, which is in accordance with the CV result. The dQ/dV vs. potential plot for the first charge-discharge curve is presented in the inset in Figure 5a. Two oxidation peaks located at 4.2 and 4.

2 3 Treatments In accordance with a two-way randomized crossover

2.3 Treatments In accordance with a two-way randomized crossover study design, participants were given two 5-day treatments (days 1–5 of each crossover phase; Fig. 1) with a once-daily oral contraceptive, once as monotherapy (treatment A) and once with once-daily prucalopride on days 1–6 of the treatment phase (treatment B). The washout

period between the two contraceptive treatments was 7 ± 2 days. The stage of the patient’s menstrual cycle was not taken into account in the timings of these treatments. The oral contraceptive Trinovum® (ethinylestradiol 0.035 mg and norethisterone 1 mg; Janssen-Cilag Ltd) was used; prucalopride was administered as 2 mg film-coated tablets containing prucalopride selleck screening library succinate, equivalent to 2.0 mg prucalopride base. Fig. 1 Overview of the trial design. OC oral contraceptive The oral contraceptive dose was taken at 0800 hours. For the combination treatment, prucalopride was administered immediately before the oral contraceptive. The drugs were taken with a total of 200 mL of non-carbonated

water. On days 1 and 5 of each treatment period, the study medication was administered in the clinic following an overnight fast of at least 10 hours, and participants were not permitted to eat or drink until 2 hours MK-4827 price after receiving the medication, at which time they received a standard breakfast. On all other days, participants took the study treatments either

at the clinic (days 2 and 6) or at home (days 3 and 4) 30 minutes before breakfast. Compliance was Transmembrane Transporters inhibitor assessed by investigator supervision of dosing (except on days 3 and 4) and daily diary entries. During the study, participants were not permitted to take medication other than the study drugs, with the exception of as-needed Thalidomide paracetamol/acetaminophen (up to a maximum of three 500 mg tablets per day, and no more than 3 g during the study). 2.4 Pharmacokinetic Assessments Serial blood samples for the determination of ethinylestradiol and norethisterone concentrations in plasma were taken on day 1 pre-dose and then at 1, 2, 3, 4, 6, 8, 10, 12, and 24 hours post-dose, and on day 5 pre-dose and then at 1, 2, 3, 4, 6, 8, 10, 12, 24, 36, and 48 hours post-dose. Participants receiving treatment B had serial blood samples collected for the determination of plasma concentrations of prucalopride on days 1 and 5 pre-dose and then at 3 hours post-dose, and on day 6 pre-dose and then at 24 hours post-dose. No pharmacokinetic parameters were calculated for prucalopride. 2.4.1 Assay Validation Plasma samples were analyzed for prucalopride, ethinylestradiol, and norethisterone, using validated liquid chromatography–tandem mass spectrometry (LC–MS/MS) methods.

For NanPSi, the wafer

was etched with a current density o

For NanPSi, the wafer

was etched with a current density of 60 mA/cm2 for 1 min. MacPSi was etched with a current density of 4 mA/cm2 for 30 min. Then, the samples were rinsed with pentane and dried under a nitrogen flow. Macro- and nanoporous silicon samples were morphologically characterized by scanning electron microscopy (ESEM-FEI Quanta 600 and SEM Quanta 450; FEI, Hillsboro, OR, USA). Porous silicon functionalization MacPSi and NanPSi substrates were oxidized at 600°C for 15 min. Then, the samples were treated in KOH 0.1 M for 3 min and HNO3 0.1 M for 10 min to increase the density of surface hydroxyl groups. Next, the samples were silanized in 5 mM solution of APTES (Gelest Inc., Morrisville, PA, USA) in anhydrous toluene for 3 h at 75°C. Then, they were washed in succession with toluene, ethanol, and deionized see more water and dried under a nitrogen flow. Cell seeding and culture this website HAECs were purchased from Cascade BiologicsTM (Portland, OR, USA) and, at the 5th passage, were thawed and seeded on NunclonTM Δ surface 12-well plates (Thermo Fisher Scientific, Waltham, MA, USA) in the presence or absence (in the case of control conditions) of sterilized silicon substrates, at a density of approximately 1.9 × 104 viable cells/mL and 4 × 103 of viable cells/cm2. Through the whole

experiment, cells were maintained in M200 medium supplemented with 2% (v/v) low serum growth supplement (LSGS), 10 mg/mL gentamicin, 0.25 mg/mL amphotericin B, 100 U/mL penicillin, and 100 mg/mL of streptomycin. Cells were seeded in find more complete cell culture medium and growth at 37°C in a humidified incubator (HERAcell 150; Heraeus, Hanau, Denmark) with atmosphere containing 5% CO2, and culture medium was cAMP replenished every 2 days with a fresh medium. Cell viability and cytotoxicity Cell viability was assessed by morphology using phase-contrast microscopy and by trypan blue exclusion (Merck & Co., Inc., Whitehouse Station, NJ, USA). The viability of the HAEC was >97%. The extent of cytotoxicity of each experimental condition was determined by a colorimetric assay, which measures released lactate dehydrogenase (LDH) activity (the LDH Cytotoxicity Detection

Kit; Roche Applied Science, Penzberg, Germany). Briefly, LDH enzyme is rapidly released into the cell culture supernatant when the plasma membrane is damaged. This result is a colorimetric reaction that can be measured at a wavelength of 492 nm. Thus, the activity of LDH released by the cells was measured in cell-free supernatants collected after 48-h incubation times. Results are expressed as mean 492-optical density (OD) and standard deviation (SD error bars) of LDH produced by the cells under each treatment condition. Scanning electron microscopy The morphology and shape of cells adhering to the functionalized PSi substrates were observed with scanning electron microscope (SEM) (JEOL model JSM-6400; JEOL Ltd., Akishima-shi, Japan).

BxPC-3 cells displayed also a dose dependency regarding the relat

BxPC-3 cells displayed also a dose dependency regarding the relative contribution of selleck chemicals necrotic and apoptotic cell death. The response on cell viability upon incubation with TRD 250 μM for 24 hours was characterized by a mixed apoptotic

and necrotic effect whereas TRD 1000 μM was characterized by an exclusive and pronounced necrotic effect. This phenomenon became even more obvious in AsPC-1 cells, were TRD 1000 μM led to a strong necrotic effect. The observed dose dependency of apoptotic and necrotic cell see more death is consistent with previous studies by others [27] as well as by our group [6, 26, 34]. The V-shaped dose effect was found in HT29 cells as well as in Chang Liver cells and was characterized by a dose response with maximal effects on cell viability and apoptosis with the intermediated concentration of TRD 250 μM whereas the highest (TRD 1000 μM) and lowest (TRD 100 μM) concentrations were less effective. This V-shaped dose effect has been described only once by our group [34]. However, to our surprise HT1080 cells presented in the current study with a anti-proportional OSI-027 research buy dose effect with decreasing effects on cell viability and apoptosis

upon treatment for 24 h with increasing TRD concentrations. We can only speculate about the reason for this inverse proportionality. Our assays were repeated with nine consecutive passages, thus excluding biological assay variability

as a possible explanation for this unusual finding. The second part of the study comprised the evaluation of the contribution of reactive oxygen species (ROS) to TRD induced PCD by co-incubation experiments with either the radical scavenger N-acetylcysteine (NAC) or the glutathione depleting agent DL-buthionin-(S,R)-sulfoximine (BSO). Previous studies have presented first evidence for involvement of TRD mediated ROS production [9, 13, 36]. Furthermore, Sitaxentan cell death induced by TRD has been shown to be reversible by application of radical scavengers like NAC [9, 12, 13, 36] and to be enhanced by inhibitors of ROS detoxification like BSO [9]. In our study, all cell lines except HT1080 fibrosarcoma cells responded to NAC co-incubation with an attenuation of TRD induced cell death. However, the magnitude of protection was divergent among cell lines ranging from partial protection (Chang Liver, AsPC-1, BxPC-3) to complete protection (HT29). To our surprise and in contrast to the available literature, HT1080 cells presented a completely contrary response to radical scavenging by NAC leading to enhancement rather than attenuation of TRD induced cell death. The biological cause behind this unexpected response pattern is currently unknown. However, ROS can be regarded as a “”double edged sword”" in terms of anti-neoplastic activity [37].

J Mater Chem 2012, 22:15599–15605 CrossRef 9 Ko SH, Lee D, Hotz

J Mater Chem 2012, 22:15599–15605.CrossRef 9. Ko SH, Lee D, Hotz N, Yeo J, Hong S, Nam KH, ABT-737 mw Grigoropoulos CP: Digital selective growth of ZnO nanowire arrays from inkjet-printed nanoparticle seeds on a flexible substrate. Langmuir 2012, 28:4787–4792.CrossRef 10. Greene LE, Law M, Goldberger J, Kim F, Johnson JC, Zhang Y, Saykally RJ, Yang P: Low-temperature wafer-scale production of ZnO nanowire. Angew Chem Int Ed 2003, 42:3031–3034.CrossRef 11. Law M, Greene LE, 4EGI-1 mw Johnson JC, Saykally R, Yang P: Nanowire dye-sensitized solar cells. Nat Mater 2005, 4:455–459.CrossRef 12. Ko SH, Chung J, Hotz N, Nam KH, Grigoropoulos

CP: Metal nanoparticle direct inkjet printing for low-temperature 3D micro metal structure fabrication. J Micromech Microengr 2010, 20:125010.CrossRef 13. Ko SH, Park

I, Pan H, Misra N, Rogers MS, Grigoropoulos CP, Pisano AP: ZnO nanowire network transistor fabrication on a polymer substrate by low-temperature, all-inorganic nanoparticle solution process. Appl Phys HCS assay Lett 2008, 92:154102.CrossRef 14. Yeo J, Hong S, Wanit M, Kang HW, Lee D, Grigoropoulos CP, Sung HJ, Ko SH: Rapid, one‒step, digital selective growth of ZnO nanowires on 3D structures using laser induced hydrothermal growth. Adv Funct Mater 2013, 23:3316–3323.CrossRef 15. Gao P, Brent JL, Buchine BA, Weinstraub B, Wang ZL, Lee JL: Bridged ZnO nanowires across trenched electrodes. Appl Phys Lett 2007, 91:142108.CrossRef 16. Park WI, Kim JS, Yi G, Bae MH, Lee HJ: Fabrication and electrical characteristics Methisazone of high-performance ZnO nanorod field-effect transistors. Appl Phys Lett 2004, 85:5052.CrossRef 17. Hong S, Yeo J, Manorotkul W, Kwon J, An G, Ko SH: Low-temperature rapid fabrication of ZnO nanowire UV sensor array by laser-induced local

hydrothermal growth. J Nanomater 2013, 2013:246328. Competing interests The authors declare that they have no competing interests. Authors’ contributions SH, JK, HL, and JY carried out the experiments and drafted the manuscript. SSL and SHK supervised the project and participated in the design of the study and analysis of its results. All authors read and approved the final manuscript.”
“Background Due to the development and expansion of industry, pollution of heavy metals in water supplies increases in the recent years. The pollution is seriously threatening the ecological systems as well as human health. Among them, mercury is one of the most hazardous elements due to its toxicological and biogeochemical behavior [1, 2]. A lot of adsorbents have been employed to extract Hg2+ from the industrial wastewaters. For example, thiol-functionalized adsorbents exhibited a specific binding capability toward highly toxic heavy metal ions including Hg2+ due to the existence of the thiol groups [3–6].