A selection bias may also have affected our results, because the data included in the present study were derived from single-center-based registrations. Nevertheless, our observations suggest that there is a potential relationship between the amount of urinary excreted Klotho and the residual renal function among PD patients, and this relationship will need to be confirmed in further studies including a larger number of PD patients. Moreover, the significant difference in the amount of urinary Klotho between PD patients and normal control subjects demonstrated in the present study led us to propose that there might be a continuum in the relationship between

Akt inhibitor the amount of urinary Klotho and renal function, characterized by the GFR, among subjects with or without chronic kidney disease. On the other hand, the clinical impact of the serum level of Klotho on renal function might need to be evaluated more carefully, because it has been demonstrated that the STAT inhibitor levels of serum Klotho in patients with early stages of chronic kidney disease were observed

to be increased in comparison to those in healthy control subjects [25]. Whether the findings demonstrated in the present study can also be demonstrated in subjects with various stages of chronic kidney disease is currently being investigated by our group. Conflict of interest None declared. References 1. Kuro-o M, Matsumura Y, Aizawa H, Kawaguchi H, Suga T, Utsugi T, et al. Mutation of the mouse klotho gene leads to a syndrome resembling ageing. Nature. 1997;390:45–51.PubMedCrossRef 2. Kuro-o M. Klotho. Pflugers Arch. 2010;459:333–43.PubMedCrossRef

3. Chen CD, Podvin S, Selleck VX-680 Gillespie E, Leeman SE, Abraham CR. Insulin stimulates the cleavage and release of the extracellular domain of Klotho by ADAM10 and ADAM17. Proc Natl Acad Sci Enzalutamide cell line USA. 2007;104:19796–801.PubMedCrossRef 4. Imura A, Iwano A, Tohyama O, Tsuji Y, Nozaki K, Hashimoto N, et al. Secreted Klotho protein in sera and CSF: implication for post-translational cleavage in release of Klotho protein from cell membrane. FEBS Lett. 2004;565:143–7.PubMedCrossRef 5. Hu MC, Shi M, Zhang J, Quiñones H, Kuro-o M, Moe OW. Klotho deficiency is an early biomarker of renal ischemia–reperfusion injury and its replacement is protective. Kidney Int. 2010;78:1240–51.PubMedCrossRef 6. Kusano E. Mechanism by which chronic kidney disease causes cardiovascular disease and the measures to manage this phenomenon. Clin Exp Nephrol. 2011;15:627–33.PubMedCrossRef 7. Haruna Y, Kashihara N, Satoh M, Tomita N, Namikoshi T, Sasaki T, et al. Amelioration of progressive renal injury by genetic manipulation of Klotho gene. Proc Natl Acad Sci USA. 2007;104:2331–6.PubMedCrossRef 8. Koh N, Fujimori T, Nishiguchi S, Tamori A, Shiomi S, Nakatani T, et al.

In the bloodstream, C. albicans is exposed to the innate immune defenses. As a part of human innate immune system, serum and its components show different degrees of protection against systemic candidiasis. In this study, the natural proliferation condition of C. albicans was monitored continuously by a Live Cell Movie Analyzer. C. albicans cells in HS moved with Brownian motion in the initial selleck stage of culture, then failed adhere to the surface of polystyrene plates. This indicates

that C. albicans may remain in a suspended status at the early period of entering the blood stream. Previous studies showed that free-flowing C. albicans can be rapidly cleared from the blood [19]. We determined that human serum facilitates the removal of C. albicans by inhibiting the adhesion of C. albicans on the surface of the endothelial cells. C. albicans possesses virulence factors that are needed to establish candidiasis that are involved in the many steps of this complicated process,

such as adhesion, phenotypic switching, morphogenesis, and biofilm learn more formation [20]. Some factors in the bloodstream, such as temperature and serum, facilitate the filamentation of C. albicans[21–23]. It is reported that filamentation is favorable for C. albicans adhesion and biofilm formation [24, 25]. However, filamentation failed to offset the biofilm formation inhibition caused by the HS-induced adhesion defect, as demonstrated in our study. We also investigated the effect of serum on germ tube formation in C. albicans. Our results LY2835219 research buy showed that the science rate of germ tube formation is high in HS medium, but compared with the control group, germ

tube formation in the experimental group was delayed in the initial stage of culture (within 90 min). This may be one of the reasons for HS-induced adhesion inhibition. Based on these results, we also think that RPMI 1640 medium may be a more suitable medium than human serum to conduct germ tube testing in C. albicans. In the initial stage of biofilm culture (the adhesion period), low serum concentrations suppressed C. albicans biofilm formation. However, the serum had no effect on pre-adhered biofilms (90 min), even if the serum was in a very high concentration. Thus, we concluded that serum may inhibit biofilm formation by preventing the adhesion of C. albicans, in consensus with previous studies [15, 16]. Recent studies showed that addition of as little as 3% human serum to media can promote C. albicans biofilm formation [14], contrary to our results. This may be explained by the use of different materials, such as serum, culture medium, strains, adhesive medium, and so on. It has been reported that IgG, LL-37, transferrin and lactoferrin, at concentrations close to those found in vivo, can reduce the capacity of C. albicans and bacteria to adhere to polystyrene [17, 26–28].

Salinity shifts characterize a boundary which is one of the most difficult barriers to cross for organisms in all

three domains of life [43]. While mechanisms to cope with high salt concentrations are relatively well studied in prokaryotes, they are still largely unknown in protists (with the selleck inhibitor exception of the model algae Dunaliella salina[44]). While there is evidence that many protists have narrow ranges of salt tolerance [45, 46], some taxa are known to occur under a wide range of salinities, from freshwater to hypersaline [47]. One example is the ciliate Cyclidium glaucoma[48], which may explain the occurrence Selleck Capmatinib of some of the same phylotypes in haloclines and brines of specific DHABs. Other examples are likely to exist. In contrast, adaptations to anoxia in ciliates are well known. Ciliates are one of the most successful eukaryotic taxon groups in hypoxic and anoxic habitats. In their long evolutionary history, they have acquired several strategies that allow for an anaerobic lifestyle, including hydrogenosomes [49, 50], anaerobic mitochondria [51], and/or symbiotic

networks [52, 53]. The high taxonomic diversity of anaerobe ciliates includes taxa such as Nyctotherus, Loxodes, Pleuronema, Strombidium, Trimyema, Cyclidium and Metopus, some of which were also detected in our genetic diversity survey. Electron microscopy and fluorescence in situ hybridization assays provide unbiased evidence that the genetic signatures we detected in our rRNA-targeted gene survey can be assigned to ciliates living

in the AG-120 clinical trial DHABs rather than reflecting ancient nucleic acids. (Figure 5, [25, 54]). Taking advantage of phylotypes that we detected exclusively in specific habitats and phylotypes that can be found in several habitats with distinct hydrochemical Amisulpride characteristics, we may assume that the latter have a character of more generalist taxa compared to the more locally restricted phylotypes. The total number of observed taxon groups is 102 distributed over eight different datasets (samples or habitats) (Additional file 1: Figure S1). In those eight samples there are 13 generalist taxonomic groups that appeared simultaneously in at least six of the datasets. Only four taxonomic groups appeared in all of the eight datasets. Specialists, i.e. taxa that are restricted to a single unique habitat account for 34 different taxonomic groups. This results in a specialist/generalist ratio of 8.5 to 1, indicating a high specialization of taxa in the habitats under study. However, there is a limitation to infer the autecology of specific evolutionary lineages based on sequence data and microscopy evidence [25]. We do not make any attempt to explain the presence or absence of specific phylotypes in individual samples, and we instead focus only on community level ciliate diversity.

In the UV-visible spectrum, a strong, broad peak at about 420 nm was observed for AgNPs (Figure 1). The specific and characteristic

features of this peak, assigned to a surface plasmon, has been well documented for various metal nanoparticles with sizes ranging from 2 to 100 nm [27, 28]. Bortezomib in vivo The silver nanoparticles were formed by adding 10 ml leaf extracts with aqueous AgNO3. After 6 h, the color of the mixed solutions of leaf extract and AgNO3 changed from pale green to deep brown indicating the formation of silver nanoparticles. The change in color of the reaction medium as an effect of presence of reducing potential substances present in the leaf extract. The color of the silver nanoparticles are due to excitation of surface plasmon vibration in silver nanoparticles and this color change is due to redox reaction between the leaf extract and AgNO3. AgNPs have free electrons, which give rise to a surface plasmon resonance click here absorption due to the combined vibration of electrons of the metal nanoparticles in resonance with the light wave. [29] It is observed from Figure 1 that the synthesized AgNPs display a clear and single surface plasmon resonance (SPR) band located at 420 nm which confirms the reduction of silver ion to metallic silver. In contrast, AgNO3 shows maximum

absorbtion at 220 nm, whereas the leaf extract shows two absorbtion peaks at 450 and 650 nm. The sharp absorption peak of AgNPs indicates that the formation of spherical and homogeneous distribution of silver nanoparticles. The similar observation was reported using leaf extract

of Delonix elata mediated synthesis of silver nanoparticles [26]. XRD analysis of AgNPs Further, the synthesized silver nanoparticles were confirmed using XRD analysis. Figure 2 shows that the XRD patterns of natural dried silver nanoparticles synthesized using leaf extract. A number of Bragg reflections with 2θ values of 24.48°, 30.01°, 33.30°, 34.50°, 46.30° sets of lattice planes are observed which may be indexed to the (111), (200), and (220) faces of silver respectively. The XRD pattern thus clearly selleckchem illustrates that the silver nanoparticles formed in this present synthesis are crystalline in nature and having face centered cubic (fcc) crystal Uroporphyrinogen III synthase structure. The XRD pattern confirmed the presence of Ag colloids in the sample. A strong diffraction peak located at 30.01 was ascribed to the (111) facets of Ag. The intensive diffraction peak at a 2θ value of 30.01° from the (111) lattice plane of fcc silver unequivocally indicates that the particles are made of pure silver. Two additional broad bands are observed at 34.50°, 46.30° correspond to the (200) and (220) planes of silver respectively (Figure 2). The Braggs reflections were also observed in the XRD pattern at 2θ = 24.48° and 32.50°. The assigned peaks at 2θ values of 24.48°, 29.0°, and 32.

Biochimie 2014. doi: 10.1016/j.biochi.2013.12.023 34. Cifuentes-Rojas C, Shippen DE: Telomerase regulation. Mutat Res 2012, 730:20–27.PubMedCentralPubMedCrossRef 35. Heaphy CM, de Wilde RF, Jiao Y, Klein AP, Edil BH, Shi C, Bettegowda C, Rodriguez FJ, Eberhart CG, Hebbar S, Offerhaus GJ, McLendon R, Rasheed BA, He Y, Yan H, Bigner DD, Oba-Shinjo SM, Marie SK, Riggins GJ, Kinzler KW, Vogelstein B, Hruban RH, Maitra A, Papadopoulos N, Meeker AK: Altered telomeres in tumors with ATRX and DAXX mutations. Science 2011, 333:425.PubMedCentralPubMedCrossRef 36. Henson JD, Reddel

RR: Assaying and investigating alternative https://www.selleckchem.com/products/gsk3326595-epz015938.html lengthening of telomeres activity in human cells and cancers. FEBS Lett 2010, 584:3800–3811.PubMedCrossRef 37. Cairney CJ, Hoare SF, Daidone MG, Zaffaroni N, Keith WN: High

level of telomerase RNA gene AR-13324 concentration expression is associated with chromatin modification, the ALT phenotype and poor prognosis in liposarcoma. Br J Cancer 2008, 98:1467–1474.PubMedCentralPubMedCrossRef 38. Venturini L, Motta R, Gronchi A, Daidone M, Zaffaroni N: Prognostic relevance of ALT-associated markers in liposarcoma: a comparative analysis. BMC Cancer 2010, 10:254.PubMedCentralPubMedCrossRef 39. Henson JD, Hannay JA, McCarthy SW, Royds JA, Yeager TR, Robinson RA, Wharton SB, Jellinek DA, Arbuckle SM, Yoo J, Robinson OSI-906 concentration BG, Learoyd DL, Stalley PD, Bonar SF, Yu D, Pollock RE, Reddel RR: A robust assay for alternative lengthening Atazanavir of telomeres in tumors shows the significance of alternative lengthening of telomeres in sarcomas and astrocytomas.

Clin Cancer Res 2005, 11:217–225.PubMed 40. Johnson JE, Gettings EJ, Schwalm J, Pei J, Testa JR, Litwin S, von Mehren M, Broccoli D: Whole-genome profiling in liposarcomas reveals genetic alterations common to specific telomere maintenance mechanisms. Cancer Res 2007, 67:9221–9228.PubMedCrossRef 41. Montgomery E, Argani P, Hicks JL, DeMarzo AM, Meeker AK: Telomere lengths of translocation-associated and nontranslocation-associated sarcomas differ dramatically. Am J Pathol 2004, 164:1523–1529.PubMedCentralPubMedCrossRef 42. Dei Tos AP: Liposarcomas: diagnostic pitfalls and new insights. Histopathology 2014, 64:38–52.PubMedCrossRef 43. Fritz B, Schubert F, Wrobel G, Schwaenen C, Wessendorf S, Nessling M, Korz C, Rieker RJ, Montgomery K, Kucherlapati R, Mechtersheimer G, Eils R, Joos S, Lichter P: Microarray-based copy number and expression profiling in dedifferentiated and pleomorphic liposarcoma. Cancer Res 2002, 62:2993–2998.PubMed 44. Pilotti S, Della Torre G, Lavarino C, Sozzi G, Minoletti F, Vergani B, Azzarelli A, Rilke F, Pierotti MA: Molecular abnormalities in liposarcoma: role of MDM2 and CDK4-containing amplicons at 12q13–22. J Pathol 1998, 185:188–190.PubMedCrossRef 45.

To determine the effect buy Cyclopamine of this energy transfer process on the luminescence properties of Er3+ in the SROEr films with different Si NCs microstructures, the PL spectra of Er3+ in the films are provided, as shown in Figure 4a. Interestingly,

the PL intensity of Er3+ decreases with the increase of the Si excesses, which is completely opposite to the evolution of the η but DAPT supplier coincident with that of the original PL intensity of Si NCs, as shown in Figures 2 and 3. To further determine the effect of Si NCs microstructures on the transition between intra-4f levels of Er3+ ions (4I13/2 – 4I15/2), PL decay curves at the emission wavelength of Er3+ (1.54 μm) are provided, as shown in Figure 4b. From their fittings by stretched exponential function, we obtained that the characteristic decay time is on the order of millisecond (the curves of SROEr with the Si excess of 36% and 58% are not shown here). The largest value is obtained from the film with the lowest Si excess, which means

that higher Si excess and the coalescence of Si NCs would enhance the nonradiative recombination of Er3+ ions. Nevertheless, the amount of Si excess has an insignificant effect on the luminescence performance of Er3+ as the variation of the characteristic decay time can be negligible, as shown in Figure 4b. Since the size and density of Si NCs for the sample with the Si excess of 36% were similar to the one with the Si excess of 88%, as shown in Figure 1b,d, while the PL intensity is significantly decreased, we ascribe the main origin of this decreased selleck chemicals PL intensity as the microstructural differences of the Si NCs in these samples. Furthermore, the decrease of the oscillator strength with the increasing size of

the Si NCs due to the coalescence might be also a partial reason for this decreased PL intensity. Besides, the influence of Si excess on the percentage of optically active Er3+ ions was also considered. Since the excitation energy in our experiment is especially low (about 3 × 1016 cm−2 s−1), the number of Er3+ ions contributing to the 1.5-μm emission could be assumed to be equal to the concentration of Si NCs acting as sensitizers [21]. mafosfamide Actually, Si NCs with similar densities have been obtained from SROEr films with different Si excesses in our experiment, as shown in Figure 1. It means that the influence of the percentage of optically active Er3+ on the luminescent property of the samples with different amounts of the Si excess is insignificant. Therefore, the microstructures of Si NCs play an extremely important role on the emission of Er3+ ions. The Si NCs with separated microstructures should be prepared for the further improvement of the luminescence performance of Er3+ ions. Figure 4 Room-temperature PL spectra and decay curves of Er 3+ ion. (a) Room-temperature PL spectra of Er3+ ion in the SROEr films.

Mulukutla R: Nanoscience and technology “case studies on research & commercialization.”. [http://​www.​kymanox.​com/​JSNN_​Presentation_​31AUG12.​pptx] 5. Sargent JF Jr: Nanotechnology: a policy primer. Congressional Research Service 2012 Mocetinostat concentration [http://​www.​fas.​org/​sgp/​crs/​misc/​RL34511.​pdf] online PDF. Accessed 5 September 2012 6. Kayat J, Gajbhive V, Tekade RK, Jain NK: Pulmonary toxicity of carbon nanotubes: a systematic report. Elsevier:

Nanomed 2011,7(1):40–49. 7. Barry P: Cloaked carbon nanotechnology become non toxic. NewScientist Health. [http://​www.​newscientist.​com/​.​.​.​/​dn9169-cloaked-carbon-nanotubes-become-no] 8. Chai C: Study reveals that carbon nanotubes have no toxic effects on green algae. [http://​www.​azonano.​com/​search.​aspx?​q=​mg&​site=​all&​page=​7] online PDF. Accessed 6 August 2012 9. European Commission: Scientific Committee on Emerging and Newly Identified Health Risks (SENIHR) report. [http://​www.​ec.​europa.​eu/​health/​scientific_​committee/​.​.​.​/​scenihr_​s_​001.​pd] online PDF. Accessed 3 August 2012 10. Allianz: Protein Tyrosine Kinase inhibitor Working Part on Innovation and Technology Policy Results of OECD Mini Survey on Nanotechnology R/D Programmes. June 7–8, 2004. [http://​oecd.​org/​science/​nanosafety/​37770473.​pdf] Selleck Wortmannin online PDF. Accessed 30 June 2012 11. TERI: Review of international nanotechnology developments and policy concerns: capability, governance and nanotechnology 6-phosphogluconolactonase development:

a focus on India. [http://​teriin.​org/​Resupdate/​nano.​php] Online PDF with citing permission. Accessed 1 August 2012 12. Cozzens S, Cortes R, Soumonni O, Woodson T: Nanotechnology and the millennium development goals: water, energy, and agri-food. J Nanopart Res 2001, 2013:15(11).

doi:10.1007/s11051–013–2001-y 13. USA_National Nanotechnology Initiative: Nanotechnology 101. What is nanotechnology. [http://​www.​nano.​gov]. Accessed 1 August 2012 14. Observatory NANO: Public Funding of Nanotechnology, Seventh Framework Programme. [http://​www.​observatorynano.​eu/​publicfundingofn​anotechnologies] Accessed 9 August 2012 15. Sergeant JF Jr: The National Technology Initiative: overview, reauthorization and appropriation issues. Congressional Research Services [https://​www.​fas.​org/​sgp/​crs/​misc/​RL34401.​pdf] online PDF. Accessed 9 September 2012 16. USA_NNI: Regional, State and Local Initiatives in Nanotechnology Report. In National Nanotechnology Initiative Workshop. Oklahoma City; 2009. [http://​www.​nano.​gov/​NNI2009RSLWorksh​opReport.​pdf] Accessed 19 June 2013 17. Cientifica: Nanotechnology White Papers on Global Funding of Nanotechnology and its Impacts. [http://​www.​cientifica.​com/​wp.​.​.​/​Global-Nanotechnology-Funding-Report-2011.​pdf] online PDF. Accessed 29 September 2012 18. Bai C: Progress of nanoscience and nanotechnology in China. J Nanopart Res 2001,3(4):251–256.CrossRef 19. Italian Trade Commission: Nanotechnology and biotechnology in China. [http://​www.​ice.

It is then tempting to speculate that the presence of HQNO will prevent S. aureus from disseminating and will rather favor tissue colonization, biofilm production and invasion of host cells. It has indeed been suggested that S. aureus FnBPs HKI-272 price mediates cellular

invasion [53, 54] whereas the capacity of the bacterium to remain intracellular is helped by the Sorafenib manufacturer repression of hla [55]. Accordingly, we showed that an exposure of S. aureus to HQNO up-regulates the expression of fnbA and represses the expression of hla. However, whether or not HQNO and P. aeruginosa increase the invasion of host cells by S. aureus remains to be confirmed. Interestingly, O’Neil et al. [32] have recently demonstrated that the FnBPs are also involved in the ica-independent Selleckchem Peptide 17 mechanism of biofilm formation. It is thus

possible that FnBPs are directly responsible for the observed HQNO-mediated SigB-dependent increase in biofilm production and, more specifically, FnBPA which is under the control of SigB for expression [15, 19, 22, 37]. As such, the FnBPs would represent the main effectors for both biofilm formation and cellular invasion in S. aureus SCVs. HQNO may be one of several bacterial exoproducts influencing S. aureus during polymicrobial Olopatadine infections. Our results and those of Machan et al. [47] suggest that other HAQs may also affect S. aureus, although not as efficiently as HQNO. Moreover, it is known that other P. aeruginosa exoproducts such as pyocyanin have an inhibitory activity against the electron transport chain of S. aureus [13]. Loss of pyocyanin production has been associated with mutations in the pqsA-E genes [45, 56], which may provide an additional explanation for the different effects of the pqsA and pqsL mutants we have observed on the growth (data not shown) and biofilm formation of S. aureus (Fig. 6C). Furthermore, Qazi et al. [7] found that an N-acyl-homoserine-lactone

from P. aeruginosa antagonizes quorum sensing and virulence gene expression in S. aureus. More precisely, it was shown that the 3-oxo-C12-HSL interacts with the cytoplasmic membrane of S. aureus and down-regulates both sarA and agr expression. Although we also observed here a down-regulation of agr, the HQNO-mediated up-regulation of sarA suggests further complexity in the response of S. aureus to P. aeruginosa exoproducts. It is possible that the outcome of the S. aureus-P. aeruginosa interaction is dependent on the amount and the types of exoproducts secreted by the specific strain of P. aeruginosa interacting with S. aureus.

The results of FP assay show that 10 of 11 synthetic peptides (except no. 6 peptide) have antigenicity. When these 10 peptides reacted with standard antibody-positive serum, we measured >200-mP FP values, which were far higher than the FP values of those peptides that reacted with standard antibody-negative serum (Figure 5). 10058-F4 Figure 5 Identification of the antigenicity of synthetic peptides by FP assay ( p < 0.05). Immunodominant SIS3 cell line peptides of HBV surface antigen The dominant epitopes of HBV surface antigen were screened by analyzing the antibody levels against 10 antigenic peptides in 159 anti-HBV surface antigen-positive antiserum by FP assay. The results show that

nos. 1, 10, and 11 antigenic peptides were immunodominant among 159 samples, for the antibody levels against these peptides were higher than those against other peptides or the ALK inhibitor antibodies against these peptides widely existed among 159 samples (Table 2).

Table 2 The results of FP assay detecting antibodies against 10 antigenic peptides in 159 serum samples No. of peptides Numbers of samples (n = 159) Average ΔmP   ΔmP ≤ 25 25 < ΔmP ≤ 50 50 < ΔmP ≤ 100 ΔmP > 100   1 5 11 90 53 129 2 29 42 79 9 67 3 19 36 88 16 73 4 13 21 83 42 111 5 17 16 90 36 89 7 10 21 87 41 107 8 13 26 77 34 92 9 25 29 83 22 86 10 3 12 114 30 93 11 9 13 89 48 121 Detection of HBV infection using immunodominant peptides based on FP assay The resulting three dominant antigenic peptides were used to develop a FP-based method for detecting anti-HBV surface antigen. After FP analysis, the FP values represent the antibody levels against HBV surface antigen. The frequency distributions of the FP assay results obtained from the 293 serum samples are shown in Figure 6.

Tacrolimus (FK506) The histograms show that the majority of the HBV-negative sera had mP values of <80 and the majority of the sera from infected people had mP values of ≥80. In order to distinguish positive and negative results of HBV infection by FP values, all samples were detected for HBV infection by ELISA method. The results of ELISA were used as criterion for HBV infection for each sample, and an optimal cutoff point of 77 mP for FP assay was recommended by ROC curve analysis (Figure 7). Using the FP assay method to detect HBV infection, the results indicated that the antibody-positive ratio was 51.9%, analyzed using the three antigenic peptides; the sensitivity and specificity estimates at this cutoff point were 85.4% and 98.6%, respectively. The area under the ROC curve was 0.959 (95% confidence interval = 0.908 to 0.986), which indicated a high level of accuracy for this assay. Figure 6 Frequency distribution of the FP assay results that were obtained from 293 serum samples. The x-axis shows the mP values, and the y-axis shows the number of serum. Figure 7 ROC curve obtained from the analysis of the FP assay results of 293 serum samples.

In 1 Hz- to 100-kHz range, the space charge region rules the conductivity process. There is a sharp decrement in the sensitivity with the increment of frequency and little variation in the gain values at frequency higher than 100 kHz, where the conductivity is mainly dependent on the surface charge of the grains. This revealed that a suitable selection of frequency could achieve maximum gain in sensitivity. The sensing mechanism can be described from the following aspects: The oxygen molecules from the ambient atmosphere were initially adsorbed onto the ZnO surface. The electrons were extracted from the conduction band of the ZnO material and were converted to a single or a double oxygen ion

and became ionosorbed on the surface [2]. This led to a decrease in electron concentration and consequently an increase in resistance. This mechanism can be find more described as follows [2, 37]: (5) The reaction of the hydrogen or any reduction gases with the ionosorbed results in the release of the captured electrons back to

the conduction band. This results in an increase in electron concentration, decreasing the resistance which could be explained by the following reaction [2]: (6) When the hydrogen is introduced, PdO is reduced to metallic palladium, returning electrons to ZnO. Hydrogen molecules adsorbed on palladium simultaneously click here spill over the surface of ZnO, activating the reaction between hydrogen and the adsorbed

oxygen: (7) At elevated temperature, Pd is oxidized by the chemisorbed oxygen: (8) The weak bonding of Pd atoms with the oxygen gas results in the dissociation of the complex at relatively low temperature releasing atomic oxygen. The oxygen atoms migrate along the surface of the grains. This migration is induced by the Pd catalyst and is known as spillover of the gaseous ions [38]. Thus, the oxygen atoms capture electrons from the surface layer selleck products forming an acceptor surface at the grain boundary. The presence of catalyst atoms activates the reaction between reducing gases and the adsorbed oxygen [39–41]. Thus, the Pd sensitization on the ZnO nanorod surface enabled the hydrogen sensing at relatively low operating temperature. Conclusions A hydrogen Phosphoprotein phosphatase sensor was successfully developed using Pd-sensitized ZnO nanorods synthesized on oxidized silicon substrate using a sol-gel spin coating technique. The sensor detected ppm level hydrogen at room temperature with more sensitivity over the literature-reported values for the ZnO-based sensors. The variation in the resistance value of the grain boundary which was the basis of analyte detection mechanism was due to the sole variation in hydrogen concentration. Nyquist plot strongly supported the impedance findings. Acknowledgments MK acknowledges the financial support of the Malaysian Ministry of Higher Education (MOHE) through FRGS grant number 9003-00276 to Professor UH.