The amino acid position 175 for Mab 62 is close to the H7 RBS but not within it. This allows the amino acid to be conserved in neutralizing epitopes. Most patients infected with H7N9 HPAI viruses had a Foretinib mouse history of poultry contact [21]. However, most avian species carrying infectious H7N9 viruses are asymptomatic [22]. Symptoms from H7N9 infection

developed rapidly and treatments are effective only when administrated within 5 days after the onset of the symptoms [23, 24]. Therefore, detection of H7 antigens at the earliest stage of infection is of crucial significance to identify infections and reduce mortality in patients. This poses a serious threat to public health and highlights the need for H7 diagnosis. Further, less cases of avian infection with H7N9 were reported than human cases, suggesting there may be other reasons for human infection besides poultry contacts. Serological assays are able to identify the history of mild or asymptomatic infection in avian species or humans, providing critical information for surveillance studies [25]. Hence, efficient serological detection in birds and humans is also important

to control and study H7 HPAI viruses. It was found previously that poultry species carrying AIV antibodies are shedding less virus than SPF poultry upon asymptomatic AIV infection or infection with mild selleck screening library microscopic lesions [26]. Therefore, ideally, diagnostic results of both antigen and antibody detection should be consulted together to create a better understanding of H7 infection among populations. However, applying those high-tech diagnosis tests, such as Real time PCR and virus neutralization, Veliparib clinical trial to routine screening in public populations and birds is neither practical nor cost effective due to the limited availability of equipment and trained manpower. User-friendly rapid tests, such as dot ELISA and lateral flow, are preferred in field investigation and clinical diagnosis in the neighborhood [10, 27]. All these immuno-tests are initially developed from an ELISA assay based on monoclonal antibodies [9]. In the current study, AC-ELISA and competitive ELISA were combined to a dual ELISA with standardized

Mabs for both H7 antigen and antibody detection. High specificity and sensitivity were confirmed for either function in the dual ELISA against H7 Morin Hydrate AIVs. Sensitivity of antigen detection is higher than HA tests and antibody ELISA detects less H7 antibodies than conventional virus neutralization. The combination of two functions in one plate paves the way for an ever simplified rapid test. For antibody detection, the dual ELISA is even easier to prepare than conventional competitive ELISAs. A small amount of baculovirus expressed H7 antigen is sufficient for antibody blocking in the dual ELISA while highly purified and concentrated H7 antigen is required for coating in other cELISAs to minimize unspecific blocking effects [12].

Figure 2 Selected GO terms related to “”GO: 0052040 modulation by symbiont of host programmed cell death”". A greatly simplified directed acyclic graph (DAG) showing key low-level terms describing modulation of programmed cell death

in one organism (the host) by another organism (the symbiont) is depicted. A simplified lineage for these terms is shown up to “”GO: 0008150 biological_process”". Only selected terms are shown, and only a few of the parent-child relationships are depicted; arrows symbolize GO “”is_a”" and “”part_of”" relationships (for more information on ontology structure, i.e. “”is_a”", “”part_of”", and “”regulates”", see [13]). Note that “”GO: 0052040 modulation by symbiont of host programmed cell death”" (denoted by a ARS-1620 in vivo dark PX-478 mw star) and “”GO: 0052031 modulation by symbiont of host defense response”" (light star) both ultimately exist under the “”GO: 0051704 multi-organism process”" node. The GO terms shaded with grey represent annotations discussed in the text; GO terms highlighted with broken lines or black serve as reference points for Additional file1and Additional

file2, respectively. The term “”GO: 0052248 modulation of programmed cell death in other organism during symbiotic interaction”" can be viewed (highlighted in black) in Figure2, which depicts a greatly simplified directed acyclic graph (DAG; for more information on ontology structure see [13]) showing some more specific GO terms used to describe aspects of symbiont modulation of host programmed cell death. “”GO: 0052040 modulation by symbiont of host programmed cell death”" (shown in Figure2, denoted by a dark star), or a child term of this more general parent term if more specific annotation information

is available, would be used instead of “”GO: 0012501 Staurosporine nmr programmed cell death”" (Additional file1) to annotate any gene product produced by a symbiont that affected PCD in a host during a typical interaction. For example, the mTOR inhibitor protein family, NPP1, comprises proteins from oomycetes, bacteria, and fungi that in plants cause HR-like cell death, pathogenesis-related gene transcription, reactive oxygen species (ROS) and ethylene (ET) generation, and apposition of callose, a (1→3)-β-d-glucan involved in both normal development and response to abiotic and biotic stress [31,32]. Annotating NPP1 family proteins with GO terms adds clarity not conferred by its literature description as a “”necrosis-inducing protein”". It would be appropriate to annotate aPhytophthora sojaemember of the family (e.g. PsojNIP; [33]) with the GO term “”GO: 0052040 modulation by symbiont of host programmed cell death”" (Figure2and Additional file2).

Several antibiotics were routinely used in the treatment of S.

aureus infections, contributing to the emergence of antibiotic-resistant strains. Widespread resistance severely complicates management of S. aureus infections. S. aureus MI-503 strains that are resistant to methicillin (methicillin-resistant S. aureus, MRSA) are pervasive in the hospital environment, and have recently also caused a global epidemic of community-associated S. aureus (CA-MRSA) infections [30]. The changing Nutlin-3 clinical trial trend of MRSA epidemiology, showed the use of PVL locus detection as a marker of CA-MRSA isolates, alongside with non multiresistant pattern and SCCmec type IV or V [31]. Vancomycin has been used successfully for over 50 years for the treatment of S. aureus infections, particularly those caused by MRSA strains [32]. However, vancomycin-resistant S. aureus (VRSA) and vancomycin-intermediate (VISA) strains have been reported, three decades after the introduction of vancomycin [33]. The presence of resistance genes may also affect toxin production. The production of multiple virulence factors, as well as the presence of antibiotic resistance genes, makes S. aureus a highly pathogenic microorganism. The objective of

learn more this work was to study the susceptibility profile and toxin production of S. aureus strains isolated from various skin, soft tissue, and bone infections. Results Prevalence of S. aureus strains according to the sample origin Using standard microbiological methods for identification of microorganisms; a total of 136 strains of S. aureus were collected during this study. The proportions

of the strains varied depending on the five types of infection: furuncle, osteomyelitis, pyomyositis, abscess, and Buruli ulcer. Almost 37% (50/136) of the collected strains originated from abscesses, followed not by strains isolated from pyomyositis patients (27%, 37/136), furuncles (14%, 19/136), Buruli ulcers (12%, 16/136), and osteomyelitis cases (10%, 14/136). Susceptibility to antibiotics There was a wide range in the susceptibility of the isolates to the various antibiotics examined. All of the strains were resistant to benzyl penicillin, while other antibiotics (vancomycin, fusidic acid, fosfomycin, and linezolid) were active against some of the strains (Figure 1). Figure 1 Global Staphylococcus aureus strains isolated from primary and secondary infections resistance profile to 22 antibiotics. Benzyl penicillin (BP), oxacillin (Ox), cefoxitin screen (Cef), gentamicin (Gen), tobramycin (Tob), kanamycin (Kan), vancomycin (Van), teicoplanin (Tei), fusidic acid (FA), fosfomycin (Fos), rifampicin (Rif), trimethopim/sulfamethoxazole (T/Sul), erythromycin (Ery), lincomycin (Lin), pristinamycin (Pri), linezolid (Line), tetracyclin (Tet). There was no significant difference in the antibiotic resistance of the strains based on their origin (Figure 2). S.

Furthermore, distance covered during the YoYo IR2 has been associated with high-intensity running performed during competitive games play [12, 13]. Therefore, the results of the present investigation suggest that β-alanine supplementation is effective at improving team sport

specific exercise capacity. Blood measures were not taken in the current investigation, although others have reported lactate values in excess of 10 mmol·L-1 at exhaustion [13], which is higher than the values shown in repeated sprint activity studies that have shown a correlation to H+ buffering capacity (~8 mmol·L-1; [5, 18]). Although the rate of muscle phosphorylcreatine and glycogen utilisation are high during Defactinib molecular weight the YoYo IR2 [13], there is no difference in muscle concentrations of these substrates between 85% and 100% of exhaustion time, indicating that depletion of these substrates is not a main contributing factor to fatigue. Interestingly, muscle pH was significantly lower at exhaustion compared with at 85% of exhaustion time, which suggests increasing muscle acidity is a limiting factor to YoYo IR2 performance. Although muscle carnosine concentrations were not directly determined in this study, Stellingwerff et al. [19] showed that

as little as two weeks of β-alanine supplementation at half the dose used in the current study was sufficient to increase muscle carnosine by 11.8 ± 7.4% in the tibialis anterior. Therefore, it can by hypothesised that 12 weeks of β-alanine supplementation at 3.2 g·day-1 significantly increased muscle carnosine concentrations in the current population. As Endocrinology antagonist such, since one of the undisputed roles of muscle carnosine is in muscle buffering, the most likely explanation Silibinin for the improvement in YoYo IR2 IACS-10759 chemical structure performance is due to an increase in intracellular buffering capacity, resulting in an attenuation of the reduction in intracellular

pH during high-intensity exercise. The YoYo IR2 has been shown to be a highly reproducible capacity test, with a CV of ~10% for two tests performed within a one week period [13]. In addition, the test is sensitive to detect training adaptions, with performance improvements of approximately 42% shown following pre-season training. In the present investigation, players in the placebo group showed a ~7% decline in performance while β-alanine supplementation improved YoYo IR2 performance by ~34%, which compares favourably with the effects of pre-season training, and exceeds the expected CV of the test. Furthermore, all 8 of the players who improved with β-alanine did so above this expected CV, while the placebo group showed more variation with 3 players exceeding the CV (1 improved and 2 decreased their performance), which suggests that performance improvements in the β-alanine group can be attributed to the nutritional intervention employed in the current investigation.

This large decrease in valley splitting due to implicit doping can be explained by the smearing of the doping layer in the direction normal to the δ-layer, thereby decreasing the quantum confinement effect responsible for breaking the degeneracy in the system. Carter

et al. [32] also shows that the arrangement of the phosphorus atoms in the δ-layer strongly influences the valley splitting value. In particular, they showed that there is a difference of NSC 683864 manufacturer up to 220 meV between P doping along the [110] direction and along the [100] direction. It should be noted, however, that deterministic nearest-neighbour donor placements are not yet physically realisable due to the P incorporation mechanism GSK458 currently employed [27, 53]. Similarly, the perfectly ordered arrangement discussed here is highly improbable, given the experimental limitations, but represents the ideal case from which effects such as disorder can be studied. Table 2 Valley splitting

values of 1/4 ML P-doped silicon obtained using different techniques Technique Number of Valley   layers splitting     (meV) Planar Wannier orbitala[30] 1,000 20 Tight binding (4 K)b[34] ∼150 ∼17 Tight binding (4 K)b[37] 120 25 Tight binding (300 K)b[36] ∼150 ∼17   40 7   80 6 DFT, SZP basis set a[32] 120 6   160 6   200 6 DFT, SZP: ordered b[31] 40 120 DFT, SZP: random disorder b[31] 40 ∼70 DFT, SZP: [110] direction alignment b[32] 40 ∼270 DFT, SZP: dimers b[32] 40 ∼85 DFT, SZP: random disorder b[32] 40 ∼80 DFT, SZP: clusters b[32] 40 ∼65 DFT, SZP: [100] direction alignment Pazopanib molecular weight b[32] 40 ∼50 DFT, SZP: ordered, M=4b,c[32] 80 153 DFT, SZP: ordered, M=6b,c[32]

80 147 DFT, SZP: ordered, M=10b,c[32] 80 147   40 145.1   60 144.7 SZP, M=9 (this work)b,c 80 144.8   120 144.7   160 144.7   200 144.7   16 118.6   32 94.1 PW, M=9 (this work)b,d 40 93.5   60 93.3   80 93.2   40 100   60 99.5 DZP, M=9 (this work)b,c 80 99.5   120 99.3   160 99.6 Techniques are grouped by similarity. aImplicit doping; bExplicit doping; c M × M × 1k-points; d M × M × N k-points; N as in Appendix 1. Our results show that valley splitting is highly sensitive to the choice of basis set. Due to the nature of PW basis set, it is SB202190 order straightforward to improve its completeness by increasing the plane-wave cut-off energy. In this way, we establish the most accurate valley splitting value within the context of density functional theory. Using this benchmark value, we can then establish the validity and accuracy of other basis sets, which can be used to extend the system sizes to that beyond what is practical using a PW basis set. As seen in Table 2, the valley splitting value converges to 93 meV using 80-layer cladding. The DZP localised basis set gives an excellent agreement at 99.5 meV using 80-layer cladding (representing a 7% difference). On the other hand, our SZP localised basis set gave a value of 145 meV using the same amount of cladding.

For the ABT-888 price yeast two-hybrid study, each wag31 Mtb allele was cloned in frame into both pJZ4-G (pCK145, pCK143, and pCK142) and pHZ5-NRT vectors (pCK146, pCK147, and pCK148) [35]. Each wag31 allele was amplified by PCR using the WagYTHF and WagYTHR primers, and pCK89, pCK90, and pCK91 as the templates. Nascent peptidoglycan biosynthesis and localization of Wag31 For observation of nascent peptidoglycan biosynthesis, the wag31 Msm deletion mutant cells of M. smegmatis containing Ptet-wag31 Mtb (pCK89), Ptet-wag31T73A Mtb (pCK90), or Ptet-wag31T73E Mtb (pCK91) or cells containing

pMV261-Ptet-wag31 (click here pCK314) with or without pknA Mtb – (KMS 2) or pknB Mtb -overexpression (KMS 4) were stained with Van-Alexa568 [11]. A stock solution of Van-alexa568 (5 mg ml-1)

was prepared according to the manufacturer’s manual (Molecular Probes). Each strain was cultured in 7H9 liquid medium with tetracycline (20 ng ml-1) overnight and was then inoculated into fresh 7H9 liquid medium selleck chemicals llc containing 20 ng ml-1 of tetracycline. Cells from each strain were taken during mid-log phase (approximate OD600 = 0.4) and incubated with Van-alexa568 (5 μg ml-1) for 20 min at 37°C. For microscopic analysis, cells were washed with PBS buffer and examined by an Olympus BX51 microscope. Pictures were taken with an Olympus DP30BW high sensitivity cooled CCD camera, acquired with 17-DMAG (Alvespimycin) HCl DP-BSW software and processed with Adobe Photoshop CS2. To minimize possible errors during the sampling process and fluorescence examination, the staining procedure was conducted in the dark, and microscopy conditions such as exposure time and opening of the aperture diaphragm were fixed for all samples.

For quantification of average fluorescence intensity at the cell poles, DIC and fluorescence images were superimposed to align cells and fluorescence signals, and fluorescence density from the poles of approximately 300 cells was measured and background-corrected by using the ImageJ software. For localization of different forms of Wag31, pMV261 containing Pacet-gfp-wag31 Mtb (pCK174), Pacet-gfp-wag31T73A Mtb (pCK175) or Pacet-gfp-wag31T73E Mtb (pCK176) was electroporated into the wag31 Msm deletion mutant expressing wag31 Mtb (KMS41), wag31T73A Mtb (KMS42) or wag31T73E Mtb (KMS43) under a tetracycline-inducible Ptet promoter [36] at the chromosomal L5 attB locus, respectively. The resulting strains (KMS69, KMS70, and KMS71) were grown in 7H9 liquid medium containing 20 ng tetracycline, and at early-log phase (approximate OD600 = 0.2) cells were induced with 0.1% of acetamide for 3 hr before being transferred onto a glass slide and observed using an Olympus BX51 florescence microscope. Quantification of GFP signals at the cell poles of approximately 300 cells was conducted with ImageJ software similar to the one for Van-Alexa568.

Horizontal reading of the graph indicates the percentage of unigenes shared by several libraries. D. GO annotation results for this website High Scoring Pairs (HSP) coverage of 0%. GO annotation was first conducted using the Score Function (SF) of the BLAST2GO software. The GO terms selected by the annotation step were then merged with InterProScan predictions (SF + IPR). Finally, the Annex annotation was run (SF + IPR + ANNEX). E. Annotation distribution of GO terms. Two

non-normalized libraries were constructed from asymbiotic and symbiotic ovaries (AO and SO) starting with 1 µg of polyA RNAs. They were prepared using Creator SMART cDNA Library Construction kit (Clontech/BD Biosciences), following the manufacturer’s instructions. cDNA was digested by SfiI, purified (BD Chroma Spin – 400 column) and ligated into pDNRlib vector for Escherichia coli transformation. Amplified double strand cDNA (ds cDNA) was prepared using a SMART approach [28]. SMART Oligo II oligonucleotide (Clontech/BD Biosciences) and CDS primer were used for first-strand cDNA synthesis. SMART-amplified cDNA samples were further digested by RsaI endonuclease. The SSH libraries from asymbiotic and symbiotic ovaries (SSH-A and SSH-S) were constructed

starting with 20 µg of total RNA. SSH libraries from specimens challenged and not challenged by S. typhimurium (SSH-C and Ruboxistaurin research buy SSH-NC) were performed on 20.4 µg of a total RNA equally pooled from different tissues (i.e., ovaries, gut, cæca, fat tissues, hemocytes, hematopoietic organ, nerve chain, and brain) harvested at each https://www.selleckchem.com/products/Pazopanib-Hydrochloride.html time point. The pooled total RNA was obtained by mixing equal amounts of total RNA

extracted separately for each tissue and for each time point. Subtractive hybridizations were performed Mirabegron using SSH method in both directions (Asymbiotic vs. Symbiotic A/S and vice-versa S/A; Not Challenged vs. Challenged NC/C and vice-versa C/NC) as described in [29, 30] using the PCR-Select cDNA Subtraction Kit (Clontech/BD Biosciences). SSH libraries were prepared by Evrogen (Moscow, Russia). The Mirror Orientation Selection (MOS) procedure was used for SSH-A/S and SSH-C/NC as described in [31] in order to reduce the number of false-positive clones in the SSH-generated libraries. Purified cDNAs from SSH-A/S and SSH-C/NC were cloned into the pAL16 vector (Evrogen) and used for E. coli transformation. Finally, the normalized library (N) was prepared with 75 µg of a pooled total RNA from an equimolar proportion of asymbiotic and symbiotic ovaries, and 6h, 9h, and 15h challenged asymbiotic females. As for the libraries of challenged specimens, total RNA was extracted separately from the same tissues. This N library was prepared by Evrogen (Moscow, Russia). Total RNA sample was used for ds cDNA synthesis using SMART approach [28]. SMART prepared amplified cDNA was then normalized using Duplex Specific Nuclease (DSN) normalization method [32].

e. multi dimensional scaling, MDS). Such graphical analysis helped MRT67307 cell line to identify exudate compounds and cultures which tended to cluster together and have high similarities. The cluster procedure was an average linking one, and all similarities used were based on Eucledian distances. Exudate compounds identified were scored ‘1’ for the presence, and ‘0’ for the absence of the compound. HPLC analysis of streptomycete secondary metabolites The chromatographic system consisted of a HP 1090 M liquid chromatograph equipped with a diode-array detector and HP Kayak XM 600 ChemStation (Agilent Technologies, Waldbronn, Germany). Multiple wavelength monitoring was performed at 210, 230, 260, 280, 310, 360, 435 and 500 nm, and UV-visible spectra

measured from 200 to 600 nm. Five-μl aliquots of the selleck chemicals llc samples were injected onto a HPLC column (125×3 mm, guard column 20×3 mm) filled with 5-μm Nucleosil-100 C-18 (Maisch, Ammerbuch, Germany). The samples were analyzed by linear gradient elution using 0.1% ortho-phosphoric acid as solvent A and acetonitrile as solvent FK228 molecular weight B, at a flow rate of 0.85 ml min-1. The gradient was from 4.5% to 100% for solvent B in 15 min with a 3-min hold at 100% for solvent B. Evaluation was carried out by means of an in-house HPLC-UV–vis database which contains nearly 1000 reference compounds, mostly antibiotics [45]. Electron microscopy The megagametophyte tissues were evaluated on those A. angustifolia seedlings, which showed interrupted cotyledon

connections. Samples were fixed in 0.05 M sodium phosphate buffer (pH 8.0) containing 2% glutaraldehyde. The samples were gradually dehydrated in acetone, critical-point dried, sputter-coated with gold and observed by scanning electron microscopy. Acknowledgements PAK5 We gratefully acknowledge the help of Elisabeth Früh, Nadine Horlacher, Martin Galic, Martina Schmollinger, Kerri Hagemann, Sarah Bayer, and Silvia Schrey for help in sample acquisition, sample analysis, and helpful suggestions. We also appreciate the helpful suggestions by the reviewers. This work was supported by a DFG (Deutsche Forschungsgemeinschaft) grant to RH. References 1. Janzen DH: The future of tropical ecology. Ann Rev Ecol Syst 1988, 17:303–324.

2. Golte W: Araucaria – Verbreitung und Standortansprüche einer Coniferengattung in vergleichender Sicht. Stuttgart, Germany: Franz Steiner Verlag; 1993. 3. Fähser L: Die Bewirtschaftung der letzten Brasilkiefer-Naturwälder, eine entwicklungspolitische Aufgabe. Forstarchiv 1981, 52:22–26. 4. Fähser L: Araucaria angustifolia. In Enzyklopädie der Holzgewächse 3. Edited by: Schütt P, Schuck HJ, Lang UM, Roloff A. Landsberg, Germany: Ecomed-Verlag; 1995. 5. Seitz R: Hat die Araukarie in Brasilien noch eine Zukunft? AFZ 1983, 38:177–181. 6. IUCN red list of threatened species. http://​www.​iucnredlist.​org/​apps/​redlist/​search (verified July 18, 2011) 7. Duarte LDS, Dos-Santos MMG, Hartz SM, Pillar VD: Role of nurse plants in Araucaria forest expansion over grassland in south Brazil.

In our recent study, we U0126 have found significantly elevated NTproBNP levels in childhood leukemia survivors at a median of 10.5 years after completion of anthracycline therapy in comparison with apparently healthy controls [27]. In the present study, this finding was

extended to show NTproBNP levels not only in survivors after ANT therapy but also in patients unexposed to anthracyclines. The NTproBNP values in unexposed survivors were found to be comparable to those determined in the control group. According to our information, only one other study reported recently NTproBNP levels in survivors who received ANT compared with patients not receiving these agents [28]. These authors confirmed higher NTproBNP values in the ANT group than in controls yet they found that not only exposed but also unexposed survivors had elevated NTproBNP. They suggest that a chronic inflammatory process may be a predisposing factor of cardiomyopathy in cancer survivors unexposed to anthracyclines. Systemic inflammation in cancer survivors has been of particular concern in recent Tariquidar pathophysiological studies. The discrepancy between the study of Lipshultz et al. [28] and the presented study might be explained by differences in characteristics of the study participants

(cancer treatment history, gender, age, body mass index and other risk factors). In the present study, the detection of cardiotoxicity was performed in childhood leukemia survivors after a low cumulative ANT dose (with median 221 mg/m2). So far only few studies have been published that assessed cardiotoxicity after such ANT doses [26, 27]. We found significantly higher serum levels of NTproBNP in patients exposed to anthracyclines than in unexposed survivors and controls. These results might reflect anthracycline-induced

cardiac abnormalities (such as loss of cardiomyocytes and damage of the learn more remaining cardiomyocytes and other myocardial cells). The sex-related differences in NTproBNP levels in our patients are consistent PTK6 with other authors demonstrating that female survivors are more vulnerable to anticancer cardiotoxic and non- cardiotoxic treatments [28]. In the study we found that 11% survivors treated with ANT (with median cumulative dose 221 mg/m2) and 6% of patients previously unexposed to anthracyclines had abnormal NTproBNP levels. In the study of Mavinkurve-Groothius et al. [26], abnormal levels of NTproBNP were detected in 13% of 122 asymptomatic survivors of childhood cancer who had received a median cumulative ANT dose comparable to our study. These authors used published reference values for adults derived from a population older or equal to 50 years [29]. The applicability of these cut-off reference NTproBNP values to our adolescent and young adult population may be debatable. In the present study, normal values of NTproBNP were different for females (<105 pg/mL) and males (<75 pg/mL) (below 97.5th percentile from our controls).

J Phys Chem C 2008,112(32):12225–12233. doi: 10.​1021/​jp8027353 ABT-263 datasheet CrossRef 3. Kanjwal M, Barakat N, Sheikh F, W-i B, Khil M, Kim H: Effects of silver content and morphology

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Defactinib supplier Pt-Co supported on single-walled carbon nanotubes as an anode catalyst for direct methanol fuel cells. Electrochim Acta 2008,53(24):7276–7280.CrossRef 10.

Shao Y, Sui J, Yin G, Gao Y: Nitrogen-doped carbon nanostructures and their composites as catalytic materials for proton exchange membrane Sulfite dehydrogenase fuel cell. Appl Catal, B 2008,79(1):89–99.CrossRef 11. Ren X, Zelenay P, Thomas S, Davey J, Gottesfeld S: Recent advances in direct methanol fuel cells at Los Alamos National laboratory. J Power Sources 2000,86(1):111–116.CrossRef 12. Liu Z, Ling XY, Su X, Lee JY: Carbon-supported Pt and PtRu nanoparticles as catalysts for a direct methanol fuel cell. J Phys Chem B 2004,108(24):8234–8240.CrossRef 13. Mu Y, Liang H, Hu J, Jiang L, Wan L: Controllable Pt nanoparticle deposition on carbon nanotubes as an anode catalyst for direct methanol fuel cells. J Phys Chem B 2005,109(47):22212–22216.CrossRef 14. Li W, Zhou W, Li H, Zhou Z, Zhou B, Sun G, Xin Q: Nano-structured Pt-Fe/C as cathode catalyst in direct methanol fuel cell. Electrochim Acta 2004,49(7):1045–1055.CrossRef 15. Yen CH, Shimizu K, Lin YY, Bailey F, Cheng IF, Wai CM: Chemical fluid deposition of Pt-based bimetallic nanoparticles on multiwalled carbon nanotubes for direct methanol fuel cell application. Energy Fuels 2007,21(4):2268–2271.CrossRef 16. Frackowiak E, Lota G, Cacciaguerra T, Béguin F: Carbon nanotubes with Pt-Ru catalyst for methanol fuel cell. Electrochem Commun 2006,8(1):129–132.CrossRef 17.