# CF-associated

CF-associated AES-1R was the only MK5108 cell line strain with detectable flagellin in the protein extracts analysed by 2-DE. AES-1R FliC has significant protein

sequence differences compared with PAO1 and PA14, and has greater sequence similarity with the type A flagellin of strain PAK (Additional file 5). Increased flagellin in AES-1R is consistent with our phenotypic data for swimming motility and with previous work showing AES-1 isolates displayed greater motility than non-clonal CF isolates [59]. Several differences in the OMP profile of AES-1R were observed. The loss of OprD in AES-1R is characteristic of carbapenem antibiotic resistance [60]. Decreased OprG expression was originally associated with Sotrastaurin increased fluoroquinolone resistance [61], however a recent study showed no significant difference in the antibiotic susceptibility profile of an oprG-deficient strain [62]. ΔoprG P. aeruginosa do show a 3-fold decrease in cytotoxicity toward the human bronchial epithelial cell line HBE, however transcriptomics revealed a rapid down-regulation of oprG in wild-type P. Selleckchem Poziotinib aeruginosa upon interaction with these cells [62]. MexX, a component of the MexXY-OprM multidrug efflux transporter, was markedly increased in abundance in AES-1R and is known to confer resistance to a number of antibiotics including erythromycin, fluoroquinolones, aminoglycosides and the ß-lactams, cefepime and ceftobiprole [63–66],

correlating well with the antibiotic resistance associated with CF infections. Quinolones are the antibiotic of choice for treatment of P. aeruginosa CF lung infections and resistance to this class of drug Bortezomib datasheet can result from mutations within DNA gyrase GyrA (PA3168), which is essential for DNA replication. The AES-1R gyrA gene sequence revealed an amino acid substitution (Thr83Ile) previously reported to result in

quinolone resistance [34] and observed in the Liverpool epidemic strain LESB58. Increased abundance of PA5178 (putative LysM domain protein), a protein containing a domain with predicted bacterial wall degradation properties may suggest a potential advantage against competing pathogens. P. aeruginosa is predicted to contain approximately 185 genes encoding lipoproteins [67]. A number of lipoproteins were observed at increased abundance in AES-1R. Induction of lipoprotein genes has been associated with an excessive proinflammatory response in lung epithelial cells via Toll-like receptor 2 [68]. OprI (PA2853) is an immunogenic lipoprotein that has been proposed as part of a multivalent vaccine [69]. We observed reduced OprI abundance in AES-1R, which may influence the efficacy of an OprI-based vaccine. LPS is a major virulence factor that is involved in initiating the pro-inflammatory response in the host. P. aeruginosa strains produce different LPS types, which are currently classified into 20 serotypes.

# Pseudoplagiostoma anamorphs are difficult to distinguish morpholo

Pseudoplagiostoma anamorphs are difficult to distinguish morphologically from Cryptosporiopsis s. str. based on this

widely-used generic concept. In this study, the three species of Pseudoplagiostoma produced conidiogenous cells that proliferated percurrently, with conidia seceding at the same level or higher, and lacking the swollen structure observed below the conidiogenous loci seen in Cryptosporiopsis anamorphs linked to Pezicula (Verkley 1999). This difference in conidiogenesis could, therefore, be used to distinguish anamorphs of Pseudoplagiostoma from other similar coelomycetous genera in the Diaporthales, and from those in the Helotiales. Moreover, based on LSU and ITS sequence data, three species of Cryptosporiopsis (C. californiae,

C. caliginosa and Cryptosporiopsis sp.) clustered with other members of Pezicula and Cryptosporiopsis within the Dermateaceae (Helotiales). Thus far, only one true other Cryptosporiopsis OSI-027 mw species (C. edgertonii) has been reported from Eucalyptus buy Torin 2 samples in New Zealand (Gadgil 2005), which has much larger conidia (30–48 × 12–15 µm; Edgerton 1908) than these taxa. Phenotypic plasticity remains a major factor leading to taxonomic uncertainty in the classification and identification of diaporthalean fungi. Castlebury et al. (2002) noted that the delimitation of diaporthalean families varied considerably among specialists, and that their morphological characters could easily lead to confusion for non-specialists. Nine diaporthalean families were previously established based on phylogenetic analysis, because it highlighted the specific differences observed among species at molecular level (Rossman et al. 2007). Digestive enzyme For Pseudoplagiostomaceae, we found that certain morphological characters are more valuable for species distinction, such as conidia, conidiogenous cells and conidiomata of anamorphs. However, only the ascomatal neck and asci-forming positions could be used to distinguish these teleomorphs from those in other families. It should be noted though, that the phylogeny

of the Diaporthales is still not fully resolved (Castlebury et al. 2002). The addition of new taxa and description of potential new genera may result in changes in relative relatedness between families. This may also indicate differences in the importance of certain morphological characteristics to delineate families. This study has resolved the taxonomy of one of the most commonly encountered fungi emerging from Eucalyptus disease surveys. The results will contribute Eltanexor substantially to a better understanding of these fungi and their role in Eucalyptus leaf diseases in many different parts of the world. A priority at this stage will be to compare the pathogenicity of the three new species of Pseudoplagiostoma that have previously been treated as the single species, C. eucalypti. The temptation to assume that they are all pathogens should be avoided until Koch’s postulates have been proven.

# Potential

Potential

arrangement variants are: arrangement as determined by genome sequencing [1], at least two head-to-tail copies of RD2, tail-to-tail, single copy arranged in reverse orientation than the integrative copy determined by genome sequencing, head-to-tail arrangement of copies in reverse orientation than the integrative copy determined by genome sequencing, head-to-head, and circular form. B. PCR screen detects product amplified Selleckchem MLN2238 with primer pairs #1+#2, #3+#4, and #2+#3, corresponding to arrangement variant (head-to-tail) or (circular form), and #1+#4 detecting chromosomal integration site lacking RD2. C. Primers #2+#3 detect arrangement variant 2 or 7 in multiple RD2 positive strains [1]. Serotype M1 strain MGAS5005 (lacks RD2) was used as a negative control of amplification. To further investigate the putative presence of multiple extrachromosomal copies of RD2 in GAS cells, we performed quantitative real time PCR using total DNA isolated from MGAS6180 strain. Performed analysis revealed that RD2 is present in 6-9 copies per chromosome (Figure 5B, see below). Also,

the amplification of chromosomal junction (primers #1+#4) suggests that RD2 can be excised from the site of integration. Figure 5 Mitomycin C treatment results in amplification of RD2. A Rapid decrease in O.D. of a liquid culture of strain MGAS6180 after mitomycin C addition. The decreased O.D. is likely due to prophage BI 2536 cell line induction followed by lytic cycle EX 527 research buy Interleukin-2 receptor phage release. Smaller drop in OD is

observed after treatment with hydrogen peroxide. B. The RD2 element is present in 6-9 copies per chromosome in the absence of inducer. C. The RD2 element is not induced by oxidative stress. Bars in each group represent the RD2 copy number after 1 h, 2 h, 3 h, and 16 h after treatment with hydrogen peroxide. D. RD2 is induced by DNA damage. Bars in each group represent the increase in copy number at 1 h, 2 h, 3 h, and 16 h after treatment with mitomycin C. The statistical significance of the increase in RD2 copy number was determined by t-test, *** on the graph denotes p value below 0.001. Taken together, these results indicate that a circular form of RD2 is present in strain MGAS6180. Response of strain MGAS6180 to mitomycin C and hydrogen peroxide treatment We hypothesized that the putative circular form detected in overnight cultures (see above) is a transient form involved in DNA transfer. DNA damaging factors as ultraviolet light, hydrogen peroxide, or mitomycin C can induce mobilization of genetic elements such as prophages or pathogenic islands as part of a response to DNA damage or oxidative stress [23]. To test hypothesis that RD2 was induced/excised by DNA damage and oxidative stress, we examined induction of RD2 and five other integrative elements present in the genome of strain MGAS 6180 by mitomycin C and hydrogen peroxide treatment.

# 1 were used for further microarray analysis at the VIB Nucleomics

1 were used for further microarray analysis at the VIB Nucleomics Core (http://​www.​nucleomics.​be). selleck chemicals llc Per sample, an amount of 100 ng of total RNA spiked with bacterial RNA transcript positive controls (Affymetrix) was amplified and labelled using the GeneChip 3′ IVT express kit (Affymetrix). All steps were carried out according to the manufacturer’s protocol. A mixture of purified and fragmented biotinylated aRNA and hybridisation controls (Affymetrix) was hybridised on Affymetrix HG U133 Plus 2.0 arrays followed by staining and washing in a GeneChip® fluidics station 450 (Affymetrix) according to the manufacturer’s procedures. To assess the raw probe signal intensities, chips were scanned using a GeneChip® scanner

3000 (Affymetrix). The RMA procedure was used to normalize data within arrays (background correction and log2-transformation) and between arrays (quintile normalization) click here (affy_1.22.0 package of Bioconductor)

[14, 15]. The MAS 5.0 algorithm (Microarray suite user guide, version 5; Affymetrix 2001) was used to assess detection above background. All probesets had a good signal and were used for further analysis. Four experimental designs were analysed: the effect of PDAC patients with a good outcome (‘Good’) versus surrounding pancreatic tissue (defined as ‘control’), the effect of PDAC patients with a poor outcome (‘Bad’) versus surrounding pancreas, the effect of ‘Bad’ versus ‘Good’ and the effect of all PDAC samples, irrespective of outcome, versus metastatic disease in the liver or peritoneum . The limma package from Bioconductor was used to assess the contrast in each experiment [16]. Statistical significance of this contrast was tested with a moderated t-test IKBKE (implemented in limma). Differentially expressed genes were defined as genes with an uncorrected p-value of p < 0.001 in combination with >2 fold-change. Classical schemes to adjust for multiple testing can result in low statistical power for microarray studies . The stringent cut-off of p < 0.001 was used as an alternative, pragmatic approach to balance the number of false positives and false negatives

[17]. Metastatic samples (LM and PM) were buy PCI-32765 contaminated with respectively normal liver and peritoneal tissue, reflecting in upregulation of liver- and peritoneal specific genes. Therefore only genes that were not differentially expressed between LM and PM samples, considered as metastatic specific genes, were used for analysis between primary tumour and metastatic tissue. All gene expression data will be available from the Gene Expression Omnibus (GEO, http://​www.​ncbi.​nlm.​nih.​gov/​projects/​geo/​). Functional pathway analysis on differentially expressed probe sets was done with the Ingenuity Pathway Analysis (IPA) program (Ingenuity Systems, http://​www.​ingenuity.​com; Redwood City, CA). For each experiment, probe sets with a corrected p-value <0.001 and a >2 fold change were used as input.

# ATRA suppressed the phosphorylation of KIT protein KIT protein is

ATRA check details suppressed the phosphorylation of KIT protein KIT protein is one of the most important molecules in the pathogenesis of GISTs. Despite clinicopathological difference, most GISTs have a similar genetic profile, gain-of-function mutations

of KIT or PDGFRA [2]. Upon the importance of KIT protein, we examined whether ATRA can suppress KIT activity in GIST-T1 cells. We treated GIST-T1 cells with 180 μM ATRA for the indicated duration. Total cell lysates were subjected to Sepantronium western blot analysis. Interestingly, ATRA treatment resulted in suppression of KIT activity after 4-day treatment in GIST-T1 cells (Figure 4A the top row) and GIST-882 cells (data not shown). The suppression of KIT activity in GIST-T1 and GIST-882 cells by ATRA required longer time compared with other reagents such as imatinib or EGCG [25]. In addition, ATRA treatment also ICG-001 manufacturer suppressed the AKT activity (Figure 4A the middle row) but not MAPK activity (Figure 4A the bottom row) in GIST-T1 cells. Figure 4 ATRA suppresses the auto-phosphorylation of KIT and AKT protein but not MAPK activity. Panel A shows the suppression of KIT and AKT activity after 2-, 4- or 6-day treatment with 180 μM ATRA. Panel B shows the suppression of KIT and AKT activity after 4 hours treatment with different ATRA concentrations in serum-free media. The results demonstrated that KIT

and AKT activity were suppressed by ATRA treatment in a dose- and time-dependent manner but not MAPK activity. Interestingly, the suppression of KIT and AKT activity by ATRA treatment was enhanced in serum-free media. However, suppression of MAPK activity was not observed even in serum-free media (Figure 4B). The similar results were observed in GIST-882 cells (data not shown). ATRA prevented the migration of GIST-T1 cells Next, to study the migration of GIST-T1 cells in vitro, the scratch assay was performed. This method is based on the observation that, upon creation of a new artificial gap, so called a scratch on a confluent cell monolayer, the cell on the edge of the newly

created gap will move toward the opening to close the scratch until cell to cell contacts are established again. In this study, GIST-T1 cells were seeded with or without ATRA (45, 90 μM) in plates. After 24 Fossariinae hour incubation to get the confluence, a scratch was created. The images of GIST-T1 cells at the beginning and 24 hour later were compared to assess the migration of GIST-T1 cells. The result revealed that 90 μM ATRA inhibited completely migration of GIST-T1 cells compared with the non-ATRA treated dishes (Figure 5A). However, at a lower concentration (45 μM), ATRA inhibited but not completely the migration of these cells (data not shown). All together, the data suggested that ATRA may be useful to prevent the invasion or metastasis of GIST cells. Figure 5 Panel A shows the result of scratch assay, GIST-T1 cells were treated with or without ATRA (90 μM).

# As shown in Figure 1A, after 24 hours of infection, the isolate 9

As shown in Figure 1A, after 24 hours of infection, the isolate 97-1505 (presence Avapritinib nmr of PLCs) was more resistant to killing by alveolar macrophage than 97-1200 (absence of PLCs). Considering that mycobacterial PLCs have cytotoxic effects on macrophages [7], we studied the viability of rat alveolar macrophages AZD5582 mw infected in vitro with the isolates 97-1200 or 97-1505 to investigate if cell death is associated to mycobacterial PLCs. In comparison to uninfected

cells, mycobacterium isolate 97-1505 reduced cell viability by more than 40%, which was approximately 20% higher than the cell death induced by 97-1200 (Figure 1B). Regarding the cell death modality, alveolar macrophages infected with 97-1505 underwent significantly more death by necrosis, and no differences were observed in apoptosis induced by 97-1200 or 97-1505 isolates (Figure 1C). These results suggest that Mtb bearing PLCs genes plays a role in host-cell death by inducing necrosis, which contributes significantly to mycobacterial resistance to microbicidal activity of alveolar macrophages. Figure 1 Intracellular killing of Mtb isolates 97-1200 or 97-1505 and cell death of infected alveolar macrophages. Alveolar macrophages were infected in vitro for 24 PI3K Inhibitor Library chemical structure h with Mtb isolates 97-1200 or 97-1505 at MOI 5. (A) Bacterial killing was assessed by resazurin

metabolisation and expressed as a percentage of phagocytised bacteria. (B) Cell viability assessed by resazurin metabolisation. Maximum viability (100%) is based on uninfected BCKDHB cells. (C) ELISA assay of apoptosis and necrosis 24 h post-infection of alveolar macrophages in vitro. Camptothecin 5 μg/mL (CAMP) was used as apoptosis-positive control and hypertonic buffer as necrosis-positive control. # P < 0.0001 for uninfected cells vs. infected cells (97-1505 or 97-1200); ***P < 0.0001; **P < 0.001 (one-way ANOVA). Data are representative

of three (A, B) and two (C) independent experiments (error bars, s.e.m.). PLCs-expressing Mycobacterium tuberculosis more efficiently stimulates the production of proinflammatory cytokines and NO by alveolar macrophages in vitro The results shown in Figure 1 indicate that the isolate 97-1505 is more resistant to bactericidal activity by inducing host-cell necrosis. Thus, we next asked if the production of pro-inflammatory cytokines and NO is affected, since these mediators are essential for host control of Mtb infection [18]. In addition, previous data from our lab revealed that lungs from mice infected with the isolate 97-1505 presented extended tissue damage, which was suggested to be associated with strong production of pro-inflammatory cytokines (data not shown). Here, in vitro infection showed that both isolates induced a strong production of NO and the cytokines TNF-α, IL-6, IL-1α, IL-1β, and IL-10.

# ““Background Any reaction in a living system is followed by

“Background Any reaction in a living system is followed by heat production. Monitoring heat production

is valuable for investigating metabolic reactions in living systems, and heat production by microorganisms has been extensively investigated [1–5]. Selleckchem Fedratinib Heat production by bacteria is related to their growth phases because the heat produced by bacteria is tightly coupled to their metabolic reactions [1]. Thus, heat output monitoring has been used to determine bacterial growth rates. The heat output of bacteria is characteristic of the particular strain because the amount of heat produced by bacteria is affected by nutrients and the bacterial products and metabolic pathways. In previous studies, heat output measurements were used to characterize bacteria [2, 5]. Heat output measurements were also used to investigate

selleck kinase inhibitor the effects of a particular compound in a medium on bacterial growth [6–8]. Detailed studies on the relationships between substrate consumption and biomass production by bacteria have suggested that some bacteria can consume higher amounts of energy without concomitant biomass production [9–12]. In these growth independent reactions, energy sources were converted to heat. Russell called these growth independent reactions energy-spilling reactions [10]. Some bacteria use RSL3 solubility dmso futile cycles to spill energy. The energy-spilling reaction of Streptococcus bovis is mediated by a futile cycle of protons through its cell membrane. A futile cycle between pyruvate and phosphoenolpyruvate was proposed in the metabolic pathway of Escherichia coli[13] and another futile cycle between fructose-6-phosphate mafosfamide and fructose-1,6-bisphosphate was proposed in the metabolic pathway of Streptococcus cremoris[14]. In the case of an energy-spilling reaction that increases under nitrogen-limited and excess glucose

conditions, the energy-spilling reaction is used to reduce glucose toxicity [11]. However, the roles of energy-spilling reactions in many bacteria are not completely understood. In the case of homeotherms, some growth independent reactions are utilized to maintain a constant body temperature. UCP1, which is located in the mitochondrial inner membrane of brown adipocytes, disrupts the mitochondrial membrane potential without the production of ATP [15]. This UCP1-mediated reaction is considered to play a major role in the thermogenesis of brown adipocytes. However, the effects of the growth independent reactions of bacteria on cellular temperature have not been investigated. The cellular temperatures of microorganisms have been considered to be the same as those of their surroundings because the cellular volume is too small to maintain a cellular temperature different from the ambient temperature. However, by forming a colony or a biofilm, microorganisms may be able to maintain a cellular temperature that is different from the ambient temperature.

# The fraction (1−F)q 2 is composed of two parts—one part comprisin

The fraction (1−F)q 2 is composed of two parts—one part comprising the compound heterozygotes (CH), and the other part combining all homozygotes non-IBD (HN). The relative frequencies of the two sets within the fraction (1−F)q 2 are (in reversed order) $$R\left( \hboxHN \right) = \sum\limits_i = 1^n \mathop a\nolimits_i^2 , \hboxand$$ (2) $$R\left( \hboxCH \right) = 1 – \sum\limits_i = 1^n \mathop a\nolimits_i^2$$ (3) In Eqs. 2 and 3, a i represents the relative frequency of the ith allele. So its square, a i 2 , is the relative frequency of homozygotes of the ith allele non-IBD. From Eqs. 1 and 3, it follows that the proportion of find more compound heterozygotes, P(CH), among affected children of consanguineous Selinexor cost Selleck Dactolisib parents is $$P\left( \hboxCH \right) = \frac\left( 1 – \sum\limits_i = 1^n a_i^2 \right) \times \left( 1 – F \right)q^2Fq + \left( 1 – F \right)q^2$$ (4) We can now calculate the expected proportion of compound heterozygotes, P(CH), if we know F, q, and the relative frequencies of the pathogenic alleles. Conversely, knowing P(CH) by observation, as mentioned in the introduction, we can estimate R(CH), R(HN), and P(HN), if we know F and q, as follows: $$R\left( \hboxCH \right) = \left( 1 – \sum\limits_i = 1^n \mathop a\nolimits_i^2 \right) = \fracP\left( \textCH \right) \times \left[ Fq + \left( 1 - F \right)q^2 \right]\left( 1 – F \right)q^2 = \fracP\left( \textCH \right) \times \left[ F + \left( 1 - F \right)q \right]\left( 1 – F \right)q,$$ (5) $$R\left( \hboxHN \right) = 1 – R\left( \hboxCH \right),\,\hboxand$$ (6) $$P\left( Anidulafungin (LY303366) \hboxHN \right) = \fracR\left( \textHN \right) \times \left( 1 – F \right)q^2Fq + \left( 1 – F \right)q^2 = \fracR\left( \textHN \right) \times \left( 1 – F \right)qF + \left( 1 – F \right)q$$ (7) We can also calculate q from (4) or (5) if we know P(CH), F and R(CH) or the relative frequencies of the pathogenic alleles. $$q = \fracP\left( \textCH \right) \times \left( F + q – Fq \right)\left( 1 – F \right) \times R\left( \hboxCH \right),\,\hboxfrom\;\hboxwhich\;q\;\hboxcan\;\hboxbe\;\hboxsolved.$$ (8) Results Table 1 shows the dependency of the proportion of compound heterozygotes among affected offspring of consanguineous parents, P(CH), upon the parameters F, q, and R(CH) (see Eqs. 3 and 4). The examples given illustrate that P(CH) is positively correlated with R(CH) and q, and negatively with F,—as expected. Table 1 Expected proportions of compound heterozygotes among affected children of consanguineous parent, P(CH), given some values of F, q, and R(CH), the relative frequency of these compound heterozygotes among non-IBD affected children F q R(CH) P(CH) 1/8 0.01 0.1 0.007 0.5 0.033 0.05 0.1 0.026 0.5 0.130 1/16 0.01 0.1 0.013 0.5 0.065 0.05 0.1 0.043 0.5 0.214 1/64 0.01 0.

# J Virol 2008, 82:6631–6643 PubMedCrossRef 26 Beltramello M, Will

J Virol 2008, 82:6631–6643.PubMedCrossRef 26. Beltramello M, Williams KL, Simmons CP, Macagno A, Simonelli L, Quyen NT,

Sukupolvi-Petty S, click here Navarro-Sanchez E, Young PR, de Silva AM, Rey FA, Varani L, Whitehead SS, Diamond MS, Harris E, Lanzavecchia A, Sallusto F: LY2874455 order The human immune response to Dengue virus is dominated by highly cross-reactive antibodies endowed with neutralizing and enhancing activity. Cell Host Microbe 2010, 8:271–283.PubMedCrossRef 27. Rodenhuis-Zybert IA, van der Schaar HM, da Silva Voorham JM, van der Ende-Metselaar H, Lei HY, Wilschut J, Smit JM: Immature dengue virus: a veiled pathogen? PLoS Pathog 2010, 6:e1000718.PubMedCrossRef 28. Chan AH, Tan HC, Chow AY, check details Lim AP, Lok SM, Moreland NJ, Vasudevan SG, MacAry PA, Ooi EE, Hanson BJ: A human PrM antibody that recognizes a novel cryptic epitope on dengue E glycoprotein. PLoS One 2012, 7:e33451.PubMedCrossRef 29. Chau TN, Hieu NT, Anders KL, Wolbers M, Lien LB, Hieu LT, Hien TT, Hung NT, Farrar J, Whitehead S, Simmons CP: Dengue virus infections and maternal antibody decay in a prospective birth cohort study of Vietnamese infants. J Infect Dis 2009, 200:1893–1900.PubMedCrossRef 30. Huang KJ, Yang YC, Lin YS, Liu HS, Yeh TM,

Chen SH, Liu CC, Lei HY: Flow Cytometric Determination for Dengue Virus-Infected cells: Its application for Antibody-Dependent Enhancement study. Dengue Bulletin 2005, 29:142–150. 31. Huang

KJ, Astemizole Yang YC, Lin YS, Huang JH, Liu HS, Yeh TM, Chen SH, Liu CC, Lei HY: The dual-specific binding of dengue virus and target cells for the antibody-dependent enhancement of dengue virus infection. J Immunol 2006, 176:2825–2832.PubMed 32. Men R, Yamashiro T, Goncalvez AP, Wernly C, Schofield DJ, Emerson SU, Purcell RH, Lai CJ: Identification of chimpanzee Fab fragments by repertoire cloning and production of a full-length humanized immunoglobulin G1 antibody that is highly efficient for neutralization of dengue type 4 virus. J Virol 2004, 78:4665–4674.PubMedCrossRef 33. Vanniasinkam T, Barton MD, Heuzenroeder MW: B-Cell epitope mapping of the VapA protein of Rhodococcus equi: implications for early detection of R. equi disease in foals. J Clin Microbiol 2001, 39:1633–1637.PubMedCrossRef 34. Viudes A, Perea S, Lopez-Ribot JL: Identification of continuous B cell epitopes on the protein moiety of the 58-kiloDalton cell wall mannoprotein of Candida albicans belonging to a family of immunodominant fungal antigens. Infect Immun 2001, 69:2909–2919.PubMedCrossRef 35. Li PC, Liao MY, Cheng PC, Liang JJ, Liu IJ, Chiu CY, Lin YL, Chang GJ, Wu HC: Development of a humanized antibody with high therapeutic potential against dengue virus type 2. PLoS Negl Trop Dis 2012, 6:e1636.PubMedCrossRef 36.

# 2 0 1778 6 1 75 72 2 541 3 33 30 63 The film thicknesses were dir

2 0.1778 6.1 75.72 2.541 3.33 30.63 The film thicknesses were directly measured by a Dektak 6 M profilometer (Veeco Instruments Inc., Plainview, NY, USA). The average grain size d was derived from the (111) X-ray diffraction (XRD) peak, measured with a Bruker D-8 this website XRD system (Cu Kα radiation, 40 kV and 60 mA, Madison, WI, USA) at room temperature,

and the grain size was also directly observed by high-resolution transmission electron microscopy (HRTEM; CM200, Philips, Amsterdam, The Netherlands). The crystalline volume fraction X C was calculated from the Raman spectra, measured with a Jobin Yvon LabRam HR800 UV micro-Raman spectrometer (backscattering configuration and Ar ion laser of 514.5 nm, Kyoto, Japan). The laser power density is 1 mW/mm2 to avoid any beam-induced crystallization. The long-wavelength limit of the refractive index n ∞ was deduced from optical transmission spectra, measured with the double-beam ultraviolet-visible-near-infrared spectrometer PerkinElmer UV Lambda 35 (300- to 1,000-nm spectral range with 0.5-nm resolution, Waltham, MA, USA). The hydrogen (oxygen) content bonded to silicon C H (C O), and its bonding

configurations were obtained from infrared (IR) absorption spectra, measured with a Nicolet Nexus 870 Fourier transform IR spectrometer (400 to 4,000 cm-1, Thermo Fisher Scientific Inc., Waltham, MA, USA). XPS was used to study the silicon core energy level of the nc-Si:H. All the spectra were obtained with an electron takeoff angle of 90° using an Al Kα source monochromatic X-ray radiation. The Kratos charge neutralizer system (Kratos Analytical, Talazoparib mw Chestnut Ridge, NY, USA) was used on all the samples to compensate

the charging effect of the sample surface. The narrow scan of the spectra was collected at a high-resolution mode with a pass energy of 20 eV. The binding energy was calibrated to the C1s emission (284.8 eV) arising Bcl-w from surface contamination. The background from each spectrum was subtracted using a Shirley-type background to remove most of the extrinsic loss structure. All the comparative data and spectra presented below are normalized with thickness. Selleckchem NVP-BSK805 Results and discussion To investigate the structural properties of the nc-Si:H thin films grown under various H dilution profiling, micro-Raman and XRD measurements were carried out. In Figure  1a, the XRD pattern for the sample with R H = 98.2% is presented, in which the three diffraction peaks appearing at 2θ ~ 29.0°, 47.5°, and 57.0° correspond to the (111), (220), and (311) planes of c-Si, respectively. The presence of large diffraction peak broadening of (111), (220), and (311) c-Si peaks indicates the appearance of a silicon nanocrystalline phase in the film. The strongest XRD peak intensity for the (111) plane indicates that the nanocrystallites have preferentially grown along the (111) direction. Based on the Scherrer formula [14], the average grain size d in the (111) direction was calculated to be approximately 5.