Methods The layer structure of a simulated deep UV LED is basically similar to that of recently reported

deep UV LEDs [3, 4]. The layer structures are assumed to be grown on a sapphire substrate and consist of a 2-μm-thick n-Al0.6GaN layer, 50-nm-thick Al0.45GaN/Al0.56GaN multiple quantum well (MQW) active layers, a 50-nm-thick p-Al0.6GaN layer, and a p-GaN contact layer. CP-673451 cell line It is assumed that the simulated UV LED chip is not encapsulated and thus exposed to air. In this work, we consider two types of LED structures: planar and nanorod structures. Figure  1 shows the cross section of the FDTD computational domain for simulated LED structures. In the nanorod LED structure, the sidewall of the nanorod is filled with SiO2 layers for passivation. The cross section of the nanorod is assumed to have a hexagonal shape as shown in Figure  1c because nanorod structures are mostly grown in the shape of a hexagon [16]. In the simulations, the dependence of LEE on the height (h) and diameter (d) of the nanorod structure will be investigated. Figure 1 Schematic diagram of FDTD computational domain. Side view of the simulated LED structure is shown for (a) the planar LED and (b) nanorod LED structures. PMLs are employed for the absorption boundary

condition of the FDTD simulation. The detection plane for extracted light is indicated as dotted red line. (c) Cross-sectional view of the simulated Dinaciclib manufacturer nanorod LED structure. In the FDTD simulation, a single dipole source is positioned in the middle of the MQW active region. The spectrum of the dipole source has a Gaussian shape. Center wavelength and full width at half maximum of the spectrum are assumed to be 280 and 10 nm, respectively. The dipole source is polarized in the direction either parallel to the MQW plane for the excitation of the TE mode or perpendicular to the MQW plane for the excitation

of the TM mode. In the computational domain shown in Figure  1, the dipole source for the TE and TM modes is set to be polarized Miconazole in the x and z directions, respectively. The propagating light is completely absorbed without reflection in the PML. The Poynting vectors are calculated on the surfaces near PMLs and used to determine LEE of LED structures. LEE is defined as the fraction of emitted power out of the LED structure to the total emitted power, which is determined by the ratio of Poynting vectors integrated over extraction surfaces to total integrated Poynting vectors [18]. The plane for detecting extracted light is shown as dotted red line of the computational domain in Figure  1. In order to obtain reliable simulation results, it is important to properly choose the refractive index and absorption coefficient of each material. The absorption coefficient of the GaN layer is chosen to be 170,000 cm-1[20, 21]. Light is strongly absorbed in the GaN layer due to the large absorption coefficient.

Through these centers, she coordinates multidisciplinary and multiagency research teams in academic research and promotes industrialization of nanotechnology with about 175 companies participating. APCTT-UNESCAP [36] reported that serious nanotechnology is ongoing C59 wnt price in the Philippines. They have developed a road map towards successful nanoscience and nanotechnology by way of proper policy formulations and definite goals set as targets. Again, her governments have put in place incentives that will lure their scientists abroad to return

and help in their science and technology development. Demonstration of interest nations – African nations and LDC Many developing countries are at various stages of unknown level either at current R/D empowerment or demonstration of interest stage [11, 25, 26]. Apart from South Africa, most countries in Africa are at the demonstration of interest stage in their nanotechnology development effort. Many have not even indicated

interest, while those that indicated are not having enough drive to push for success [37]. These African nations are only at the level of individual research and incidental funding [38]. Recently, on August 7, 2012 in Abuja, Nigeria, the Federal Ministry of Environment signed a joint agreement to promote training and capacity building for the development of a nanosafety pilot project in Nigeria with financial CT99021 mw support Phosphatidylinositol diacylglycerol-lyase from the government of Switzerland – the overall aim was to create awareness [38]. Zainab [39] reported that ‘nanotechnology is a new field in Nigeria, and systematic efforts are being made by the academia, research institutes and government to create awareness and interest in nanotechnology development.’ Nigeria is one of the up-comer nations with nothing in place indicating nanotechnology activities and the big question is: When will such rich

nation like Nigeria key into this technological revolution and practically start their own nanotechnology programs? This is because most of these countries are for too long standing at this demonstration of interest stage not necessarily because of fund scarcity but probably because of political issues that blind them against realities of life. This is true when some of them are by far richer than Sri Lanka with GDP per capita of about US$2,000 [24] yet shows high commitment in developing nanotechnology with a unique private-public partnership and dedicated scientists. We think the problem is basically because there is no well-developed materials science research curriculum and infrastructural platform in these countries upon which such sensitive research can stand.

J Med Entomol 2011,48(2):389–94.PubMedCrossRef Competing interests The

authors X-396 declare that they have no competing interests. Authors’ contributions CVM conceived the design of the study, participated in all the tasks and performed sequence analysis. FHT carried out the molecular identification of bacteria (ARDRA, PFGE, plasmid profiles). FNR participated in the sampling of mosquitoes and the isolation of bacteria. PR participated in the design of the study. PM conceived of the study and drafted the manuscript. All authors read and approved the final manuscript.”
“Background Bacteriocins are antimicrobial peptides produced by many species of bacteria and some members of the Archaea domain. Nisin, the most well-known bacteriocin, is produced by Lactococcus lactis strains and it belongs to the lantibiotic class of bacteriocins; nisin has GRAS status (Generally Recognized as Safe) and is currently the only bacteriocin approved for use as a food preservative [1]. Other bacteriocins, such as pediocin PA-1/AcH and lacticin 3147, are also

commercially available, but are marketed as fermentates of lactic acid bacteria (LAB) having GRAS status [2]. The targeted mechanism of action and the relatively low propensity to select resistant bacteria are attractive properties of the lantibiotics. Moreover, previous studies have demonstrated the find more efficacy of many lantibiotics against target bacteria [3] and also the Cediranib (AZD2171) potential for biotechnological and therapeutic applications of these peptides [4]. Despite the good results obtained in vitro, the large scale application of lantibiotics remains limited due to the lack of data regarding clinical aspects, including the destiny of the peptides after ingestion, the loss of antimicrobial activity, the cytotoxicity and the immunostimulatory effects triggered by these peptides

in vivo [5]. In order to evaluate the in vivo toxicity, an antimicrobial peptide should be administered daily and repeatedly to an animal model for a required period of time [6, 7], and the route of administration should be the same proposed for use in vivo [8]. Because lantibiotics generally have low molecular mass and little intrinsic immunogenicity, coupling of these peptides to protein carriers or the use of adjuvants can be useful strategies to enhance the immunogenicity [9, 10]. Bovicin HC5, a lantibiotic produced by the ruminal bacterium Streptococcus bovis HC5, has desirable properties, such as broad spectrum of activity, stability to low pH and high temperatures [11, 12]. The mechanism of action of bovicin HC5 was recently elucidated and it is based on the specific interaction with lipid II molecule, leading to inhibition of the bacterial cell wall synthesis and eventually to pore-formation [13].

9% and 60.3%, respectively, a typical feature of oomycete genes [34]. CHI2 and CHI3 code for open reading frames of 596 and 522 amino acids (Figure 2) with molecular masses of 64.0 kDa and 56.7 kDa and isoelectric points of pH 6.14 and 6.63 predicted for the mature secreted enzymes Chi2 and Chi3 (see below), respectively. The mRNAs possess an identical 42-bp 5′ untranslated region (UTR) carrying the major part of the oomycete consensus sequence for the start site of transcription (TATTCAATTTGCCAT, [33]). The 3′ UTRs of CHI2 and CHI3

contain check details the polyadenylation signal WAUAAC (W = A or T) [35] (Additional file 2). In both genes the translation start codon is part of the eukaryotic consensus ACCATGA [33]. The enzymes are predicted to be cleaved by signal peptidase between positions A20 and A21 producing a hydrophobic signal peptide of 20 amino acids (Figure 2). Overall, the deduced amino acid sequences of CHI2 and CHI3 are highly homologous with an identity of up to 79.0% (overlapping residues 1 to 596 and 1 to 522, respectively). The proline-, serine-, and threonine-rich domain [36] of Chi2 contains extra residues resulting in an extended amino acid sequence of Quizartinib price the whole protein compared to Chi3 (Figure 2). This domain also represents the most heterologous part of the enzymes regarding primary sequence. Chi2 and

Chi3 possess an oomycete-type catalytic GH18 domain (A21 to G400/403, Figure 3). It contains a conserved chitin-binding (CB) site [37] (CB site 1 in Figure 2), and an active site consensus [LIVMFY] – [DN] – G – [LIVMF] – [DN] – [LIVMF] – [DN] – x – E (Prosite no. PS01095) being variant at one position (Additional file 3). The catalytic-site residues D154, D156 and E158 are putatively

required for catalytic activity [27]. A second putative, highly homologous CB site was identified in the C-terminal part of the chitinases (CB site 2 in Figure 3). It contains four cysteines, instead of the five residues found in a diatom chitinase (GenBank:EED92972) or six in most insect chitinases [38]. Figure 3 The A. astaci chitinases Chi2 and Chi3 possess an oomycete type-GH18 catalytic domain. Maximum likelihood phylogenetic analysis was performed with TreePuzzle using the diatom Thalassiosira pseudonana as an outgroup. Oomycete and fungal sequences are given Cytidine deaminase in blue and grey, respectively. GenBank accession numbers of partial or complete amino acid GH18 domain sequences are indicated in parentheses. The scale bar represents 0.1 substitutions per site. The numbers at the nodes are quartet puzzling values indicating the frequencies of occurrence for 1,000 replicate trees and can be interpreted in much the same way as bootstrap values. The group A-V – one of six separate fungal groups classified [27, 28] – showing the closest homology to the sequences identified in this work, is represented by two members. An asterisk denotes partial sequences.

J Clin Oncol 2008, 26:2442–2449.PubMedCrossRef 21. Sugio K, Uramoto H, Onitsuka T, Mizukami M, Ichiki Y, Sugaya M, Yasuda M, Takenoyama M, Oyama T, Hanagiri T, Yasumoto HM781-36B clinical trial K: Prospective phase II study of gefitinib in non-small cell lung cancer with epidermal growth factor receptor gene mutations. Lung Cancer 2009, 64:314–318.PubMedCrossRef 22. Douillard JY, Shepherd FA, Hirsh V, Mok T, Socinski MA, Gervais R, Liao ML, Bischoff H, Reck M, Sellers MV, Watkins CL, Speake G, Armour AA, Kim ES: Molecular predictors of outcome with gefitinib and docetaxel in previously treated non-small-cell

lung cancer: data from the randomized phase III INTEREST trial. J Clin Oncol 2010, 28:744–752.PubMedCrossRef 23. Mu XL, Li LY, Zhang XT, Wang MZ, Feng RE, Cui QC, Zhou HS, Guo BQ: Gefitinib-Sensitive Mutations

of the Epidermal Growth Factor Receptor Tyrosine Kinase Domain in Chinese Patients Cisplatin in vivo with Non-Small Cell Lung Cancer. Clin Cancer Res 2005, 11:4289–4294.PubMedCrossRef 24. Tiseo M, Rossi G, Capelletti M, Sartori G, Spiritelli E, Marchioni A, Bozzetti C, De Palma G, Lagrasta C, Campanini N, Camisa R, Boni L, Franciosi V, Rindi G, Ardizzoni A: Predictors of gefitinib outcomes in advanced non-small cell lung cancer (NSCLC): study of a comprehensive panel of molecular markers. Lung Cancer 2010, 67:355–360.PubMedCrossRef 25. Ma F, Sun T, Shi Y,

Yu D, Tan W, Yang M, Wu C, Chu D, Sun Y, Xu B, Lin D: Polymorphisms of EGFR predict clinical outcome in advanced non-small-cell lung cancer patients treated with Gefitinib. Lung Cancer 2009, 66:114–119.PubMedCrossRef 26. Jian G, Songwen Z, Ling Z, Qinfang D, Jie Z, Liang T, Caicun Z: Prediction of epidermal growth factor receptor mutations in the plasma/pleural effusion to efficacy of gefitinib treatment in advanced non-small cell lung cancer. J Cancer Res Clin Oncol 2010,136(9):1341–7.PubMedCrossRef 27. Yamaguchi H, Soda H, Nakamura Y, Takasu M, Tomonaga N, Nakano H, Doi S, Nakatomi K, Nagashima S, Takatani H, Fukuda M, Hayashi T, Tsukamoto K, much Kohno S: Serum levels of surfactant protein D predict the anti-tumor activity of gefitinib in patients with advanced non-small cell lung cancer. Cancer Chemother Pharmacol 2010, in press. Competing interests The authors declare that they have no competing interests. Authors’ contributions YQS contributed to conception and design, and gave final approval of the version to be published. ZXW contributed to conception and design. YMY acquired the data and revised the manuscript critically for important intellectual content. YTG acquired the data and drafted the manuscript. YFS acquired the data. XLH and WL contributed to statistic analysis. All authors have read and approved the final manuscript.

5 (±28.6) min. remained no longer statistically significant when adjusted for the personal best time in a 100 km ultra-marathon. Personal best time proved to be an important variable regarding performance in ultra-endurance races [37]. Thus, adjusting for personal best time resulted in a non-significant difference in

race time between the two groups. The number of athletes might also have affected the result. A decrease of 0.6 kg in body mass seems to be relevant. In a recent study of male 100 km ultra-marathoners, skeletal muscle mass decreased by 0.7 selleck kg [2]. Regarding statistical power, we would have needed to include 42 subjects per group to detect a clinical relevant difference between the groups of 80% power. With our actual sample size, we had only 60% power. However, it was not possible to increase the sample https://www.selleckchem.com/products/XL184.html of athletes under field conditions since only these 28 ultra-marathoners from the total field of athletes volunteered to participate. Since variables of skeletal muscle damage, such as creatine kinase and myoglobin, remain increased for up to seven days after a marathon [38], they should be measured not only immediately

after the race but also in the recovery phase. Presumably the intake of amino acids during the race would lead to lower values of creatine kinase and myoglobin in the recovery phase. In a multi-stage ultra-endurance run, skeletal muscle mass decreased continuously throughout the race [11, 12]. Presumably, amino acid supplementation would have an Temsirolimus effect on variables of skeletal muscle damage rather in a multi-stage race than in a single ultra-marathon. It has been shown that the oral administration of amino acids resulted in a faster recovery of muscle strength after eccentric exercise [39]. The

ingestion of protein during rest periods might enhance recovery [40]. In runners, especially, the combined ingestion of carbohydrate and protein after each training session over 6 days reduced the post exercise increase in serum creatine kinase and muscle soreness [34]. Conclusions The ingestion of 52.5 g of amino acids immediately before and during a 100 km ultra-marathon had no beneficial effect on variables of skeletal muscle damage, muscle soreness, and race performance. A positive effect of amino acid supplementation in ultra-runners might be expected when amino acid or protein would be supplemented in the rest period during a multi-stage ultra-endurance run. Recovery might be enhanced and increase in variables of skeletal muscle damage might be reduced, effects that should be investigated in future studies. Acknowledgements We thank Mary Miller for her help in translation. References 1.

Figure 2 The capacity of pathogenic mycobacteria to grow intracellularly in macrophages treated with IFN-γ or IL-10. Cultures of BMDM were pretreated with exogenic murine r-IFN -γ or r-IL-10 for 2 h, infected with the mycobacterial strains at a MOI of 1, as indicated in the legend to Figure 1, and incubated in the presence of these cytokines for an additional 6 days. The intracellular CFU numbers determined at day 0 and day 6 are presented. The data of

three independent experiments Dorsomorphin concentration are shown as mean ± SD of samples in triplicate. Asterisks represent statistical significance (p < 0.05) compared to infected cells cultured without addition of the cytokines. Innate macrophage activation by the pathogenic mycobacterial strains differing in growth kinetics in macrophages To study the effects of pathogenic Mbv isolates on MΦ activation, we evaluated characteristic markers of M1- and M2- type macrophage polarization induced in infected BMDM, in the presence or absence of IFN-γ and IL-10. First, we investigated the innate MΦ activation induced by infection. Evaluation of expression of the M1 proinflammatory markers, including factors mediating recruitment of the phagocytic cells (MCP-1/CCL2 and MIP-2/CXCL2), and contributing to the MΦ microbicidity (TNF-α, IL-12, IL-6 and NO), demonstrated

that the studied pathogenic mycobacterial strains induced different patterns of cytokine secretion check details by the BMDM (Figure 3A). Both clinical isolates of Mbv induced less IL-6 and MCP-1, and, additionally, the Mbv strain MP287/03 induced less TNF-α, Protirelin than the reference strain H37Rv. In contrast, the level of secretion of MIP-2, an important chemokine regulating migration of granulocytes, was significantly increased in cultures infected with the Mbv strains. These cells secreted 10-fold more MIP-2 than the cells infected by H37Rv strain, and 3-fold more than those infected by the strain B2. Neither mycobacterial strain tested in this study was

able to induce in MΦ the production of NO or IL-12, although production of these mediators was induced by the LPS (Figure 3A). Figure 3 The activation profiles of macrophages infected with pathogenic mycobacteria. BMDM were infected with the studied mycobacterial strains at a MOI of 5:1, washed and incubated for an additional 48 h. The cells left untreated and cells stimulated with LPS for 48 h were used as a negative and positive controls of proinflammatory activation, respectively. To evaluate markers of M1-type activation (A), the culture supernatants of infected cultures were harvested and tested for TNF-α, IL-6, MCP-1, MIP-2 and IL-12 by Bioplex test, and for NO production by Griess reaction. Assays were completed with duplicate samples, and results are expressed as a mean of three independent experiments.

(PDF 12 KB) Additional file 4: Table S2. Score table for the geochemical parameters. The table shows the scores of the geochemical parameters fitted onto the PCA ordination shown in Figure 3. The first two columns gives the direction cosines of the vectors,

r2 gives the squared correlation coefficient. The parameters are sorted by increasing p-values. (DOC 112 KB) Additional file 5: Table S3. Metagenomic parameter scores. The table shows metagenomic parameters scores Raf tumor for the first and second principal component in the PCA analysis. (DOCX 21 KB) Additional file 6: Figure S3. PCA plot showing all measured geochemical parameters. The figure shows the same PCA plot as Figure 3, but displays all the measured geochemical parameters labeled by numbers. (PDF 30 KB) Additional file 7: Table S4. Reads assigned at the domain level in MEGAN. Numbers are given as percent

of total reads (numbers based on the reads assigned to the 16S rRNA gene). (DOCX 13 KB) Additional file 8: Figure S4. Taxonomic distribution of prokaryotes based on all reads at the phylum level. The figure shows the taxonomic distribution of HM781-36B mw prokaryotes in the metagenomes at the phylum level (Proteobacteria are presented at the class level) based on MEGAN analysis (Min Score: 35, Top percent: 10 and Min Support: 5) of all reads after blast against NCBIs non redundant Protein database. (PDF 94 KB) Additional file 9: Figure S5. Taxonomic distribution of prokaryotes based on reads assigned to the 16S rRNA gene at the phylum level. The figure shows the taxonomic distribution of prokaryotes in the metagenomes at the phylum level (Proteobacteria Non-specific serine/threonine protein kinase are presented at the class level) based on MEGAN analysis (Min Score: 50, Top percent: 10 and Min Support: 1) of reads assigned to the 16S rRNA gene after blast against the SILVA SSU and LSU databases. (PDF 16 KB) Additional file 10: Table S5. Significantly over or underrepresented genera in Troll metagenomes compared to both Oslofjord metagenomes. Genera differing significantly in one or more Troll metagenomes compared to both

Oslofjord metagenomes after statistical analysis in STAMP. (DOCX 26 KB) Additional file 11: Table S6. Abundant bacterial and archaeal taxa at the genus level. Taxa with ≥ 0.1% of the reads in one or more metagenomes are presented. Numbers are given as percent of total reads. (DOCX 19 KB) Additional file 12: Table S7. Relative proportion of reads assigned to SEED subsystems (level I). Abundances are presented as percent of total reads. Subsystems where a Troll metagenome showed significant differences compared to both Oslofjord metagenomes in the STAMP analysis are marked with an asterisk. (DOCX 15 KB) Additional file 13: Table S8. Significantly over or underrepresented subsystems (level III) in Troll metagenomes compared to both metagenomes from the Oslofjord.

Indeed, USA400 was the far most common CA-MRSA clone recovered from three northern remote communities of Saskatchewan,

Canada [11]. In 2005, a novel variant of the lineage ST1-SCCmecIV emerged in Rio de Janeiro city as an important cause of bloodstream infections (BSI) [12]. It is intriguing that despite the genetic relationship with Australian WA-1 and MW2/USA400, isolates of this novel clone were PVL-negative, multiresistant and mostly involved in hospital-associated BSI [12]. It is still poorly understood why isolates of CA-MRSA have become successful so quickly [13]. Nevertheless, for hospital-associated AZD1152-HQPA cost MRSA (HA-MRSA), the bacterial ability to produce biofilm has been recognized as an important virulence factor for the pathogenesis of intravenous catheter-related bacteremia and infections associated with the use of medical prosthesis. In addition, the bacterial ability to adhere to, colonize and invade host tissues is considered important factor associated with bacterial virulence, adaptation and spread

[14, 15]. Different surface proteins have been implicated in biofilm formation/accumulation and host colonization, including fibronectin-binding Adriamycin proteins A and B (FnBPAB), S. aureus surface protein G (SasG) and staphylococcal protein A (Spa) [16–19]. In addition, extracellular DNA (eDNA) has also been associated with bacterial biofilms [20]. It is also well known that virulence in S. aureus is modulated by an intricate regulatory network [21]. The accessory gene regulator (agr), the major S. aureus quorum sensing system, down-regulates a number of genes encoding for cell-surface proteins involved in colonization processes, and up-regulates (by an indirect mechanism involving RNAIII dependent down-regulation of Rot) different exoproteins

associated with host-cell damages [22]. Previous works have suggested that inactivation of Agr could be very effective at inhibiting S. aureus infections [23], including those associated with implantable medical devices [24, 25]. Studies have demonstrated that biofilm production, host cell adhesion and invasion as well as other mechanisms involved in the establishment and course of staphylococcal diseases were affected by knockout of the agr locus [26–28]. Despite the improvements Temsirolimus achieved in staphylococcal virulence, most of the investigations have been carried out using relatively few laboratory constructions or clinical isolates [28]. In addition, those results have not been validated using current clinical isolates of MRSA. In this paper we characterized the biofilm formed by USA400-related (ST1-SCCmecIV) MRSA emergent in Rio de Janeiro, investigated the adhesive and invasive properties of naturally agr-dysfunctional isolates and analyzed the impact of the agr inhibition on S. aureus infections associated with the use of medical device.

The dotted horizontal line represents the cut-off value for adherence. The dashed vertical line indicates the separation of the biofilm formation assay. vs: versus, ***P < 0.0001, **P < 0.001, black dot: isolate AC 7070, black triangle: isolate AC 1181. The analysis of biofilm formation demonstrated that all strains have the

capability to adhere to polystyrene surfaces and form biofilms (Fig. 4). Isolates 10672, AC1135 and strain DSM 16831 revealed the highest biofilm formation; remarkably, strain DSM 16831 had no capacity to invade cells. Correlation analysis of adherence to or invasion of endothelial cells and biofilm formation revealed no correlation. Additionally, no correlation was found between adherence to different ECM proteins and biofilm formation. Discussion and Conclusions S. gallolyticus NVP-BGJ398 order is an important pathogen with an underestimated relevance causing IE. The frequent changes in the taxonomy resulted in an inadequate or incorrect identification of the causative pathogens, because non-experts were often not aware of the new nomenclature (e.g. [42]). In contrast to RG7420 chemical structure other streptococci, little is known about virulence factors and pathogenesis. The adherence of circulating bacteria to damaged heart tissues and subsequent colonization and persistence of bacteria are the crucial factors in streptococcal IE. The prevention of tissue colonization, with special

attention to targeting therapy against ECM-binding, potentially provides a promising alternative in human medicine [43]. Therefore, we analyzed the factors which contribute to S. Rolziracetam gallolyticus adhesion and invasion in IE using an experimental in vitro cell culture model. Investigation

of the adhesion to ECM proteins identified or confirmed putative adhesive sites on the endothelial cell surface. Additionally, virulence factors were detected and biofilm formation was analyzed in order to identify different strain characteristics. Most S. gallolyticus strains tested in this study adhere to and invade endothelial cells. The diversity in adhesion and invasion characteristics appears considerably higher for invasion. Strain DSM 16831 exclusively demonstrated no invasive capability. Invasion was also not induced using higher concentrations of bacteria, usage of primary endothelial cells or mechanical stretched cells. In contrast, strain DSM 13808 present a considerably high invasion. The distinct behaviour of these two strains may be due to the fact that they were the only strains tested that were isolated from non-human sources. In general, the observed differences may reflect distinctions in the bacterial equipment with virulence factors or gene expression of virulence factors. We have shown that isolate represent a different distribution of the virulence-associated genes gtf, fimB and pilB. However, the presence of a putative virulence gene does not necessarily indicate expression. For example, Stipp et al.