Since SrRuO3 (SRO) is often chosen as the lower electrode for the BFO thin film as well as for the buffer layer to control its nanoscale

domain architecture [11], it is desirable to investigate the optical properties of the BFO thin film grown on SRO. Spectroscopic ellipsometry (SE) is a widely used optical characterization method for materials and related systems at the nanoscale. It is based on the measuring the change in the polarization state of a linearly polarized light reflected from a sample surface which consists of Ψ, the amplitude ratio of reflected p-polarized light to s-polarized light and Δ, the phase shift difference between the both [12]. The obtained ellipsometry spectra (Ψ and Δ at measured wavelength range) are fitted to the optical model for thin film nanostructure, and thus, rich information including surface roughness, film thickness, and optical constants of nanomaterials are revealed [13, 14]. QNZ Since Compound C solubility dmso SE allows various characterizations of the material, our group has studied some thin-film nanostructure using SE methods [15–18]. In this paper, we report the optical properties of epitaxial BFO thin film grown on SRO-buffered STO substrate prepared by pulsed-laser deposition (PLD) and measured by SE. The dielectric functions of STO, SRO, and BFO are extracted from the ellipsometric spectra,

respectively. And the optical constants of the BFO thin film are obtained. The bandgap of 2.68 eV for the BFO thin film is also received and is compared to that for BFO thin film deposited on different substrate as well as BFO single crystals. Methods The epitaxial BFO thin film was deposited

by PLD on SRO-buffered (111) STO single-crystal substrate. The SRO buffer layer was directly deposited on the STO substrate by PLD in advance. More details about the deposition PR 171 process can be taken elsewhere [19]. The crystal phases in the as-grown BFO thin film were identified by X-ray diffraction (XRD, Bruker X-ray Diffractometer D8, Madison, WI, USA). The surface morphologies of the BFO thin film were investigated by atomic force microscopy (AFM, Veeco Instruments Inc., Atomic Force Microscope System VT-1000, Plainview, NY, USA). Both XRD and AFM investigation are employed to show growth quality of the BFO thin film for further optical find more measurement and analysis. SE measurements were taken to investigate the optical properties of the BFO film. Considering the optical investigation with respect to a substrate/buffer layer/film structure, we should firstly obtain the optical response of the STO substrate and SRO buffer layer and then research the optical properties of the BFO thin film. The ellipsometric spectra (Ψ and Δ) were collected for the STO substrate, the SRO buffer layer, and the BFO film, respectively, at an incidence angle of 75° in the photon energy range of 1.55 to 5.

It is thus necessary to eliminate or reduce the presence of mycotoxins in the food chain. An important step in controlling contaminants in the food production chain is by identifying food-borne fungi. The conventional methods used for the detection of fungal contamination are based on phenotypic and physiological characteristics that make use of standard culture and biochemical/serological tests. However, these

methods are very time-consuming, laborious and do not detect mycotoxins. Recently, a variety of molecular methods have DZNeP been used for fungal pathogen identification and for their potential to produce mycotoxins [5]. Molecular methods were used for Aspergillus species differentiation using Southern blot hybridization assays [6] and PCR-based restriction fragment length polymorphisms [7]. Most assays that have been developed included PCR-based methods that exploited the highly conserved ribosomal RNA gene sequences for the design of species-specific primers [8] as well as generic PCR detection assays

developed for genes involved in the biosynthesis of some mycotoxins [9, 10]. Although these assays are an improvement compared to conventional methods, the overall throughput is still limited. Only a limited number of diagnostic regions can be identified for a single organism at a time. If all potentially mycotoxigenic fungi must be included, these assays become laborious Glutamate dehydrogenase and expensive. MM-102 manufacturer The use of integrated platforms that Selleckchem FG-4592 combine identification and typing methods for several fungi would facilitate the rapid and accurate identification of possible mycotoxigenic fungi in food commodities. The microarray technique allows the rapid and

parallel characterization of a range of organisms and has the intrinsic ability to perform multiplexed and low-volume biological assays. This technique has been increasingly used for diagnostic purposes as it has the ability to detect more than one parameter at a time [11, 12]. Leinberger et al. [13] exploited the polymorphisms of the internal transcribed regions in the ribosomal RNA cassette for the microarray-based detection and identification of Candida and Aspergillus species. In a similar experiment, DeSantis et al. [14] generated a 62358-probe oligonucleotide of small subunit ribosomal RNA (ssu rRNA) for the detection of 18 different orders of microbes from environmental samples and novel variants exhibiting mutations in their ssu rRNA. Microarrays have also been successfully used to study the expression levels of mycotoxin gene clusters. Schmidt-Heydt and Geisen [15] developed a microarray which contained oligonucleotide probes for the biosynthesis pathways of fumonisin, aflatoxin, ochratoxin, patulin and trichothecene.

Biochemistry (Moscow) 2008, 73 (9) : 985–989.CrossRef 25. Brun R, Schoenenberger M: Cultivation and in vitro cloning of procyclic culture forms of Trypanosoma brucei in a semi-defined medium. Acta Trop 1979, 36 (3) : 289–292.PubMed 26. Hesse F, Selzer PM, Muehlstadt K, Duszenko M: A novel cultivation technique for long-term maintenance of bloodstream form trypanosomes in vitro. Mol Biochem Parasitol 1995, 70 (1–2) : 157–166.PubMedCrossRef 27. Wirtz E, Leal S, Ochatt C, Cross GAM: A tightly regulated inducible expression system for conditional gene knock-outs and dominant-negative genetics in Trypanosoma brucei . Mol Biochem Parasitol 1999, 99 (1)

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reticulum translocation of a phospholipase C. FEBS J 2006, 273 (10) : 2110–2126.PubMedCrossRef 29. Eixler S, Selig U, Karsten U: Extraction and detection methods for polyphosphate storage in autotrophic planktonic organisms. Hydrobiologia 2005, 533: 135–143.CrossRef 30. Diaz JM, Ingall ED: Fluorimetric quantification of natural inorganic polyphosphate. Environ Sci Technol 2010, 44: 4665–4671.PubMedCrossRef 31. Tartof KD, Hobbs CA: Improved media for growing plasmid and cosmid clones. Bethesda Res Lab Focus 1987, 9: 12. 32. Wentzinger L, Bopp S, Tenor H, Klar J, Brun R, Beck HP, Seebeck T: Cyclic nucleotide-specific phosphodiesterases of Plasmodium falciparum : PfPDEalpha, a nonessential cGMP-specific PDE that is an Ruxolitinib integral membrane protein. Int J Parasitol 2008, 38 (14) : 1625–1637.PubMedCrossRef 33. Hojman P, Eriksen J, Gehl J: Tet-On induction with doxycycline after gene transfer in mice: sweetening of drinking water is not a good idea. Animal Biotechnol 2007, 18 (3) : 183–188.CrossRef 34. Pillai

R, Kytle K, Reyes A, Colicelli J: Use of a yeast expression system for the isolation and analysis of drug-resistant mutants of mammalian phosphodiesterases. Proc Natl Acad SB-3CT Sci USA 1993, 90 (24) : 11970–11974.PubMedCrossRef 35. Espiau B, Lemercier G, Ambit A, Bringaud F, Merlin G, Baltz T, Bakalara N: A soluble pyrophosphatase, a key enzyme for polyphosphate metabolism in Leishmania . J Biol Chem 2006, 281 (3) : 1516–1532.PubMedCrossRef Authors’ contributions EL and TS conceived the project, and EL conducted most of the work. LW contributed to recombinant protein expression and PDE assays, SK provided the expertise and conducted many of the yeast experiments, FF contributed to polyphosphatase activity measurements. TS drafted and wrote the manuscript. All authors have read and approved the final text.

Arab J Sci Eng 2013, 38:1289–1304.Selleck Flavopiridol CrossRef 15. Cai X, Lin MS, Tan SZ, Mai WJ, Zhang YM, Liang ZW, Lin ZD, Zhang XJ: The use of polyethyleneimine-modified reduced graphene oxide as a substrate for silver nanoparticles to produce a material with lower cytotoxicity and long-term antibacterial activity. Carbon 2012, 50:3407–3415.CrossRef 16. Sundaram RS, Steiner M, Chiu HY, Engel M, Bol AA, Krupke R, Burghard M, Kern K, Avouris P: The graphene–gold interface and its implications for nanoelectronics. Nano Lett 2011, 11:3833–3837.CrossRef www.selleckchem.com/products/lxh254.html 17. Zhou KF, Zhu YH, Yang XL, Jiang X, Li CZ: Preparation of graphene–TiO 2 composites with enhanced photocatalytic activity.

New J Chem 2011, 35:353–359.CrossRef 18. Cheng JS, Tang LH, Li JH: Palladium nanoparticles-decorated graphene nanosheets as highly regioselective catalyst for cyclotrimerization reaction. J Nanosci Nanotechno 2011, 11:5159–5168.CrossRef 19. Kim H, Son Y, Park C, Cho J, Choi HC: Catalyst-free direct growth of a single to a few layers of graphene on a germanium nanowire for the anode material of a lithium battery. Angew Chem 2013, 52:5997–6001.CrossRef 20. Chockla AM, Panthani MG, Holmberg VC, Hessel

CM, Reid DK, Bogart TD, Harris JT, Mullins CB, Korgel BA: Electrochemical lithiation of graphene-supported silicon and germanium for rechargeable batteries. J Phys Chem C 2012, 116:11917–11923.CrossRef Protein Tyrosine Kinase inhibitor 21. Anota EC, Hernandez GM: Electronic properties of germanium carbide blade of graphene type. Rev Mex Fis 2011, 57:30–34. 22. Cheng JS, Du J: Facile synthesis of germanium–graphene nanocomposites and their application as anode materials for lithium ion batteries. CrystEngComm 2012, 14:397–400.CrossRef 23. Ren JG, Wu QH, Tang H, Hong G, Zhang WJ, Lee ST: Germanium–graphene composite anode for high-energy lithium batteries with long cycle life. J Mater Chem A 2013, 1:1821–1826.CrossRef 24. Hummers

WS, Offeman RE: Preparation of graphitic oxide. J Am Chem Soc 1958, 80:1339.CrossRef 25. Kovtyukhova NI, Ollivier PJ, Martin BR, Mallouk TE, Chizhik SA, Buzaneva EV, Gorchinskiy AD: Layer-by-layer assembly of ultrathin composite films from micron-sized graphite oxide sheets and polycations. Chem Mater 1999, 11:771–778.CrossRef 26. Bagri A, Mattevi C, Acik M, Chabal YJ, Chhowalla M, Shenoy VB: Structural evolution during the Nintedanib (BIBF 1120) reduction of chemically derived graphene oxide. Nature Chem 2010, 2:581–587.CrossRef 27. Leroy P, Tournassat C, Bizi M: Influence of surface conductivity on the apparent zeta potential of TiO 2 nanoparticles. J Colloid Interf Sci 2011, 356:442–453.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions PY supervised the study, HY did the experiments, and JL help modify the manuscript. Pinghe Yin provided detection technical support. PY and HY analyzed the data and gave the final approval of the version of the manuscript to be published. All authors read and approved the final manuscript.

innocua were higher than those of L. monocytogenes. More strikingly, recombination rates of L. innocua subgroup A were particularly AZD1480 ic50 high (Table 5). Wirth et al. [32] proposed from the data for Escherichia coli that epidemic and virulent bacteria face an increased selective pressure

for rapid diversification in response to host immune defenses, resulting in higher recombination rates. L. monocytogenes is an opportunistic pathogen with wide host ranges as well as a saprotroph found in different environments [2, 33]. Though lineage I strains were responsible for almost all major human listeriosis outbreaks and the majority of sporadic cases [6], those of lineage II this website exhibited higher recombination rate according to our observation and the findings by Bakker et al. [24]. Bakker et al. [24] proposed that higher recombination in lineage PCI-32765 research buy II was not due to selective forces involved in its

virulence. Recombination may be critical for lineage II to successfully compete and survive in a board range of different environments. Lineage II strains are more commonly found at higher levels than lineage I strains in natural environments including foods [24, 34]. Similarly, we postulate that the nonpathogenic species L. innocua descending from its pathogenic ancestor has better adaptability to contemporary environmental niches. Removal of some gene loci related to virulence (e.g., LIPI-1, inlAB and bsh) in Listeria could be regarded as adaptive gene loss, which favors its survival in

environmental niches as a saprotroph [9, 11]. L. innocua subgroups A and B strains have similar TMRCA and exhibit similar genetic distances to L. monocytogenes, suggesting that these two subgroups appeared at approximately the same time (Fig 2). However, subgroup A experienced a recent expansion of the population size, consistent with the higher recombination frequency (r/m) and effect (ρ/θ) of subgroup A as compared to those of subgroup B. This further AMP deaminase implies that these two subgroups have distinct inclinations and adaptive abilities to environments and occupy different habitats, while subgroup A might face increased selective pressures resulting in higher recombination rates. Additional support for this indication is that the majority of subgroup A isolates (belonging IT1) contain a whole set of L. monocytogenes-L. innocua common and L. innocua-specific internalin genes which may play broad roles in enhancing the adaption to various environments. Hence, the L. innocua subgroup A strains might represent the possible evolutionary direction towards adaptation. Interestingly, the higher recombination rate of L. innocua subgroup A did not seem to contribute to nucleotide diversity.

Mortality was analyzed by survival analysis using Cox’s proportional hazard rate including censoring. The follow-up time for one person was from the day the fracture occurred to death or the censoring date in January 1, 2009. The analyses were

performed using the Statistical Package for Social Sciences version 15.0 (SPSS, Chicago, IL, USA), Microsoft Office Excel version 2007 and the statistical program R, version 2.11.0 (The R Foundation for Statistical Computing). Results Fracture incidence and time trends Of the 603 fractures, 73% (95% CI: 69.5, 76.5) occurred in women providing a female:male ratio of 2.7. The mean age at fracture in this population (aged 50 years and above) was 80.0 years (95% CI: 79.1, 80.9) in women and 76.7 years (95% CI: 75.1, 78.3) Selleck YAP-TEAD Inhibitor 1 in men (p < 0.001). The median age at hip fracture was 81.7 and 79.3 years in women and men, respectively. Age at fracture did not change during the 15 years, neither in women (p = 0.43) nor in men (p = 0.26). The incidence of hip fractures rose exponentially with increasing

age from 5.8 to 349.2 per 10,000 in men, VX-689 and from 8.7 to 582.2 per 10,000 in women (Table 1 and Fig. 1). Table 1 Age- and sex-specific annual incidence of hip fractures Ribonucleotide reductase in Harstad, Northern HSP inhibitor Norway Age groups (years) Number of hip fractures Person years in total Incidence per 10,000 (SD) 95% CI Men  50–54 7 12,060 5.8 (2.2) 1.5, 10.1  55–59 6 10,095 5.9 (2.4) 1.2, 10.7  60–64 6 7,740 7.8 (3.2) 1.5, 14.0  65–69 20 6,360 31.4 (7.0) 17.7, 45.2  70–74 20 5,595 35.7 (8.0) 20.1, 51.4  75–79 27 4,545 59.4 (11.4) 37.0, 81.8  80–84 37 2,970 124.6 (20.5) 84.4, 164.7  85–89 28 1,050 266.7 (50.4) 167.9, 365.4  90+ 11 315 349.2 (105.3) 142.8, 555.6 Women  50–54 10 11,520 8.7 (2.7) 3.3,14.1  55–59 13 9,810 13.3 (3.7) 6.0, 20.5

 60–64 11 7,980 13.8 (4.2) 5.6, 21.9  65–69 22 6,990 31.5 (6.7) 18.3, 44.6  70–74 41 6,750 60.7 (9.5) 42.2, 79.3  75–79 74 6,075 121.8 (14.2) 94.1, 149.6  80–84 127 4,620 274.9 (24.4) 227.1, 322.7  85–89 81 2,460 329.3 (36.6) 257.6, 401.0  90+ 62 1,065 582.2 (73.9) 437.2, 727.1 Fig. 1 Hip fracture incidence rates pr 10,000 in women and men in Harstad (1994–2008) and Oslo (1996–1997), Norway Table 2 displays the incidence rates in Harstad compared with reported rates from four studies from other parts of Norway.

Res Microbiol 1991, 142:541–549.PubMedCrossRef 26. Huff WE, Huff GR, Rath NC, Balog JM, Donoghue AM: Bacteriophage treatment of a severe Escherichia coli respiratory infection in broiler chickens. Avian Dis 2003, 47:1399–1405.PubMedCrossRef 27. Khakhria Serine/threonin kinase inhibitor R, Lior H: Extended phage-typing scheme for Campylobacter Osimertinib jejuni and Campylobacter coli. Epidemiol Infect 1992, 108:403–414.PubMedCrossRef 28. Salama S, Bolton FJ, Hutchinson DN: Improved method for the isolation of Campylobacter

jejuni and Campylobacter coli bacteriophages. Lett Appl Microbiol 1989, 8:5–7.CrossRef 29. Connerton PL, Loc Carrillo CM, Swift C, Dillon E, Scott A, Rees CE, Dodd CE, Frost J, Connerton IF: Longitudinal study of Campylobacter

jejuni bacteriophages and their hosts from broiler chickens. Appl Environ Microbiol 2004, 70:3877–3883.PubMedCrossRef 30. Grajewski BA, Kusek JW, Gelfand HM: Development of a bacteriophage typing system for Campylobacter jejuni and Campylobacter coli. J Clin Microbiol 1985, 22:13–18.PubMed 31. Mdivi1 Atterbury RJ, Connerton PL, Dodd CE, Rees CE, Connerton IF: Isolation and characterization of Campylobacter bacteriophages from retail poultry. Appl Environ Microbiol 2003, 69:4511–4518.PubMedCrossRef 32. Atterbury RJ, Dillon E, Swift C, Connerton PL, Frost JA, Dodd CE, Rees CE, Connerton IF: Correlation of Campylobacter bacteriophage with reduced presence of hosts in broiler chicken ceca. Appl Environ Microbiol 2005, 71:4885–4887.PubMedCrossRef 33. El-Shibiny A, Scott A, Timms A, Metawea Y, Connerton P, Connerton I: Application of a group II Campylobacter bacteriophage to reduce strains

of Campylobacter jejuni and Campylobacter Thalidomide coli colonizing broiler chickens. J Food Prot 2009, 72:733–740.PubMed 34. Loc Carrillo CM, Connerton PL, Pearson T, Connerton IF: Free-range layer chickens as a source of Campylobacter bacteriophage. Antonie Van Leeuwenhoek 2007, 92:275–284.PubMedCrossRef 35. Carvalho C, Susano M, Fernandes E, Santos S, Gannon B, Nicolau A, Gibbs P, Teixeira P, Azeredo J: Method for bacteriophage isolation against target Campylobacter strains. Lett Appl Microbiol 2009, 50:192–197.PubMedCrossRef 36. Atterbury RJ, Connerton PL, Dodd CE, Rees CE, Connerton IF: Application of host-specific bacteriophages to the surface of chicken skin leads to a reduction in recovery of Campylobacter jejuni. Appl Environ Microbiol 2003, 69:6302–6306.PubMedCrossRef 37. Lavigne R, Darius P, Summer E, Seto D, Mahadevan P, Nilsson A, Ackermann H, Kropinski A: Classification of Myoviridae bacteriophages using protein sequence similarity. BMC Microbiol 2009, 9:224.PubMedCrossRef 38. Rosenquist H, Sommer HM, Nielsen NL, Christensen BB: The effect of slaughter operations on the contamination of chicken carcasses with thermotolerant Campylobacter. Int J Food Microbiol 2006, 108:226–232.PubMedCrossRef 39.

After drying at 60°C for 30 min, Au was coated onto the silica sphere array by e-beam evaporation. In order to ensure adhesion, 20 nm of Cr as an insertion layer was also deposited on the surface of the silica sphere array before

deposition of the Wortmannin Au layer. Figure 1 Schematic diagram for fabrication procedure. Schematic diagram for the fabrication of the Au-coated silica sphere array as a top electrode of ZnO NRA-based NGs: (i) preparation of colloidal solution (i.e., dispersed by silica spheres) on the PET substrate, (ii) rolling and drying the colloidal solution, and (iii) e-beam evaporation of Au onto the silica sphere array. Results and discussion Figure 2a shows the field-emission scanning electron microscope (FE-SEM) images of (i) the deposited silica sphere on the PET substrate and (ii) the Au-coated silica sphere array on the PET substrate by e-beam evaporation with a deposition rate of 5 Å/s for 400 s. As shown in the FE-SEM image of Figure 2a (i), the multilayer of silica spheres of approximately 75- to 100-nm diameters was coated on the PET substrate, which could provide a rough surface of the template for Au coating as a top electrode. When Au was deposited on the silica sphere array in Figure 2a

(ii), it covered well the whole surface of the silica sphere array with a somewhat thick and angulate morphology. For click here comparison of the surface roughness in topography, 5 μm × 5 μm scan AFM images and histograms of (i) the Au film on the PET substrate and (ii) the Au-coated silica sphere array on the PET PD-1/PD-L1 Inhibitor 3 substrate are shown in Figure 2b. As can be seen in the AFM topographic images for each sample, it is clearly observed that the Au-coated silica sphere array had such a rough surface as compared to the surface of the Au film on the PET substrate. From the roughness analysis, the root mean square

(RMS) surface roughness of (i) and (ii) were 5.78 and 88.27 nm, respectively. Also, the Au-coated silica sphere array exhibited a high average particle height of 259.6 nm, while the Au film on the PET substrate exhibited a low average Methane monooxygenase particle height of 5.78 nm. This highly rough surface of the Au-coated silica sphere array could lead to a good electrode for efficient bending of ZnO nanorods on NG devices. Figure 2 FE-SEM and AFM images. (a) FE-SEM images of (i) the deposited silica sphere array on the PET substrate and (ii) the Au-coated silica sphere array on PET. (b) 5 μm × 5 μm scan AFM images and histograms of (i) the Au film on the PET substrate and (ii) the Au-coated silica sphere on the PET substrate. Figure 3 shows (a) the measured I-V curves and (b) simulation results for the strain distributions of (i) the flat Au film on PET and (ii) the Au-coated silica sphere array on PET. To obtain the sheet resistivity (R s), the I-V curves were characterized by a line four-point probe measurement setup with a fixed distance between the probes (1 mm).

Three genes (papGI, sat, hlyA) were exclusively detected in isolates of human origin, but only sat showed significant differences (P = 0,023) with APEC. The other virulence markers analyzed did not show statistical differences, either because they were not detected in any of the 59 isolates (focG, afa/draBC, bmaE, nfaE, gafD, cnf1) or only in one strain (sfaS, cdtB), or because they were highly prevalent (fimH, papC, fyuA, iutA, traT, malX, usp) (P > 0.05). Table 3 Results of genotyping PRN1371 in vivo studies in relation to the phylogenetic group   B2 (n = 40) D (n = 19) P value* Genes APEC n = 20 NMEC n = 6 Septicemic/UPEC n = 14 TOTAL B2 n = 40 APEC n Tideglusib ic50 = 1 NMEC

n = 9 UPEC-Sepsis n = 9 TOTAL D n = 19 B2 vs D FimAv MT78 2/20(10%) 1/6(16%) 2/14(14%) 5/40(12,5%) 0 5/9(55%) 8/9(89%) 13/19(68%) + (0.000) papGII 20/20(100%) 5/6(83%) 14/14(100%) 39/40 (95%) 1/1(100%) 6/9(67%) 3/9 (33%) 10/19(53%) + (0.000) sat 0 2/6(33%) 2/14(14%)

4/40(10%) 0 8/9(89%) 9/9(100%) 17/19(89%) + (0.000) tsh 6/20(30%) 1/6(17%) 2/14(14%) 9/40(22,5%) 1/1(100%) 0 0 1/19(5%) – (0.096) iro N 20/20(100%) 4/6(67%) 10/14(71%) 34/40(50%) 1/1(100%) 1/9(11%) 0 2/19(10,5%) + (0.000) cva C 12/20(60%) 3/6(50%) 6/14(43%) 21/40(52,5%) 1/1(100%) 0 0 1/19(5%) + (0.000) iss 19/20(95%) ABT-263 in vivo 3/6(50%) 8/14(57%) 30/40(75%) 1/1(100%) 0 0 1/19(5%) + (0.000) Genes showing statistical differences in relation to pathogenic groups were compared for the phylogenetic groups, using Fisher’s exact test. *For each comparison, a P value of < 0.05 was considered statistically significant (+), and a P value of > 0.05 was not considered statistically significant (-). All the 59 isolates O1:K1:H7/NM showed Dolutegravir ic50 to accumulate a high number of virulence markers. Thus, 85% of the 40 ExPEC B2 and 74% of the 19 ExPEC D strains were positive for at least eight virulence genes. Twenty-eight different profiles based on the combination of positive virulence genes were observed (Table 4). The 40 isolates belonging to the

phylogroup B2 exhibited 19 profiles (1 to 19) with 15 to five virulence genes, and the most prevalent virulence profile was 6–10 detected in 16 isolates of the three ExPEC pathotypes (10 APEC, four UPEC/septicemic E. coli, and two NMEC) positive for fimH, papC, iroN, fyuA, iutA, cvaC, iss, traT, malX, and usp. The 19 isolates belonging to the phylogroup D exhibited nine profiles (20 to 28) with 10 to five virulence genes, and the most prevalent profile was 21–9 detected in five isolates (three NMEC and two UPEC/septicemic E. coli) positive for fimH, fimAv MT78, papC, sat, fyuA, iutA, traT, malX, and usp. Table 4 Relationship between virulence genotype and phylogenetic group B2 (n = 40) D (n = 19) Profile-no. genes* No. strains PFGE clusters (no. strains) Profile-no. genes* No. strains PFGE pulsotypes (no.

CD and RZ drafted the manuscript. All authors contributed to, read, criticized and approved

the final manuscript.”
“Background Shigella is the major cause of endemic bacillary dysentery (shigellosis) in developing countries. It is estimated that there are about 164.7 LY411575 supplier million cases of shigellosis annually worldwide, of which 163.2 million were in developing countries, resulting in 1,1 million deaths, most of which JMJD inhibitor were children under 5 years of age [1]. Among the four Shigella species, S. dysenteriae, S. flexneri, S. boydii, and S. sonnei, S. flexneri is the predominant species. Based on the combination of antigenic determinants present in the O-antigen of the cell envelope lipopolysaccharide (LPS), S. flexneri is further divided into various serotypes. To date, at least 16 serotypes have been recognized [2–4]. Except for serotype 6, all share a basic repeating tetrasaccharide unit, comprised of one GlcNAc and three rhamnoses [4]. Modifications to the side chain of the tetrasaccharide by the addition of glucosyl and/or O-acetyl groups give rise to various EPZ-6438 concentration antigenic determinants [3]. The genes responsible for the O-antigen modification are always either the gene cluster

gtrABC for glucosyl groups or the single oac gene for the O-acetyl group; all encoded by serotype-converting bacteriophages [3, 5–10]. In all glucosylation modification phages, the gtrABC gene cluster is always located immediately upstream of the attP site, followed by the int and xis genes [6]. Up to now,

four S. flexneri serotype-converting bacteriophages, SfV, SfX, Sf6 and SfII, have been induced and purified by different groups [8, 11–13]. Morphologically, SfV and SfII, which many have an isometric head and a long tail, belong to Group A in the family of Myoviridae[8, 11]; while SfX and Sf6, which possess a short tail linked to an isometric head, belong to the family of Podovirida[12, 13]. The complete genome sequences of phage SfV and Sf6 have been obtained by directly sequencing the phage DNA purified from phage particles, and their genetic features have been well characterized [9, 10]. Recently, the prophage genome of SfX was determined from the sequenced S. flexneri serotype Xv strain 2002017; which is presumably the whole genome of phage SfX, because a SfX phage particle can be induced and isolated from 2002017 [2]. The SfX genome is 37,355 bp length, encoding 59 ORFs (unpublished data). The genome of SfII has not yet been sequenced from free phage particles, but prophage genomes can be derived from sequenced S. flexneri serotype 2a strains Sf301 and 2457T [14, 15], which show considerable variation with one or both being prophage remnants. S.