However, for co-doped Tm3+-Nd3+:KPb2Cl5, the presence of the Tm3+ is known to increase the absorption of the pump and enhance the IR emission from the Nd3+ ions [44]. An additional example is co-doped Tm3+-Pr3+:CsCdBr3, in which pumping the 3H4 level of Tm3+ results in energy transfer and up-conversion to emitting

states in the visible [45]. Energy transfer from the 3H4 state of Tm3+ to the IR-emitting states of Pr3+ in a low phonon energy host crystal is also an interesting phenomenon. Like Ho3+, the Pr3+ ion also lacks absorption at 800 nm. However, transitions out of the first three excited states of Tm3+ that populate through cross-relaxation are resonant with absorption transitions out of the Pr3+ ground state to excited states of Pr3+ that radiate

in the mid-IR. Figure 6 selleck kinase inhibitor compares the lower energy levels of Tm3+ to the lower levels of Pr3+ and illustrates three possible pathways for resonant energy transfer that involve excited-state Tm3+-sensitizing ions interacting with ground-state Pr3+ acceptor ions. Figure 6 Energy INCB024360 molecular weight transfer processes for co-doped Tm 3+ -Pr 3+ :KPb 2 Cl 5 . The first three excited states of Tm3+-sensitizing ions are all resonant with ground-state transitions of Pr3+ acceptor ions. In contrast to Pr3+:YAG or Pr3+:YLF, Pr3+ ions in a chloride host crystal will radiate at mid-IR wavelengths because the lower energy levels are no longer quenched by multi-phonon relaxation. This effect was exploited to make 5.2- and 7.2-μm lasers using Pr3+:LCl3[11, 12]. For Pr3+ doped into KPb2Cl5, the lower energy

levels will also radiate in the mid-IR. The mid-IR fluorescence can be observed in singly doped Pr3+:KPb2Cl5 when the 3F4 level is pumped directly with a 1.5-W, 1,483-nm laser diode. For Pr3+:KPb2Cl5 under this pump, the room temperature fluorescence that results from 1,600 to 2,800 nm is shown in Figure 7 and from 3,000 to 5,500 nm is shown in Figure 8[32]. Each feature in the spectra is labelled with the associated Pr3+ energy level transition. Figure 7 Fluorescence from 1,600 to 2,800 nm resulting from 1,483-nm pumping of Pr 3+ :KPb 2 Cl 5 . The sample has a Pr3+ concentration of 1.5 × 1020 ions/cm3. Figure 8 Fluorescence Florfenicol from 3,000 to 5,500 nm resulting from 1,483-nm pumping of Pr 3+ :KPb 2 Cl 5 . The sample has a Pr3+ concentration of 1.5 × 1020 ions/cm3. The Tm3+ sensitization of Pr3+:KPb2Cl5 allows for more convenient 800-nm diode pumping. For a co-doped Tm3+-Pr3+:KPb2Cl5 crystal using a 1.5-W, 805-nm laser diode as a pump source, the same broadband mid-IR emission between 4,000 and 5,500 nm from the Pr3+ ions is observed. The room temperature fluorescence that results from 805-nm pumping of the co-doped crystal overlapped with the fluorescence that results from the 1,483-nm pumping of the same co-doped crystal from 1,600 to 2,800 nm is shown in Figure 9 and from 3,000 to 5,500 nm is shown in Figure 10[32].

g. H. luteocrystallina, H. moravica, H. pachypallida or H. parapilulifera. These species differ markedly in their anamorphs except H. luteocrystallina. The latter species is similar to H. lutea in both teleomorph and anamorph, but can be distinguished by yellow crystals on the mature stroma surface turning violet in KOH, a conspicuous white young stage, subglobose conidia, slower growth, a growth optimum at 25°C and virtually no growth at 35°C. The red pigment is produced by both species. According to G.J. Samuels (pers. comm.), isolates of H. lutea are known that do not produce a reddish pigment.

H. lutea typically occurs on the upper side of logs or branches or on standing branches, find more i.e. freely exposed to climatic elements. This correlates with its growth at 35°C. Species concept and history: Tode (1791) described Sphaeria gelatinosa with the two varieties α. lutea and β. viridis. Petch (1937) summarised the history of the two varieties check details and the interpretations of Tode’s (1791) protologues by various mycologists.

The notion whether the stromata were gelatinous or not varied among authors, and S. gelatinosa was regarded as having hyaline ascospores until Saccardo (1883a) described it with green ascospores. Petch (1937) determined that Tode meant two different species, i.e. Sphaeria gelatinosa f. viridis representing the green-spored Hypocrea gelatinosa and a hyaline-spored Sphaeria gelatinosa f. lutea Tode, which he elevated to species rank as Hypocrea lutea. He based this latter species on yellow stromata collected by F. Currey

in 1856 and Hawley in 1905 on leaves. An anamorph was never included in the description of H. lutea. Also Petch’s scant material is not particularly informative due to the lack of conidiophores. Doi (1966) observed during a gliocladium-like anamorph in ascospore-derived cultures of Hypocrea lutea, and later (Doi in Samuels et al. 1990) he named it Gliocladium cf. deliquescens. The connections H. lutea/G. viride (= G. deliquescens) was accepted by Chaverri and Samuels (2003), Domsch et al. (2007) and Samuels (2006) and is also accepted here. The anamorph name: Matruchot (1893) described Gliocladium viride Matr. from a Stereum sp. with conidia 3–6 × 2–3 μm. Sopp (1912) described Gliocladium deliquescens from Cerrena unicolor with conidia 1.5–2 × 1 μm on top of phialides during their formation, noting that ‘later the conidia become more roundish and larger, but not much’. Morquer et al. (1963) kept the two species separate, stating nearly identical conidial sizes for them, but obviously these authors studied a generically heterogeneous assemblage of species, because G. deliquescens and other species were characterised by catenate conidiation. Matsushima (1975, 1989), Domsch et al. (2007) and the MycoBank database (CBS; under G.

1) Picocyanobacteria 103 cell mL-1* 1.4 (±0.09) 1.5 (±0.06) Non-pigmented Euk. 102 cell mL -1 7.3 (±0.6) 7.2 (±0.6) Pigmented Euk. 103 cell mL -1 4.3 (±0.6) 4.4 (±0.6) Means values (±SD) are presented for the two sets of experimental microcosms (with and without nutrient addition) at T0, for nitrogen and phosphorus compounds, bacteria, viruses, picocyanobacteria, Olaparib supplier non-pigmented and pigmented small eukaryotes. * data obtained by flow-cytometry. Abundances

and structure of the small eukaryotic community The microscope counts showed that the eukaryotic community was largely dominated by pigmented cells (85.8% of total eukaryotes). Their mean abundance was 4.3 x103 cells mL-1 and 13 of the 26 OTUs identified at T0 from sequencing results were affiliated to pigmented groups (Additional file 2: Table S1). Mamiellophyceae was the dominant group (nearly 83.7% of all pigmented eukaryotes observed by microscopy) and they were represented by 3 OTUs affiliated to Micromonas

pusilla and Ostreococcus tauri (Figure 2 Additional file 2: Table selleck screening library S1). The microscope observations allowed detection of other Viridiplantae at low densities. In particular, some Pyramimonadales (genus Cymbomonas) were observed but were not recorded among sequences at T0. The mean relative abundance of Cryptophyceae (4 OTUs) was 10.9%, while very low relative abundances of Bacillariophyceae (1 OTU) and Prymnesiophyceae (represented by Chrysochromulina-like cells, and 2 OTUs) were found by microscopy (Figure 2) and sequencing. Finally, Dinophyceae (cells larger than 6 μm) accounted for only 3% of total pigmented eukaryotes abundance, and was represented by 1 OTU (Figure 2 Additional for file 2: Table S1). Figure 2 A. Mean (±SD) abundance of pigmented and non-pigmented small eukaryotes (cell mL -1 ) at T0 and T96 h in each treatment. Mean values and SD were calculated from values obtained from treatment triplicates. B. Relative abundance of different groups

identified at T0 and T96 h in each treatment (data obtained from microscopic observation). The mean abundance of non-pigmented eukaryotes was 776 cells mL-1 at T0, accounting for about 15% of total eukaryotes. In comparison to microscope counting, the proportion of typical non-pigmented eukaryotes was over-estimated in the clone library, accounting for 43.2% of total clones (such over-representation of non-pigmented groups in 18S rRNA gene clone libraries has been discussed previously e.g.[50–52]). The diversity of these non-pigmented groups cannot be discriminated by classical microscopy due to a lack of distinct morphological features and/or their small size. However, from cloning-sequencing results, 11 different OTUs could be attributed to non-pigmented groups: Cercozoa (2 OTUs), Stramenopiles affiliated to Hyphochytrids (1 OTU), Syndiniales affiliated to Amoebophrya (2 OTUs), uncultured alveolates (4 OTUs), and Choanoflagellida (2 OTUs) (Figure 2 Additional file 2: Table S1).

Nanopillar arrays have been employed in the study of field emission [1], solar cell industry [2], biological sensing [3], micro-/nanoscale fluidics, near-field optics, and the lab-on-a-chip technology [4]. Nanopore arrays have also been recognized as valuable structures in many advanced fields such as photovoltaic [5] and photonic crystal research [6], high throughput screening gas detection [7], and especially in biological molecules detection and separation [8]. Fitting with foregoing scientific

advancements, the nanoscale fabricating methods and technologies have been made good progress. Nanopillar and nanopore arrays can be fabricated with direct growth approaches (metal-organic chemical

vapor deposition, hydride vapor phase epitaxy, molecular beam epitaxy) [9–11], nanosphere-assist etching [12, 13], electronic beam lithography [14, 15], nanoimprint technology [16], and laser lithography [17]. Since the merits of fabricating speediness and cleanliness, maskless process, controllable pattern shape and size, and capability of lithograph in three Acalabrutinib manufacturer dimensions [18, 19], laser direct lithography technology is one of the most attractive approaches to fabricate nanoscale functional structures as compared with the disadvantages such as expensive, heavy, or low precision of other methods. Choi’s group has reported implementing 100-nm-level nanostructure arrays over a large scale by means of laser interference lithography [20–23]. Scott and Li have respectively fabricated sub-100-nm isotropic voxel [24] and voxel with a 40-nm axial size [25] by photo-initiation

inhibiting technology. Cao has obtained a nanoline with a width of 130 nm and nanodots with a diameter of 40 nm [26] by polymerization inhibiting, too. In Andrew’s work, the nanolines with an average width of 36 nm were drawn employing absorbance modulation lithography [27]. Tanaka and Thiel have shown fabricating spatial voxel to sub-120 nm with the two-photo-absorption technology [28, 29]. Qi got a single polymerized tip with a diameter of 120 nm with the same technical route [30]. However, the utilization of femtosecond laser systems makes the lithography system complex and Exoribonuclease expensive. Even, in a continuous wave (CW) laser two-photon absorption method, photoresist is tailored and the whole system is costly. Furthermore, two laser sources are required in both photo-inhibiting and absorbance modulation methods, and the photoresist materials should have particular properties that result in restrictions in choosing light sources and resist materials. In the paper, we will report a kind of nanopillar array with a pillar diameter much smaller than Abbe’s diffraction limitation by visible CW laser direct lithography technology.

Carcinogenesis 2003,24(9):1445–1454.PubMedCrossRef 10. Langenfeld EM, Langenfeld J: Bone morphogenetic protein-2 stimulates angiogenesis in developing tumors. Mol Cancer Res 2004,2(3):141–149.PubMed 11. Langenfeld EM, Kong Y, Langenfeld J: Bone morphogenetic protein 2 stimulation of tumor growth involves the activation of Smad-1/5. Oncogene 2006,25(5):685–692.PubMedCrossRef 12. Kumagai T, Tomari K, Shimizu T, Takeda K: Alteration of gene expression in response to bone morphogenetic protein-2 in androgen-dependent

human prostate cancer LNCaP cells. Int J Mol Med 2006,17(2):285–291.PubMed 13. Orui H, Imaizumi S, Ogino T, Motoyama T: Effects of bone morphogenetic protein-2 on human GSI-IX ic50 tumor cell growth and differentiation: a preliminary report. J Orthop Sci 2000,5(6):600–604.PubMedCrossRef 14. Horvath LG, Henshall SM, Kench JG, Turner JJ, Golovsky D, Brenner PC, O’Neill GF, Kooner R, Stricker PD, Grygiel JJ, et al.: Loss of BMP2, Smad8,

and Smad4 expression in prostate cancer progression. Prostate 2004,59(3):234–242.PubMedCrossRef 15. Hardwick JC, Van Den Brink GR, Bleuming SA, Ballester I, Van Den Brande JM, Keller JJ, Offerhaus GJ, Van Deventer SJ, Peppelenbosch MP: Bone morphogenetic protein 2 is expressed by, and acts upon, mature epithelial cells in the colon. Gastroenterology 2004,126(1):111–121.PubMedCrossRef Selleck JNK inhibitor 16. Soda H, Raymond E, Sharma S, Lawrence R, Cerna C, Gomez L, Timony GA, Von Hoff DD, Izbicka E: Antiproliferative effects of recombinant human bone morphogenetic protein-2 on human tumor colony-forming units. Anticancer Drugs 1998,9(4):327–331.PubMedCrossRef 17. Urist MR: Bone: formation by autoinduction. Science 1965,150(698):893–899.PubMedCrossRef 18. Wozney JM, Rosen V,

Celeste AJ, Mitsock LM, Whitters MJ, Kriz RW, Hewick RM, Wang EA: Novel regulators of bone formation: molecular clones and activities. Science 1988,242(4885):1528–1534.PubMedCrossRef 19. Waite KA, Eng Y-27632 purchase C: BMP2 exposure results in decreased PTEN protein degradation and increased PTEN levels. Hum Mol Genet 2003,12(6):679–684.PubMedCrossRef 20. Wen XZ, Miyake S, Akiyama Y, Yuasa Y: BMP-2 modulates the proliferation and differentiation of normal and cancerous gastric cells. Biochem Biophys Res Commun 2004,316(1):100–106.PubMedCrossRef 21. Feeley BT, Krenek L, Liu N, Hsu WK, Gamradt SC, Schwarz EM, Huard J, Lieberman JR: Overexpression of noggin inhibits BMP-mediated growth of osteolytic prostate cancer lesions. Bone 2006,38(2):154–166.PubMedCrossRef 22. Kiyozuka Y, Nakagawa H, Senzaki H, Uemura Y, Adachi S, Teramoto Y, Matsuyama T, Bessho K, Tsubura A: Bone morphogenetic protein-2 and type IV collagen expression in psammoma body forming ovarian cancer. Anticancer Res 2001,21(3B):1723–1730.PubMed 23.

Uninfected HeLa cells were incubated in the presence of 10 μM compound D7 or DMSO, and cell density was assessed at 0, 22, 44 and 66 hours using a spectrophotometric assay. Compound D7 had little or no effect on HeLa cell growth rate compared to DMSO (fig. 4A). We also examined cell cytotoxicity at these times using an adenylate kinase release assay. Compound D7 exhibited the same level of cytotoxicity as DMSO at 0, 22 and 44 hours, and only slightly higher cytotoxicity levels

at 66 hr compared to DMSO-exposed cells (fig. 4B). Therefore compound D7 had little or no effect on HeLa cell viability and the inhibitory effect of D7 on chlamydial growth is not likely due to a non-specific cytotoxic effect on the host cell. Figure 4 Compound D7 does not reduce LDK378 HeLa cell viability. A: subconfluent HeLa HIF cancer cell monolayers incubated in MEM containing either DMSO (0.1%) or compound D7 (10 μM) with 2 μg/mL cycloheximide (+), were collected by trypsinization and the cell density was measured by absorbance at 800 nM at the times indicated. Compound D7 did not significantly alter HeLa cell number compared to DMSO alone. B: cell culture supernatant adenylate kinase activity from the samples in (A).

Exposure of HeLa cells to 10 μM compound D7 for 44 hours was not more cytotoxic than cells exposed to DMSO. At 66 hours there was a small increase in HeLa cell release of adenylate kinase in the D7-exposed group. Error bars represent means plus 2 standard deviations. Compound D7 does not block activation of the MEK/ERK pathway It has been shown previously that activation of the MEK/ERK pathway is necessary for chlamydial invasion of host cells [43] and sustained activation of this pathway is required for acquisition of host glycerophospholipids by Chlamydia

[48]. To rule out the possibility that the inhibitory effect of compound D7 on C. pneumoniae growth could be due to an inhibition of the MEK/ERK pathway we assessed the level of ERK1 and ERK2 (p44/p42 MAP kinase, respectively) phosphorylation in the presence of compound D7. HeLa cells exposed to either 10 or 100 μM of compound D7 contained high levels of phosphorylated p44 and p42 MAP kinase following EGF stimulation. HeLa cells exposed to 10 or 25 μM U0126, a specific inhibitor of MEK1/2, were used as control and did not contain phosphorylated p44 or p42 MAP kinase following EGF stimulation (fig. Megestrol Acetate 5). This result demonstrates that compound D7 does not block phosphorylation of p44/p42 MAP kinase in HeLa cells, suggesting that chlamydial growth inhibition caused by D7 was not due to a non-specific blockage of the MEK/ERK pathway. Figure 5 Compound D7 does not block activation of the MEK/ERK pathway in EGF-stimulated HeLa cells. HeLa cells incubated with DMSO, compound D7 or U0126 were activated with EGF and the levels of MAP kinase phosphorylation were determined by Western blot using anti-phospho ERK1/2 antibody. Compound D7 at 10 and 100 μM, and DMSO at 0.

Next day, beads were washed three times with PBS, and the captured proteins were resolved on a 12% SDS-PAGE gel. Proteins were transferred into a nitrocellulose membrane and blocked overnight with Odyssey blocking

buffer (Li-Cor) in TBS (Tris-buffered saline). The membranes were probed with EEA1, CREB-1, MARCO and α-tubulin antibodies (Santa Cruz Biotechnology) for 1 h and after, incubated with appropriate secondary antibodies (Li-Cor) in TBS for 1 h. Proteins were visualized by scanning of the membranes in the Odyssey Imager (Li-Cor, Lincoln, NE). Concentration of single elements in the phagosome Human monocyte-derived macrophages were purified as previously described [17, 28], seeded on 200-mesh click here Formvar-coated London finder gold grids (Electron Microscopy Sciences) and cultured Src inhibitor in RPMI-1640 supplemented with 10% FBS. The monolayers were infected with mycobacteria (MOI 10) for 1 h and subsequently washed with PBS. The monolayers were maintained in culture for 1 h or 24 h, then fixed and prepared for x-ray microscopy, as previously reported [17, 44], and the phagosome was obtained [17, 44, 45]. Elemental maps were extracted from x-ray fluorescence spectra, using the software package MAPS [47], and quantification was achieved by measuring x-ray fluorescence

from NIST thin-film standards NBS 1832 and NBS 1833 (National Bureau of Standards, Gaithersburg, MD, USA), prior to, during, and after the experiments. Calibration curves and calculations were carried out as described [17, 44, 45]. Statistical analysis of observed elemental changes was performed by comparing the concentration of the respective elements using Student’s-t test. A p < 0.05 was considered significant. Statistical analysis Comparisons between control and experimental groups were submitted to statistical analysis to determine the significance. Statistical analysis of the means ± SD was determined by ANOVA. A p < 0.05 was considered significant. A DNA microarray was carried out three independent times, while the proteomic analysis of vacuole proteins was performed twice. Acknowledgements We are grateful for the support of the Mass Spectrometry

Core Facility of the Environmental Health Sciences Center, Oregon State University, and from grant number P30 ES00210, from National Institute Etofibrate of Environmental Health Sciences, National Institutes of Health. This work was also supported by the NIH grants # AI47010 and AI043199. We thank Denny Weber for help in preparing the manuscript. References 1. Falkinham JO: Epidemiology of infection by nontuberculous mycobacteria. Clin Microbiol Rev 1996,9(2):177–215.PubMed 2. Inderlied CB, Kemper CA, Bermudez LE: The Mycobacterium avium complex. Clin Microbiol Rev 1993,6(3):266–310.PubMed 3. Aksamit TR: Mycobacterium avium complex pulmonary disease in patients with pre-existing lung disease. Clin Chest Med 2002,23(3):643–653.PubMedCrossRef 4.

Edited by: Flannigan B, Samson RA, Miller JD. Boca Raton: CRC Press; 2001:231–246. PD0325901 18. Kaarakainen P, Rintala H, Vepsäläinen A, Hyvärinen A, Nevalainen A, Meklin T: Microbial content of

house dust samples determined with qPCR. Sci Total Environ 2009, 407:4673–4680.PubMedCrossRef 19. Meklin T, Haugland RA, Reponen T, Varma M, Lummus Z, Bernstein D, Wymer LJ, Vesper SJ: Quantitative PCR analysis of house dust can reveal abnormal mold conditions. J Environ Monit 2004, 6:615–620.PubMedCrossRef 20. Vesper S, McKinstry C, Haugland R, Wymer L, Bradham K, Ashley P, Cox D, Dewalt G, Friedman W: Development of an Environmental Relative Moldiness index for US homes. J Occup Environ Med 2007, 49:829–833.PubMedCrossRef 21. Amend AS, Seifert KA, Samson R, Bruns TD: Indoor fungal composition is geographically patterned and more diverse in temperate zones than in the tropics. Proc Natl Acad Sci 2010, 107:13748–13753.PubMedCrossRef 22. Noris F, Siegel JA, Kinney KA: Evaluation of HVAC filters as sampling mechanism for indoor microbial communities.

Atmos Environ 2011, 45:338–346.CrossRef 23. Pitkäranta M, Meklin T, Hyvärinen A, Paulin L, Auvinen P, Nevalainen A, Rintala H: Analysis of fungal flora in indoor dust by ribosomal DNA sequence analysis, quantitative PCR, and culture. Appl Environ Microbiol Ibrutinib nmr 2008, 74:233–244.PubMedCrossRef 24. Tringe SG, Zhang T, Liu X, Yu Y, Lee WH, Yap J, Yao F, Suan ST, Ing SK, Haynes M, Rohwer F, Wei CL, Tan P, Bristow J, Rubin EM, Ruan Y: The airborne metagenome in an indoor urban environment. PLoS One 2008, 3:e1862.PubMedCrossRef 25. Green CF, Scarpino PV, Gibbs SG: Assessment and modeling of indoor fungal and bacterial concentrations. Aerobiologia 2003, 19:159–169.CrossRef 26. Lawton MD, Dales RE, White J: The influence

of house characteristics in a Canadian community on microbiological contamination. Indoor Air 1998, 8:2–11.CrossRef 27. Fröhlich-Nowoisky J, Pickersgill DA, Despres VR, Poschl U: High diversity of fungi in air particulate matter. Proc Natl Acad Sci 2009, 106:12814–12819.PubMedCrossRef 28. Lee SH, Lee HJ, Kim SJ, Lee HM, Kang H, Kim YP: Identification of airborne bacterial and fungal community structures in an urban area by T-RFLP analysis and quantitative real-time PCR. Sci Total Environ 2010, 408:1349–1357.PubMedCrossRef Decitabine molecular weight 29. Chao HJ, Milton DK, Schwartz J, Burge HA: Dustborne fungi in large office buildings. Mycopathologia 2002, 154:93–106.PubMedCrossRef 30. Chew GL, Rogers C, Burge HA, Muilenberg ML, Gold DR: Dustborne and airborne fungal propagules represent a different spectrum of fungi with differing relations to home characteristics. Allergy 2003, 58:13–20.PubMedCrossRef 31. Horner WE, Worthan AG, Morey PR: Air-and Dustborne Mycoflora in Houses Free of Water Damage and Fungal Growth. Appl Environ Microbiol 2004, 70:6394–6400.PubMedCrossRef 32.

For the 30 CC-23 strains examined, PI-1 was present in 12 (40%), which is considerably higher than the frequency detected in CC-23 strains from Spain [27], suggesting that there is considerable Dorsomorphin research buy geographic variation in PI profiles. Such variation may be due to baseline frequencies of PI-1 in specific populations as it may be more susceptible to horizontal gene transfer, a plausible hypothesis since the island is flanked by direct repeats and contains transposable elements [15]. The absence of PI-1 in CCs unrelated to CC-23

and in specific STs within CC-23 provides additional support for this hypothesis. Following horizontal gene transfer, PI-1 may remain incorporated into the chromosome in some strains, thereby resulting in an increased

fitness and colonization potential. Alternatively, it may also be excised from others, which may be due to both host-specific pressures and bacterial stress responses. Indeed, increased horizontal gene transfer and mutation rates have been documented in other pathogens following exposure to certain stressors [34]. Because the GBS PIs are highly immunonogenic [14, 24], the loss of PI-1 could also provide a mechanism to evade the RG7420 purchase host immune responses, a process that could be advantageous to certain genotypes that are more prone to cause invasive disease or after exposure to new niche. The eBURST analysis demonstrated that the neonatal invasive lineage, Farnesyltransferase ST-17, is related to the ST-67 bovine lineage and suggests that PI-1 was either acquired in the ST-17 strain population or lost in the ST-67 bovine population. Although a close relationship was previously identified between STs 17 and 67 [7],

it is important to note that eBURST results are greatly impacted by the number and type of STs included in any given analysis. More recent data of all STs available in the PubMLST database [35] suggest that ST-17 is part of eBURST group 1 with STs 19 and 1, which has subsequently diversified into several host-specific complexes including one containing ST-67 and other bovine-associated STs [33]. Further, it was suggested that the ST-17 subpopulation emerged via a series of evolutionary events including recombination among strains belonging to multiple clonal complexes [9] (Figure 2) as well as the acquisition of mobile genetic elements. This hypothesis is supported by our finding that many of the bovine strains were related to human strains containing PI-1 (e.g., ST 83 and 64, Figure 5) or had a PI-1 integration site occupied by another genetic element (e.g., STs 61, 64 and 67, Figure 5) unlike the human-derived strains. Those bovine strains with an occupied integration site may not be capable of acquiring PI-1, which may limit their ability to be transmitted to and sustained in the human host. Collectively, these data suggest that the human vs.

Of the other probes listed in Table 1, ABI1246 was strongly positive with all four Abiotrophia/Granulicatella reference strains tested (Granulicatella adjacens CCUG 27809T and HE-G-R 613A, Granulicatella elegans CCUG 38949T and Abiotrophia defectiva CCUG 36937), whereas ABI161 labeled only the Granulicatella strains. Probe LCC1030 was positive with Lactococcus lactis subsp. lactis reference strain NCC2211 [17], and the S. mutans and S. sobrinus probes Smut590 and L-Lsob440 stained reference strains UA159T and OMZ 176, respectively, while

none of the probes was positive with strains from other streptococcal species. Probe Decitabine concentration L-Ssob440-2 yielded better fluorescence intensity than the previously described probe SOB174 [10], but had to be used at high stringency. All these findings 5-Fluoracil were as expected from in silico data. Table 2 Reactivity of FISH probes to lactobacilli with target and non-target strains     16S rRNA probes Group, Strain OMZ LGC358a LAB759 + LABB759-comp Lpla759 Lpla990 + H1018 L-Lbre466-2 L-Lbuc438-2 Lcas467 Lsal574 L-Lsal1113-2 Lreu986 + H1018 Lfer466 + H448+ H484 L-Lcol732-2 Lvag222 Lgas458 Lgas183 L. buchneri et rel.                                     L. plantarum FAM 1638

945 2-4+*,a 3-4+ 3-4+ 2-4+* – - – - – - – - – - –     L. brevis ATCC 14869 625 3-4 + 2-3 + – - 4+ – - – - – ± -b – - –     L. brevis OMZ 1114 1114 2-4+ 2-3+* – - 3-4+ – - – - – - -b – - –     L. buchneri ATCC 4005 626 2-4 + 1-2 + – - – 3-4 + – - – - – -b – - –     L. buchneri 1097 2-4 +* 2-3 +* – - – 3+ – - – - – -b – - – L. casei et rel.                                     L. casei ATCC 393 939 2-4+ 3-4+ – - – -c 3+ – - – - – - – -     L. casei Cl-16 638 3-4 + 3-4 + – - – -c 3-4 + – - – - – - – -     L. paracasei ATCC 25598 624 2-4 +* 2-4 +* – - – -c 3-4 +* – - – - – - – -     L. rhamnosus AC 413 629 2-4 + 2-4 + – - – - 3-4 + – - – - – - – -     L. rhamnosus ATCC 7469T 602 2-4 + 2-4 + – - – - Thiamet G 3 + – - – - – - – - L. salivarius                                     L. salivarius ATCC 11741 525 3-4+ 3-4+ – - – - – 2-4+ 3-4+ ± – - – - –     L. salivarius OMZ 1115 1115 2-4+ – - – - – - 3-4+ 3-4+ – - – - – -

L. reuteri et rel.                                     L. coleohominis DSM14060T 1113 1-3 + 2-4 + – - -d – - – - 3 + – 3-4 + – - –     L. fermentum ATCC 14931 524 2-4 +* 2 +*, e – - – - – - – 2-4 + 3-4 + – - – -     L. fermentum OMZ 1116 1116 2-4 + 2 +*, e – - – - – - – 2-4 + 3-4 + – - – -     L. reuteri CCUG 33624T 1100 2-4 + 3-4 + – - – -c ± – - 2-4 + 2-4 + – - – -     L. vaginalis UMCG 5837 1095 2-4 + 3-4 + – - – -c – - – 1-3 +* – - 3-4 + – - L. gasseri et rel.                                     L. acidophilus ATCC 4357 523 2-4+ 3-4+ – - – - – - – ± ± – - 2-4+ –     L. crispatus ATCC 33820 522 3-4 + 3-4 + – - – - – - – -   – - 3-4 + –     L. gasseri ATCC 19992 520 2-4 + 2-4 + – - – - – - – ± 1 + – - 1-3 + 2-4 +     L.