To date, several leptospiral ECM binding adhesins have been descr

To date, several leptospiral ECM binding adhesins have been described [6–18]. After the adhesion, pathogens have to overcome tissue barriers in order to reach blood circulation and organs. We have reported that leptospires have the ability of binding PLG at their surface and that plasmin (PLA) can be generated in the presence of activator [19]. In addition, Verma and colleagues [20] and our group have described several leptospiral proteins as PLG – binding receptors [17, 18, 21]. More recently, we have reported that PLA generation on Leptospira decreased opsonization and that it might be an important aspect

of the immune escape strategy and survival [22]. L. interrogans serovar Copenhageni genome Barasertib purchase annotation identified many unknown coding sequences predicted to be surface exposed proteins. Characterization

of these proteins, with no previously assigned function, should increase our understanding of this intriguing pathogen’s biology. In this work, we present our studies with two leptospiral coding sequences, selleck chemicals llc LIC11834 and LIC12253, named Lsa33 and Lsa25, respectively. The genes were cloned and the proteins expressed using E. coli. The recombinant proteins were purified and their ability to bind various ECM and serum components was evaluated. We report that these proteins are novel surface adhesins capable of binding to laminin. In addition, Lsa33 can also interact to PLG and both proteins bind the complement regulator of the classical pathway C4bp. We believe that these proteins are likely to be involved in Leptospira – host interactions. Results Bioinformatic

analysis The selected coding this website sequences, LIC11834 and LIC12253, are genome annotated as hypothetical proteins, and one of them, LIC11834, is a putative lipoprotein, having lipoprotein signal peptide (signal peptidase II) and a cleavage site between amino acids 17–18. According to SMART web server, LIC11834 has a signal peptide from 1 to 21 amino acids and a FecR domain from amino acid 60 to 162. PFAM predicts that this domain is involved in regulation of iron dicitrate transport and that FecR is probably a sensor that recognizes iron dicitrate in the periplasm. Protein kinase N1 LIC12253 presents a signal peptide from amino acid 1 to 21 and a DUF1566 (Domain of Unknown Function) from amino acid 58 to 164 [23, 24]. The LIC11834 coding sequence can be classified as alpha – beta protein, being the percentage of 36.57 for alpha-helix and 29.13 for beta strands secondary structure. In the case of coding sequence LIC12253, the protein can be classified as mixed, having a predicted secondary structure composition percent of 11.01, 19.38 and 69.60 for alpha – helix, beta strands and others, respectively. Cellular localization predicts as extra – cellular (non-cytoplasmic branch) for both proteins. The solvent accessibility composition (core/surface ratio) for the CDs LIC11834 and LIC12253 is expected to be 59.87 and 66.

However, due to the scarcity of the element indium on earth and c

However, due to the scarcity of the element indium on earth and consequently the soaring prices, the advantages in nanomaterials were recently investigated for the current-spreading layer, such as graphene, metal nanowires, and carbon nanotubes (CNTs) [6–8]. find more graphene has high mobility and high optical transmittance [9]. However, large work function of graphene caused the large turn-on

voltage with inefficient current spreading, which resulted in light emission occurring only near the p-metal regions, especially on p-GaN due to high sheet and contact resistance [10]. Also, the obvious degradation of graphene layer under 20 mW of input power restricted its actual application [11]. Ag nanowire is the strong competitor of graphene due to its intrinsically Momelotinib cost high conductivity and favorable optical transparency. However, except for the easy oxidation at ambient environment, the electromigration of silver ions under bias could pose a long-term stability issue [12]. Recently, the optical output power of LEDs was first improved by using the combination of graphene film and Ag nanowires Fedratinib ic50 as current-spreading layer. The sheet resistance decreases from 500 Ω of bare graphene to about 30

Ω because the silver nanowires bridged the grain boundaries of graphene and increased the conduction channels [13]. Among these three GPX6 nanomaterials, CNTs have the most mature fabrication technology. In this work, AlGaInP LEDs with CNTs only and 2-nm-thick Au-coated CNTs as current-spreading layers were fabricated. The LEDs with Au-coated CNTs showed good current spreading effect. Methods The AlGaInP LEDs

were grown on n-GaAs substrate by metal-organic chemical vapor deposition. Fifteen pairs of Al0.6Ga0.4As/AlAs with distributed Bragg reflectors (DBRs) were grown on 100-nm-thick GaAs buffer layer. The active region was composed of 800-nm-thick 60-period (Al0.5Ga0.5)0.5In0.5P/(Al0.1Ga0.9)0.5In0.5P multiquantum wells, which were sandwiched in p- and n-(Al0.7Ga0.3)0.5In0.5P cladding layer for electron and hole confinement. In order to study the current-spreading effect of CNTs, only 500-nm-thick Mg-doped p-GaP window layer with the doping density of 5 × 1018 cm−3 was grown on top. The 50/150/200-nm-thick Au/BeAu/Au with 100-μm diameter was first deposited and then patterned by wet etching as a p-type electrode. A super-aligned CNT (SACNT) film is drawn continuously from multiwalled CNT arrays [14]. To improve the conductivity of the as-drawn SACNT films, 2-nm-thick Au was further coated on the SACNTs by magnetron sputtering methods [15]. Then the SACNT thin film was put and stuck on the surface of the LED wafer by Van der Waals force. In order to keep the tubes in place, additional 150/300-nm-thick Ti/Au was deposited and patterned on the p-type electrode.

In some cases, special structures, such

as a haustorium o

In some cases, special structures, such

as a haustorium or an arbuscle, are formed in host cells for the symbiont to absorb nutrition [22, 23]. To describe invasive growth, 15 new GO terms were developed that are children or lower level offspring of “”GO ID 0044412 growth or development of symbiont within host”". The term “”GO ID 0075065 growth or development of symbiont in host cell”" has two children, “”GO ID 0052094 formation by symbiont of haustorium for nutrient acquisition from host”" and “”GO ID 0075066 growth or development of symbiont in host organelle”". Additionally, arbuscules produced by mycorrhizal fungi are a type of MK-8776 datasheet structure functionally similar to haustoria, and thus “”GO ID 0075328 formation by symbiont of arbuscule for nutrient acquisition from host”" is a sibling of “”GO ID 0052094″” (see find more details in Figure 4). The 15 new GO terms in this section meet the need to annotate pathogen genes that are involved see more in invasive growth. For example, the MST12 gene in the rice blast fungus M. grisea was found to regulate infectious growth but not appressorium formation [46]. In particular, no obvious defects in vegetative growth, conidiation, or conidia germination were observed in MST12 deletion mutants. Also, MST12 mutants produce typical dome-shaped

and melanized appressoria. When inoculated through wound sites, MST12 mutants fail to cause spreading lesions and appear to be defective in infectious growth. As a result, MST12 mutants are nonpathogenic [46]. Thus, the MST12 gene can be annotated with the term “”GO ID 0075061 formation of symbiont invasive hypha within host”". Lesion development Methocarbamol in the host The eventual result of infection in most cases is lesion development. A lesion can be defined as any abnormality involving any tissue or organ due to any disease or any injury (cited from MedicineNet.com). Not

surprisingly, there are many types of lesions including those caused by damage such as cold injury or insects’ bites etc. It is difficult to define lesions objectively, as this requires a subjective judgment on what constitutes abnormal or damage and from what perspective, ranging for example from perturbation of a few cells to death of an entire tissue or organ. Similarly, formation of a lesion is not a specific process belonging to either the pathogen or the host and can be highly dependent on the environment. Therefore, at this time only one term, “”GO ID 0009405 pathogenesis”", is appropriate for genes involved in lesion formation. Other new GO terms Six new terms were placed jointly under the nodes “”GO ID 0006914 autophagy”" and “”GO ID 0044403 symbiosis, encompassing mutualism through parasitism”".

e , PDMS) represent the access channels to lower scale nanochanne

e., PDMS) represent the access channels to lower scale nanochannels (see Additional file 1 for examples of fabricated PDMS replica). The gaps have been successfully connected with the fabricated structure showing a continuous pattern as shown in the CRT0066101 profile 2 of Figure  7d. Figure 7 Example of finalized prototype. (a) AFM mTOR inhibitor topography of multiple line pattern written at a 2-μm s−1 speed and a bias of 12 V used as mask for an 8-s etching in SF6 plasma; on the right, the height

profiles before RIE (black) and after RIE (red). (b, c) SEM images showing the finalized result of fabrication; in the details, the effective size and section of features are available. (d) AFM topography of a finalized Si prototype; Al microfeatures are connected to nanofeatures deposited by SPL. Profile 1 shows the obtained section, and section 2 shows the junction profile (no gap is observed). Conclusions We illustrated a simple and inexpensive nanofabrication method that can produce oxide or pure graphitic nanofeatures by means of SPL, employing almost any commercial AFM, avoiding subtractive fabrication methods including electron beam lithography and focused ion beam. Secondly, choosing a proper organic Selleckchem BV-6 precursor, we show that the technique is accessible to most AFM users with no need of dedicated setups in ambient environment. The reaction leading

to carbon deposition is likely to happen in both polarities, but when the tip is biased negatively, the competing oxidation masks solvent decomposition. The method, combined with dry etching allows the fast prototyping of Si masters ideal for replica molding/nanoimprinting. As a possible prototype, we realized several Si masters with satisfactory aspect ratio and we showed how to hybridize microlithography with SPL, connecting Al micropatterns with nanopatterns. Acknowledgments Histone demethylase This work was entirely supported by the Italian Institute of Technology (IIT). We specially appreciate the support coming from

the facilities of the Nanostructures Department. Electronic supplementary material Additional file 1: Oxidative and carbonaceous patterning of Si surface in an organic media by scanning probe lithography. The file contains experimental details (Figures S1 and S2) and supplementary examples of fabrication capabilities (Figures S3 to S5). (DOCX 3 MB) References 1. Xie XN, Chung HJ, Sow CH, Wee ATS: Nanoscale materials patterning and engineering by atomic force microscopy nanolithography. Mater Sci Eng R Rep 2006,54(1–2):1–48.CrossRef 2. TsengAA SJI, Pellegrino L: Nanofabrication using atomic force microscopy. In Encyclopedia of Nanoscience and Nanotechnology. 2nd edition. Edited by: Nalwa HS. Valencia, CA: American Scientific Publishers; 2012:171–207. 3. Garcia R, Martinez RV, Martinez J: Nano-chemistry and scanning probe nanolithographies. Chem Soc Rev 2006,35(1):29–38.CrossRef 4.

The change of epitaxial relationship for ZnO films on as-received

The change of epitaxial relationship for ZnO films on as-received and etched STO substrates is accompanied with the increase of lattice mismatch, decrease of bond density, and increase of substrate surface roughness. This investigation presents a very simple way to control

epitaxial relationship of ZnO films with STO substrates, which is of technological selleckchem interest in optoelectronic and electronic devices. Acknowledgments This work was supported by the 973 program (2012CB921304, 2012CB619306) and the National Natural Science Foundation of China (check details 60990313, 51202057). References 1. Perez JZ, Sanjose VM, Lidon EP, Cochero J: Facets evolution and surface electrical properties of nonpolar m-plane ZnO thin films. Appl Phys Lett 2006, 88:261912.CrossRef

2. Jia CH, Chen YH, Liu GH, Liu XL, Yang SY, Wang ZG: Growth of c-oriented ZnO films on (001)SrTiO3 substrates by MOCVD. J Crystal Growth 2008, 311:200.CrossRef 3. Perez JZ, Sanjose VM, Lidon EP, Colchero J: Polarity effects on ZnO films grown along the nonpolar [11–20]-direction. Phys Rev Lett 2005, 95:226105.CrossRef 4. Baker TJ, Haskell BA, Wu F, Fini PT, Speck JS, Nakamura SJ: Characterization of planar semipolar gallium nitride films on spinel substrates. selleck chemical Jpn J Appl Phys 2005, 44:L920.CrossRef 5. Peruzzi M, Pedarnig JD, Bauerle D, Schwinger W, Schaffler F: Inclined ZnO thin films produced by pulsed-laser deposition. Appl Phys A 1873, 2004:79. 6. Bellingeri E, Marre D, Pallecchi I,

Pellegrino L, Siri AS: High mobility in ZnO thin films deposited on perovskite substrates with a low temperature nucleation layer. Appl Phys Lett Org 27569 2005, 86:012109.CrossRef 7. Wei XH, Li YR, Zhu J, Huang W, Zhang Y, Luo WB, Ji H: Epitaxial properties of ZnO thin films on SrTiO3 substrates grown by laser molecular beam epitaxy. Appl Phys Lett 2007, 90:151918.CrossRef 8. Wu YL, Zhang LW, Xie GL, Zhu JL, Chen YH: Fabrication and transport properties of ZnO/Nb-1 wt%-doped SrTiO3 epitaxial heterojunctions. Appl Phys Lett 2008, 92:012115.CrossRef 9. Karger M, Schilling M: Epitaxial properties of Al-doped ZnO thin films grown by pulsed laser deposition on SrTiO3 (001). Phys Rev B 2005, 71:075304.CrossRef 10. Fujisawa H, Nonomura H, Shimizu M, Niu H: Observations of initial growth stage of epitaxial Pb(Zr, Ti)O3 thin films on SrTiO3(1 0 0) substrate by MOCVD. J Crystal Growth 2002, 237–239:459.CrossRef 11. Infortuna A, Muralt P, Cantoni M, Setter N: Epitaxial growth of (Sr, Ba)Nb2O6 thin films on SrTiO3 single crystal substrate. J Appl Phys 2006, 100:104110.CrossRef 12. Chae RH, Rao RA, Gan Q, Eom CB: Initial stage nucleation and growth of epitaxial SrRuO3 thin films on (0 0 1) SrTiO3 substrates. J Electroceramics 2000, 4:345.CrossRef 13. Yoshimura T, Fujimura N, Ito T: The initial stage of BaTiO3 epitaxial films on etched and annealed SrTiO3 substrates.

In this case the final form of Equation 16 is similar to De Ruijt

In this case the final form of Equation 16 is similar to De Ruijter’s model [30] (σ(cos θ 0 − cos θ) = ζU + 6ηΦ(θ)U ln(r/a)) where Φ = sin 3 θ/2 − 3 cos θ + cos 3 θ and a is the cutoff length in De Ruijter’s model). In Equation 16, the base radius (r) is in millimeter length scale while the cutoff length (x m) is in nanometer length scale. Go6983 cell line Thus, r ≫ x m , and consequently r 1−n ≫ x m 1−n for n ranging

from 0.04 to 0.92 (see Table 1). Also, for a sessile droplet of spherical geometry (see Figure 2), the base radius is geometrically related to the dynamic contact angle: (17) where V is the volume of the droplet. Neglecting x m 1 − n and substituting r with Equation 17 gives: (18) Equation 18 shows the dynamic contact angle (θ) as a function of contact line velocity (U), solid–liquid molecular interactions (ζ), and non-Newtonian viscosity (n, K). Finally, substituting U with dr/dt = (dr/dθ) × (dθ/dt) the following equation can be obtained for the time evolution of the dynamic contact angle: (19) in which the dynamic contact angle θ = π − α. To compare with experimental data θ is used. Equation 19 is an implicit ordinary differential equation, which cannot be solved analytically, and thus numerical solutions to this equation will be sought. Results and discussion The effective diameter of nanoparticles was equal to 260 Apoptosis inhibitor nm at the lowest

solution concentration of 0.05 vol.%. At higher particle concentrations, the increased interparticle interactions result in larger clusters. This increases the possibility of clusters to deposit on the surface of solid and form a new eFT-508 solubility dmso hydrophilic surface. Due to their larger size, these clusters are less possible to deposit on the three-phase contact line, and thus a heterogeneous surface will form:

within the wedge film and away from the three-phase Arachidonate 15-lipoxygenase contact line, deposition of TiO2 clusters results in a hydrophilic surface with higher surface energy (approximately 2.2 J/m2[34]) than the three-phase contact line where the bare borosilicate glass is present (approximately 0.11 J/m2[35]). The higher surface energy inside the droplet shrinks the wetted area by increasing the equilibrium contact angle (denser solutions are more hydrophilic inside than outside). As a result, solid–liquid interfacial tension increases which on the other hand enhances the equilibrium contact angle [21]. Surface tension of these solutions decreases with particle concentration that is in accordance with Gibb’s adsorption isotherm. The shear thinning viscosity of the solutions is due to strong interparticle interaction of the nanoparticle clusters [19, 23, 36]. Other nanofluids such as ethylene glycol-based ZnO nanofluid [23] and CuO nanofluid [37] also exhibited shear thinning viscosity at low shear rates.

0 Discussion To the best of our knowledge, this is

the f

0. Discussion To the best of our knowledge, this is

the first report of prevalence of S. lugdunensis in clinical specimens obtained from mainland China. An earlier case of S. lugdunensis was reported in a 31-year-old Chinese patient (suffering from right ear sinus) in Singapore in 2000 [23]. Recently, community acquired S. lugdunensis were reported in clinical infections associated with Akt inhibitor co-morbidities in Southern Taiwan [24]; however the study did not observe widespread antimicrobial resistance even though there was widespread genetic diversity in the confirmed isolates. In the current study, our detection rate was 0.7% (5/670), which is comparatively on the lower end [12, 14, 15], but similar to what has been reported in Korea [13]. In the revised LY294002 mouse manuscript, we have described in details (in the legend of Table 1) what –ve (negative)

signifies for the tube coagulase, slide coagulase, and latex agglutination p38 MAPK inhibitor test, respectively. The latex agglutination test and slide coagulase test are used for rapid identification or for ruling out Staphylococcus aureus. However, some Staphylococcus isolates produce a membrane-bound form of the clumping factor, which can yield a positive result in slide coagulase and/or rapid latex agglutination tests, thus requiring the confirmatory tube coagulase test. However, an isolate that is positive in the Latex Agglutination test has a high probability of a positive slide coagulase test and our assay for Isolate 2 does not conform to this, whereas Isolate 4 does. In addition, recent results have shown that the

prevalence of the fibrinogen-binding adhesion (fbl) is 100% in Staphylococcus lugdunensis isolates mafosfamide [25]. However, one recent study reported that of the 17 Staphylococcus lugdunensis isolates studied, though fbl gene could be detected in all cases, only 47% gave a positive slide coagulase test result [26]. This perhaps suggests that varying levels of fbl gene product dictates the apparent sensitivity of Staphylococcus lugdunensis isolates to slide coagulase test. On comparing the results for Isolate 2 and 4 (both positive for latex agglutination test, but only Isolate 4 positive in slide coagulase test), they differ markedly in drug resistance and β-lactamase expression, with Isolate 4 being susceptible to all drugs tested and the only isolate not expressing β-lactamase. It is difficult to say whether the fbl gene expression pattern dictates this apparent difference between these isolates; however, it will be very interesting to see in the future if there is any difference in sensitivity to latex agglutination and slide coagulase test based on fbl gene expression in Staphylococcus lugdunensis isolates. We used PYR and ODC tests to preliminarily screen CNS isolates, VITEK 2 GP and API 20 Staph to validate, and gap gene sequence to confirm S. lugdunensis isolates.

67) and norC (83 98 ± 19 98) and de novo overexpression of norA (

67) and norC (83.98 ± 19.98) and de novo overexpression of norA (8.36 ± 4.63) and mepA (45.86 ± 13.86). Likewise, exposure of the EtBrCW-negative SM2 to higher ciprofloxacin

concentrations resulted in increased levels of norB expression (4.48 ± 2.48) that was accompanied by de novo overexpression of norC (5.33 ± 0.73) and mepA (10.58 ± 0.73). Discussion The few studies on efflux among S. Small molecule library aureus clinical isolates use the decrease of antibiotic MICs in the presence of EIs, particularly reserpine, as indicative of efflux activity [10]. This approach is laborious and dependent on the susceptibility of the efflux system(s) to reserpine, which varies considerably [19]. More recently, Patel and colleagues have proposed the use of EtBr MICs to identify S.

aureus effluxing strains [20]. This approach has the advantage of assessing efflux activity using a broad range efflux pump substrate, EtBr, which LY2606368 clinical trial is pumped out by most efflux systems described for S. aureus, and thus, is an useful marker for the detection of efflux pump activity [7, 12, 14, 20]. Nevertheless, it is still an indirect assessment of efflux activity. CYT387 purchase In the present study, we have applied two methods for the direct assessment of efflux activity among a collection of 52 ciprofloxacin resistant S. aureus clinical isolates, both also based on EtBr efflux. We first applied the EtBr-agar Cartwheel Method to select isolates with increased efflux activity. The presence of increased efflux in the 12 isolates selected was supported by the data collected from the semi-automated fluorometric method, which demonstrated that EtBrCW-positive isolates had a higher efflux activity than the EtBrCW-negative isolates. Thus, both methods proved to be adequate to assay efflux activity in S. aureus cells. In particular, the EtBrCW method proved to be a valuable tool for the rapid screening of efflux pump activity, allowing its application to screen large collections of clinical isolates. Branched chain aminotransferase Furthermore, the use of a broad range efflux pump substrate such as EtBr warrants its wider application as compared to the analysis of EIs effect

on MIC values, which can be severely impaired by the susceptibility of each efflux system to the EI being used and for which the mechanism of action at the cellular level remains, in most cases, to be clarified. In addition, the semi-automated fluorometric method also allowed the characterization of this efflux activity, in terms of maximal concentration of EtBr that the cells were able to extrude without observable accumulation over a 60 min period and susceptibility toward several EIs. The results obtained clearly showed a distinct capacity of the two groups of isolates to extrude EtBr from their cells, with the EtBrCW-positive isolates being able to handle higher EtBr concentrations with no detectable accumulation. It was also observed that for both groups of isolates, EtBr extrusion/accumulation was most affected by the EI verapamil.

N Engl J Med 1998, 339:1341–1348 PubMedCrossRef 10 Ghavamzadeh A

N Engl J Med 1998, 339:1341–1348.PubMedCrossRef 10. Ghavamzadeh A, Alimoghaddam K, Ghaffari SH, Rostami S, Jahani M, Hosseini R, Mossavi A, Baybordi E, Khodabadeh A, Iravani M, Bahar B, Mortazavi Y, Totonchi M, Aghdami N: Treatment of acute promyelocytic leukemia with arsenic trioxide without ATRA and/or chemotherapy. Ann Oncol 2006, 17:131–134.PubMedCrossRef 11. Ghavamzadeh A, Alimoghaddam K, Rostami S, Ghaffari SH, Jahani M, Iravani M, Mousavi SA, Bahar B, Vadimezan concentration Jalili M: Phase

II study of single-agent arsenic trioxide for the front-line therapy of acute promyelocytic leukemia. J Clin Oncol 2011, 29:2753–2757.PubMedCrossRef 12. Park WH, Seol JG, Kim ES, Hyun JM, Jung CW, Lee CC, Kim BK, Lee YY: Arsenic trioxide-mediated Selleck AZD5582 growth inhibition in MC/CAR myeloma cells via cell cycle arrest in association with induction of cyclin-dependent kinase inhibitor, p21, and apoptosis. Cancer Res 2000, 60:3065–3071.PubMed 13. Soriano C, Creus A, Marcos R: Arsenic trioxide mutational spectrum analysis in the mouselymphoma assay. Mutat Res 2008, 646:1–7.PubMedCrossRef 14. Patlolla AK, Tchounwou PB: Cytogenetic evaluation of arsenic trioxide toxicity in Sprague–Dawley rats. Mutat Res 2005, 587:126–133.PubMedCrossRef 15. Stevens JJ, Graham B, Walker AM, Tchounwou PB, Rogers C: The effects of arsenic trioxideon DNA synthesis and genotoxicity in human colon cancer cells. Int J Environ Res Public Health 2010, 7:2018–2032.PubMedCentralPubMedCrossRef

16. Jiang XH, Wong BC, Yuen ST, Jiang SH, Cho CH, Lai KC, Lin MC, Kung HF, Lam SK: Arsenic trioxide induces apoptosis in human gastric cancer cells through up-regulation of p53 and activation of caspase-3. Int find more J Cancer 2001, 91:173–179.PubMedCrossRef 17. Tchounwou PB, Yedjou CG, Dorsey WC: Arsenic trioxide-induced transcriptional activation and expression of stress

genes in human liver carcinoma cells (HepG2). Cell Mol Biol (Noisy-le-Grand) 2003, 49:1071–1079. 18. Alarifi S, Ali D, Alkahtani S, Siddiqui MA, Ali BA: Arsenic trioxide-mediated oxidative stress and genotoxicity in human hepatocellular Thiamet G carcinoma cells. Onco Targets Ther 2013, 6:75–84.PubMedCentralPubMed 19. Wang ZG, Rivi R, Delva L, König A, Scheinberg DA, Gambacorti-Passerini C, Gabrilove JL, Warrell RP Jr, Pandolfi PP: Arsenic trioxide and melarsoprol induce programmed cell death in myeloid leukemia cell lines and function in a PMLand PML-RARa independent manner. Blood 1998, 92:1497–1504.PubMed 20. Akao Y, Mizoguchi H, Kojima S, Naoe T, Ohishi N, Yagi K: Arsenic induces apoptosis in B-cell leukemic cell lines in vitro: activation of caspases and down-regulation of Bcl-2 protein. Br J Haematol 1998, 102:1055–1060.PubMedCrossRef 21. Zhang W, Ohnishi K, Shigeno K, Fujisawa S, Naito K, Nakamura S, Takeshita K, Takeshita A, Ohno R: The induction of apoptosis and cell cycle arrest by arsenic trioxide in lymphoid neoplasms. Leukemia 1998, 12:1383–1391.PubMedCrossRef 22.

Laukoetter MG, Bruewer M,

Laukoetter MG, Bruewer M, Nusrat A: Regulation of the intestinal epithelial barrier by the apical junctional complex. Curr Opin Gastroenterol 2006, 22:85–89.CrossRefPubMed 28. Saadat I, Higashi H, Obuse C, Umeda M, Murata-Kamiya

N, Saito Y, Lu H, Cell Cycle inhibitor Ohnishi N, Azuma T, Suzuki A, et al.:Helicobacter pylori CagA targets PAR1/MARK kinase to disrupt epithelial cell polarity. Nature 2007, 447:330–333.CrossRefPubMed 29. Boudeau J, Glasser AL, Masseret E, Joly B, Darfeuille-Michaud A: Invasive ability of an Escherichia coli strain isolated from the ileal mucosa of a patient with Crohn’s disease. Infect Immun 1999, 67:4499–4509.PubMed 30. Neish AS: Microbes in gastrointestinal Cytoskeletal Signaling inhibitor health and disease. Gastroenterology 2009, 136:65–80.CrossRefPubMed 31. Su L, Shen L, Clayburgh DR, Nalle check details SC, Sullivan EA, Meddings JB, Abraham C, Turner JR: Targeted epithelial tight junction dysfunction causes immune activation and contributes to development of experimental colitis. Gastroenterology 2009, 136:551–563.CrossRefPubMed 32. Barnich N, Darfeuille-Michaud A: Adherent-invasive Escherichia coli and Crohn’s disease. Curr Opin Gastroenterol 2007, 23:16–20.CrossRefPubMed 33. Gray-Owen SD, Blumberg RS: CEACAM1: contact-dependent control

of immunity. Nat Rev Immunol 2006, 6:433–446.CrossRefPubMed 34. Sasaki M, Sitaraman SV, Babbin BA, Gerner-Smidt P, Ribot EM, Garrett N, Alpern JA, Akyildiz A, Theiss AL, Nusrat A, et al.: Invasive Escherichia coli are a feature of Crohn’s disease. Lab Invest

2007, 87:1042–1054.CrossRefPubMed 35. Ivanov AI, Hunt D, Utech M, Nusrat A, Parkos CA: Differential roles for actin polymerization and a myosin II motor in assembly of the epithelial apical junctional C1GALT1 complex. Mol Biol Cell 2005, 16:2636–2650.CrossRefPubMed 36. Bagnoli F, Buti L, Tompkins L, Covacci A, Amieva MR:Helicobacter pylori CagA induces a transition from polarized to invasive phenotypes in MDCK cells. Proc Natl Acad Sci USA 2005, 102:16339–16344.CrossRefPubMed 37. Eaves-Pyles T, Allen CA, Taormina J, Swidsinski A, Tutt CB, Jezek GE, Islas-Islas M, Torres AG:Escherichia coli isolated from a Crohn’s disease patient adheres, invades, and induces inflammatory responses in polarized intestinal epithelial cells. Int J Med Microbiol 2008, 298:397–409.CrossRefPubMed 38. Hanajima-Ozawa M, Matsuzawa T, Fukui A, Kamitani S, Ohnishi H, Abe A, Horiguchi Y, Miyake M: Enteropathogenic Escherichia coli, Shigella flexneri, and Listeria monocytogenes recruit a junctional protein, zonula occludens-1, to actin tails and pedestals. Infect Immun 2007, 75:565–573.CrossRefPubMed 39. Wine E, Chan VL, Sherman PM:Campylobacter jejuni mediated disruption of polarized epithelial monolayers is cell-type specific, time dependent, and correlates with bacterial invasion. Pediatr Res 2008, 64:599–604.CrossRefPubMed 40. Monteville MR, Konkel ME: Fibronectin-facilitated invasion of T84 eukaryotic cells by Campylobacter jejuni occurs preferentially at the basolateral cell surface.