This pretreatment resulted in complete inhibition of PGE2-induced phosphorylation of EGFR, ERK, and Akt, while the EGF-induced phosphorylation of these proteins was not affected (Fig 5C and D), indicating that the transactivation

is dependent on mechanisms involving ADAM-mediated release of EGFR ligand(s). We also examined the effect of this inhibitor in the primary cultures of rat hepatocytes, and found neither inhibition of PGE2-induced phosphorylation selleck products of ERK and Akt in these cells nor any effect on EGF-induced phosphorylation of EGFR, ERK and Akt (Figure 5E). Discussion We have shown that in the MH1C1 hepatocarcinoma cells stimulation with PGE2 or PGF2α causes phosphorylation of the EGFR and learn more an EGFR-dependent phosphorylation of ERK and Akt, indicating that these prostaglandins induced transactivation of EGFR. Further study of the PGE2 effect suggested that the transactivation was mediated by the Gq-coupled FP receptor and activation

of PLCβ with downstream signalling by Ca2+ release, Src, and ADAM-mediated shedding of membrane-bound EGFR ligand precursors. In contrast, in primary hepatocytes, PGE2 did not phosphorylate the EGFR, and gefitinib did not prevent phosphorylation of Akt or ERK after PGE2-stimulation, which lends further support to our previous data suggesting that GPCR agonists do not transactivate the EGFR in normal rat hepatocytes, but rather signal via PTK6 mechanisms that synergistically enhance the effects of EGF [34, 37, 38, 51, 52] (Figure 6). Figure 6 Mechanisms by which PGE 2 interacts with EGFR-mediated signalling in hepatocytes and MH 1 C 1 hepatocarcinoma cells. A) In normal rat hepatocytes, PGE2 does not elicit transactivation of EGFR, but induces upregulation of the effectiveness in Ras/ERK and PI3K/Akt buy Barasertib pathways downstream of EGFR, leading to an

enhanced mitogenic response to EGF family growth factors [37, 38, 51]. Although not fully clarified, previous studies have indicated that this effect of PGE2 is mediated primarily through EP3 receptors and Gi proteins, requires several hours to develop, and is most likely a result of altered gene expression [34, 37, 38, 51, 52]. B) In MH1C1 rat hepatocarcinoma cells, PGE2 transactivates EGFR and thereby activates the Ras/ERK and PI3K/Akt signalling pathways. The results of the present study suggest that this effect is exerted via FP receptors, Gq proteins, PLCβ, intracellular Ca2+ (but not PKC), Src, and ADAM-mediated release of EGFR ligands. Different receptors and pathways may be involved in mitogenic and tumour-promoting effects of prostaglandins [28]. qRT-PCR analysis showed that the prostaglandin receptors expressed in these cells are EP1, EP4, and FP.

“
“Background Self-assembled nanowires (NWs) of metal silicides have received much attention recently for their potential applications as electrical interconnects on a scale that cannot be attained with conventional lithographic methods [1–4]. In addition, such structures are expected to display novel physical

properties related to the structural anisotropy and quantum confinement effects and could be used as active elements for the new generation of electronic, optoelectronic, magnetic, and thermoelectric devices [5–7]. In the past decade, it has been reported that NWs of rare-earth silicides such as ScSi2[7], ErSi2[8, 9], DySi2[2, 10, 11], GdSi2[12, 13], and HoSi2[14, 15] and 3d transition metal silicides such as VRT752271 research buy FeSi2[1], CoSi2[3], NiSi2[16], and TiSi2[17–19] can be formed on silicon substrates by the molecular beam epitaxy method. While the NW shape of rare-earth silicides is thought to result from an anisotropic lattice mismatch that is small (<1%) in length direction https://www.selleckchem.com/products/Cyt387.html and large (>5%) in width direction of the NW, the NW shape of FeSi2, CoSi2, and NiSi2 results from an ‘endotaxial’ growth mechanism which involves the growth of silicide into the Si substrate [1, 3]. Very recently, we have reported that MnSi~1.7 NWs can also be grown on the Si substrates with reactive epitaxy method at temperatures above approximately 500°C [20–22]. The growth mechanism of the

NWs was considered to be anisotropic lattice mismatch between the silicide and the Si substrates. The growth direction of the NWs is confined along Si<110>, resulting in the NWs orienting with the long axis along one direction (Si ), two orthogonal directions (Si and [011]), and three directions (Si , , and ) on the Si(110), (001), and (111) surfaces, respectively. However, for scientific investigation as well as device applications, it would be highly expected to grow NWs with a single orientation because ifenprodil the NWs grown in this mode would never cross and have larger length. Parallel NW arrays can be used as nanomechanical devices [23], and using parallel NWs, the anisotropic electronic

structure of silicide NWs can be investigated by angle-resolved photoelectron spectroscopy [11]. On the other hand, the Si(110) surface is currently attracting renewed interests because of its click here unusual properties such as high hole mobility, unique surface reactivity, and strong structural anisotropy. The Si(110) surface has a potential use in fabricating vertical double-gate metal oxide semiconductor field effect transistors that enable much higher integration [24]. Although the formation of MnSi~1.7 NWs with sole orientation on Si(110) was demonstrated in our previous works [20], a detailed investigation on how the growth parameters affect the growth of MnSi~1.7 NWs on Si(110), which is of key importance for a comprehensive understanding of the growth kinetics and thus the controllable growth of the NWs, is still lacking.

Infect Immun 1992, 60:1499–1508.PubMed 34. Chaffin WL, López-Ribot JL, Casanova M, Gozalbo D, Martínez JP: Cell wall and secreted proteins of selleck compound Candida albicans : identification,

function, and expression. Microbiol Mol Biol Rev 1998, 62:130–180.PubMed 35. Chaffin WL: Candida albicans cell wall proteins. Microbiol Mol Biol Rev 2008, 72:495–544.PubMedCrossRef 36. Gow NA, Van de Veerdonk FL, Brown AJ, Netea MG: Candida albicans morphogenesis and host defence: discriminating invasion from colonization. Nat Rev Microbiol 2011, 10:112–122.PubMed 37. Walker LA, Munro CA, de Bruijn I, Lenardon MD, McKinnon A, Gow NA: Stimulation of chitin synthesis rescues Candida albicans from echinocandins. PLoS Pathog 2008, 4:e1000040.PubMedCrossRef 38. Mora-Montes HM, Netea MG, Ferwerda Androgen Receptor Antagonist G, Lenardon MD, Brown GD, Mistry AR, Kullberg BJ, O’Callaghan CA, Sheth CC, Odds FC, Brown AJ, Munro

CA, Gow NA: Recognition and blocking of innate immunity cells by Candida albicans chitin. Infect Immun 2011, 79:1961–1970.PubMedCrossRef 39. Hoyer LL, Payne TL, Bell M, Myers AM, Scherer S: Candida albicans ALS3 and insights into the nature of the ALS gene family. Curr Genet 1998, 33:451–459.PubMedCrossRef 40. Hoyer LL, Payne TL, Hecht selleck chemical JE: Identification of Candida albicans ALS2 and ALS4 and localization of als proteins to the fungal cell surface. J Bacteriol 1998, 180:5334–5343.PubMed 41. Silverman RJ, Nobbs AH, Vickerman MM, Barbour ME, Jenkinson HF: Interaction of Candida albicans cell wall Als3 protein with Streptococcus gordonii SspB adhesin promotes development of mixed-species communities. Infect Immun 2010, 78:4644–4652.PubMedCrossRef 42. Bastidas RJ, Heitman J, Cardenas ME: The protein BCKDHA kinase Tor1 regulates adhesin gene expression in Candida albicans . PLoS Pathog 2009, 5:e1000294.PubMedCrossRef 43. Otoo HN, Lee KG, Qiu W, Lipke PN: Candida albicans Als adhesins have conserved amyloid-forming sequences. Eukaryot Cell 2008, 7:776–782.PubMedCrossRef 44. Alsteens D, Ramsook CB, Lipke PN, Dufrene YF: Unzipping a functional microbial

amyloid. ACS Nano 2012. Competing interests The authors declare that they have no competing interest. Authors’ contributions ESO, BPK, HJB, HCM designed the experiment, ESO performed the experiments, ESO, BPK, HJB, HCM analyzed the data and wrote the paper. All authors read and approved the final manuscript.”
“Background Bats (Order: Chiroptera) are the only mammals capable of true sustainable flight and one of the most diverse and species rich mammals on earth [1]. They assist in the regulation of insect populations in their habitats, pollination of flowers and dispersal of seeds of economically important tress, and these ecological roles support forest regeneration and maintenance [2]. However, they roost near human habitation and their association with emerging infections has increased attention on these flying mammals as vectors of zoonotic pathogens [3–5].

In addition, we compared the results for the concave spherical mirror with those obtained using a Fizeau interferometer, as shown in Figures 8 and 9. The result for the Fizeau interferometer is 70.0 nm PV. Table 2 Selleck Entospletinib summarizes the results for both the profilers. Figure 8 Fizeau interferometer results for concave spherical mirror in three dimensions. Figure 9 Fizeau interferometer results for concave spherical mirror in two dimensions. Table 2 Results of nanoprofiler and Fizeau interferometer for concave spherical mirror   Nanoprofiler Fizeau interferometer In three dimensions PV 70.5 nm PV 70.0 nm In two dimensions PV 40.0 nm PV 45.0 nm Measurement range 20 × 20 mm 30 × 30 mm The difference between

the nanoprofiler and Fizeau interferometer results for the figure error may depend on each device’s system error. On the other hand, the phase-shift Fizeau interferometer is affected by the precision of the reference

mirror. We cannot conclude that the difference in these results is caused only by the greater precision of the nanoprofiler. Therefore, Selleckchem R406 we conclude that the profiles of both the mirrors are consistent within the range of systematic error. Measurement of a flat mirror We measured a flat mirror three times. The measurement time was 20 min. When measuring a flat mirror, we need to move the sample system which has two sets of two pairs of goniometers, optical system which has two sets of two pairs of P5091 order goniometers and one straight stage, and the reflected beam returns to the QPD within its dynamic range. During the measurement, each axis is controlled numerically. The numerical control parameter is calculated in advance from the ideal shape of the sample. We detect the gap in the normal vector for the figure error using QPD because the sample has a figure

error. Therefore, we can acquire the declination of the normal vectors from the QPD output signal. Figure 10 shows the average figure error for the three measurements, which is 21.0 nm. Next, we evaluated the repeatability of the measurements, as shown in Figures 11, 12, and 13. The repeatability of the first, second, and third measurements was 1.08 selleckchem nm PV, 1.26 nm PV, and 1.25 nm PV, respectively. Figure 10 Figure error for flat mirror (average of three measurements). Figure 11 Repeatability for flat mirror (first time). Figure 12 Repeatability for flat mirror (second time). Figure 13 Repeatability for flat mirror (third time). When we compare the repeatability results, we see that the repeatability in each direction varies depending on the measurement. Because we used a raster scan method for these measurements, the acceleration and deceleration provided a rigorous method of measurement. Therefore, every measurement point is slightly different. The repeatability is expected to be enhanced by improving the dynamic stiffness of the optical head. In addition, when we measure a flat mirror, five axles are controlled and moved.

2006 (Fig. S3), which might explain why CyanoQ had not until now been detected in isolated His-tagged PSII complexes. In contrast, we have so far been unable to find conditions where CyanoP remains fully attached to PSII complexes. CyanoQ is a likely lipoprotein in T. elongatus Like the situation Selleck Repotrectinib in Synechocystis (Ujihara et al. 2008), both CyanoP and CyanoQ from T. elongatus contain a characteristic lipobox sequence, as detected by Prosite (De Castro et al. 2006), suggesting that they might be processed at the N-terminus and anchored to the membrane via lipidation of a cysteine residue (Fig.

S4). CBL0137 molecular weight Previous membrane washing experiments using either a high-salt treatment (2 M NaCl or 1 M CaCl2) or an alkaline treatment (pH 12.0), coupled with immunochemical detection, have shown that CyanoP

is tightly bound to the membrane consistent with its assignment as a lipoprotein, whereas the non-lipidated extrinsic PsbO subunit is more easily removed (Michoux et al. 2010). Analysis of the same samples revealed that CyanoQ behaved like CyanoP and the lipidated Psb27 subunit of PSII (Nowaczyk et al. 2006) and was more resistant to extraction than PsbO (Fig. S5). Expression and crystallisation of the CyanoQ protein from T. elongatus CyanoQ in Synechocystis and T. elongatus are relatively divergent with only 31 % sequence identity (Fig. 3 and Fig. S4). To gain insights into the structure SIS3 of CyanoQ from T. elongatus, a Venetoclax cleavable N-terminal His6-tagged derivative lacking the predicted lipidated Cys24 (Fig. 3) residue was over-expressed in E. coli and the protein purified by immobilised nickel-affinity chromatography to near homogeneity (Fig. S6a). The His-tag was removed by thrombin

cleavage and CyanoQ was re-purified and concentrated to 10 mg/ml (Fig. S6b). The predicted product contains residues 25–152 of CyanoQ plus 5 additional residues (GSELE) at the N-terminus. Crystallisation screens, performed using hanging drop plates, resulted in the formation of crystals, which were further optimised to grow in 1.8 M ammonium sulphate (Fig. S6c). Fig. 3 Sequence alignment of CyanoQ from T. elongatus, Synechocystis and PsbQ from spinach. Secondary structures are shown for CyanoQ from T. elongatus (3ZSU) and PsbQ from spinach (1VYK). Zinc-binding sites and lipidated cysteine residues are highlighted in green and yellow, respectively. Predicted signal peptides for CyanoQ are boxed in black. Numbering according to CyanoQ sequence from T. elongatus. Absolutely conserved and similar residues are shown as white letters on red background and red letters on white background, respectively, as calculated by ESPript (Gouet et al.

Genes Dev 1994, 8: 757–769.PubMedCrossRef 5. Koga H, Kaji Y, Nishii K, Shirai M, Tomotsune D, Osugi T, Sawada A, Kim JY, Hara J, Miwa T, Yamauchi-Takihara K, Shibata Y, Takihara Y: Overexpression of Polycomb-group gene rae28 in cardiomyocytes does not complement abnormal cardiacmorphogenesis inmice lacking rae28 but causes dilated cardiomyopathy. Lab Invest 2002, 82: 375–385.PubMed 6. Caretti G, DiPadova M, Micales B, Lyons GE, Sartorelli

V: The Polycomb Ezh2 methyltransferase regulates muscle gene expression and skeletalmuscle differentiation. Genes Dev 2004, 18: 2627–2638.PubMedCrossRef 7. Alkema MJ, IWP-2 purchase van der Lugt NM, Bobeldijk RC, Berns A, Koseki H: Transformation of axial skeleton due to overexpression of bmi-1 in transgenic mice. Nature 1996, 374: 724–727.CrossRef 8. Heard E: Recent advances in buy SAR302503 X-chromosome inactivation. Curr

Opin Cell Biol 2004, 16: 247–255.PubMedCrossRef 9. Lessard J, Baban D, STA-9090 mw Sauvageau G: Stage-specific expression of polycomb group genes in human bone marrow cells. Blood 1998, 91: 1216–1224.PubMed 10. Lessard J, Schumacher A, Thorsteinsdottir U, van Lohuizen M, Magnuson T, Sauvageau G: Functional antagonism of the Polycomb-group genes eed and Bmi-1 in hemopoietic cell proliferation. Genes Dev 1999, 13: 2691–2703.PubMedCrossRef 11. Peytavi R, Hong SS, Gay B, d’Angeac AD, Selig L, Bénichou S, Benarous R, Boulanger P: HEED, the product of the human homolog of the murine eed gene, binds to the matrix protein of HIV-1. J Biol Chem 1999, 274: 1635–1645.PubMedCrossRef 12. Fukuyama T, Otsuka T, Shigematsu H, Uchida N, Arima

F, Ohno Y, Iwasaki H, Fukuda T, Niho Y: Proliferative involvement of ENX-1, a putative human polycomb group gene, in haematopoietic cells. Br J Haematol 2000, 108: 842–847.PubMedCrossRef 13. Raaphorst FM, Otte AP, van Kemenade FJ, Blokzijl T, Fieret E, Hamer KM, Satijn DPE, Otte AP, Meijer CJLM: Coexpression of BMI-1 and EZH2 polycomb group genes in Reed-Sternberg cells of Hodgkin’s disease. Am J Pathol 2000, 157: 709–715.PubMedCrossRef 14. Raaphorst FM, Otte AP, van Kemenade FJ, Blokzijl T, Fieret E, Hamer click here KM, Satijn DPE, Meijer CJLM: Distinct BMI-1and EZH2 expression patterns in thymocytes and matureT cells suggest a role for Polycomb genes in humanTcell differentiation. J Immunol 2001, 166: 5925–5934.PubMed 15. Raaphorst FM: Deregulated expression of polycomb-group oncogenes in human malignant lymphomas and epithelial tumours. Hum Mol Genet 2005, 14: 93–100.CrossRef 16. Valk-Lingbeek ME, Bruggeman SW, van Lohuizen M: Stem cells and cancer; the polycomb connection. Cell 2004, 118: 409–418.PubMedCrossRef 17. Gil J, Bernard D, Peters G: Role of Polycomb group proteins in stem cell-renewal and cancer. DNA Cell Biol 2005, 24: 117–125.PubMedCrossRef 18.

Based on the pattern of AeCPA promoter-based expression, impairing of the RNAi pathway was supposed to last for only 36 h during digestion of the bloodmeal in the midgut. Before the onset of Aa-dcr2 mRNA silencing in midgut cells of Carb/dcr16 females, most likely there were sufficient quantities of dicer2 protein synthesized, which could turn the RNAi mechanism this website against itself. Possibly during the entire 36 h period of RNAi silencing certain quantities

of functional dicer2 prevailed in the midgut cells so that the pathway was compromised in its efficiency and capacity but never completely shut off. Similar lack of complete inhibition of RNAi was observed before when transiently silencing dcr2 in Drosophila S2 cells [27]. This could explain the pattern of find more the Aa-dcr2 mRNA expression profiles in Carb/dcr16 females, where the efficiency of Aa-dcr2 mRNA silencing fluctuated over time but its expression was never eliminated. Moreover, infection with SINV resulted in increased Aa-dcr2 mRNA accumulation in Carb/dcr16 females, showing that the midgut epithelial cells were still able to mobilize additional dicer2 protein, even though the pathway was impaired in the midgut tissue. Increase in Aa-dcr2 mRNA accumulation confirms earlier findings that the TR339 strain of SINV triggers the

RNAi pathway in Ae. aegypti [3]. However, no mechanism for Aa-dcr2 induction has been described so far. We have no clear explanation as to why at 2 days pbm Aa-dcr2 mRNA levels were increased in both HWE and Carb/dcr16 females. We observed that levels of transgenic Aa-dcr2 silencing varied considerably between the different transgenic mosquito lines that were initially tested. This could be caused by corresponding variations in Aa-dcr2 IR RNA expression levels. Based on

previous observations with transgenic mosquitoes expressing a marker gene in midgut tissue (A.W.E. Franz, K.E. Olson, A.A. James, Enzalutamide unpublished results), the TE integration site in the genome of the mosquito can strongly affect gene-of-interest expression levels. Even though maximal silencing of Aa-dcr2 in LCL161 in vivo midguts of SINV-TR339EGFP infected Carb/dcr16 females appeared to be no more than ~50%, it had profound effects on intensity of infection, midgut infection and dissemination rates of the virus at 7 days pbm. Average virus titers in midguts increased from 1750 pfu/ml in HWE to 14,000 pfu/ml in Carb/dcr16 mosquitoes. Accordingly, midgut infection rates increased from 33% (HWE) to 69% (Carb/dcr16) and virus dissemination rates from 30% (HWE) to 60% (Carb/dcr16). These data suggest that the RNAi pathway in the mosquito midgut tightly controls SINV infection by modulating its replication. Thus, MIB and MEB for SINV-TR339EGFP in Ae. aegypti were virus dose-dependent and in this way affected by the RNAi pathway.

For the sole application of prothioconazole

no major effects on DON production were observed since none of the tested concentrations were sub lethal. In an additional experiment using an extra intermediate concentration of 1/50 of the field concentration of prothioconazole, a reduced spore germination of about 50% was observed (data not shown). Concomitant with this observation, this sub lethal dilution resulted in an increased DON production (32 μg/μg of fungal Salubrinal order DNA). Hence, application of sub lethal concentrations of respectively prothioconazole + fluoxastrobin and prothioconazole seems to result in the activation of the trichothecene biosynthesis machinery leading to an accumulation of DON as fast as 48 h after the start of the experiment. Figure 2 Effect of prothioconazole + fluoxastrobin (a), prothioconazole (b) and azoxystrobin (c) alone or in combination with Veliparib cost catalase (d,e,f) on production of deoxynivalenol (DON) by F. graminearum. Conidia at a concentration this website of 106 conidia/ml were challenged with a tenfold dilution series of fluoxastrobin + prothioconazole, azoxystrobin and prothioconazole starting from 0.5 g/l + 0.5 g/l, 0.83 g/l and 0.67

g/l in absence (a,b,c) or presence (e,f,g) of 1000 U/ml catalase. DON content in the medium was determined using a competitive ELISA approach 48 h after start of the experiments. Each bar is the result of two pooled samples to reduce variance. Bay 11-7085 The experiment was repeated twice in time of which one representative experiment is shown in the figure. Different letters above bars indicate significant differences after analysis with a Kruskall-Wallis and Mann-Whitney test with a sequential Bonferroni correction for multiple comparisons. Timely production of H2O2 precedes DON accumulation in combined strobilurin and triazole fungicide application As several lines of evidence in literature corroborate an important role for reactive oxygen species (ROS) and more specifically H2O2 in stress responses of fungi,

the accumulation of H2O2 upon fungicide application was monitored in the established in vitro germination assay. In these experiments, we unequivocally demonstrated that sole application of respectively azoxystrobin and prothioconazole at the given concentrations did not result in elevated H2O2 concentrations at any of the time points (Figure 3). In addition, prothioconazole at field dose resulted in lower H2O2 concentrations than those observed in control samples possibly reflecting the reduction in microbial metabolic activity due to the application of the fungicide. Sub lethal dilutions of the combined application of fluoxastrobin + prothioconazole (i.e. 1/10 and 1/100) resulted in an increased H2O2 content in the medium compared to the control and the other treatments as fast as 4 h after the start of the germination assay.

Statistical analysis The Student’s t test was used to calculate the statistical differences between the mean levels of polysaccharide expression of experimental samples (biofilm grown cells) and control samples (Small molecule library concentration planktonic cells). A P value < 0.05 was considered significant. All statistical analyses were done using InStat software (InStat, San Diego, CA). Results Identification of a novel H. somni surface component produced during anaerobic growth To determine if there was variation in expression of membrane components under different environmental conditions, H. somni 738 was grown on CBA plates in 3-5% CO2 or

under anaerobic conditions for 48 h at 37°C. The bacteria were harvested from the plates as described in methods, and Cetavlon was added to the supernatant (0.005 M, final concentration); LOS and protein-enriched outer membranes were prepared

this website from the cell pellets [46, 47]. No substantial qualitative differences were detected in the electrophoretic profiles of the LOS or membrane proteins of bacteria grown Ruboxistaurin mouse on CBA under CO2 or anaerobic conditions (data not shown), although growth of H. somni under anaerobic conditions was poor. Nonetheless, when Cetavlon was added to the supernatant of cells washed off CBA plates incubated under anaerobic conditions, a large precipitate formed, whereas little or no precipitate formed from the supernatant of cells grown on CBA in CO2 (data not shown). The Cetavlon precipitate was solubilized in distilled Silibinin water, and greater than 90% of the precipitate was determined to be carbohydrate. However, it was not LOS, as determined by polyacrylamide gel electrophoresis and silver staining for LOS (data not shown). Electrophoresis of the Cetavlon precipitate followed by staining with alcian blue and ammoniacal silver demonstrated a heterogeneous profile, typical of high molecular size polysaccharide (Figure 1). Figure 1 Electrophoretic profiles of semi-purified Cetavlon precipitates and biofilm. Bacteria were grown anaerobically on plates or to late stationary phase, Cetavlon added, and precipitates

extracted, as described in Methods. Each extract was loaded onto 25% polyacrylamide gels, followed by electrophoresis and staining with Alcian blue and silver. Lanes: 1 and 2, 20 μg and 30 μg of EPS extracted under growth conditions favorable to biofilm formation; 3 and 4, 20 μg and 30 μg of EPS extracted from cells grown to late stationary phase in broth, respectively; 5, buffer alone; 6 and 7, 20 μg and 30 μg of EPS extracted from cells grown anaerobically on plates, respectively. Immuno-transmission electron microscopy of H. somni grown under anaerobic conditions or CO2 The polysaccharide from Cetavlon precipitates obtained from scaled up anaerobic cultures was further purified, as described in methods, and used to immunize a rabbit.

The 350-nm-wide computational cell used comprises a 63-nm-thick layer of a 100-nm-wide BARC stripe sandwiched between two 125-nm-wide Py stripes, atop a 2-μm-thick selleck Si substrate, with its bottom boundary fixed. It is to be noted that unlike the case of the 1D Py/Fe

nanostripe array of [7], no interfacial air gaps were considered in the calculations, as the fabrication process employed here precludes their formation. Elastic parameters used in the simulations for Py, BARC, and Si are Young’s moduli = 180, 6.26, and 169 GPa; Poisson ratios = 0.31, 0.34, and 0.064; and mass densities = 8600, 1190, and 2330 kg/m3, respectively [19–21]. The simulated dispersion relations for the lowest three SAW branches, below the

longitudinal bulk wave threshold [22, 23], presented in Figure  2a, accord well with the Brillouin measurements. Also shown in the figure are the dispersion relations of the vertically polarized transverse (T) and longitudinal (L) bulk waves, in the [110] direction, of the Si substrate. Simulated mode profiles for q = π/a, shown in Figure  2b, of the lowest two modes exhibit characteristics of the surface Rayleigh wave (RW). These RWs are standing Bloch waves satisfying the Bragg scattering condition. The mode profile of the third branch at the BZ boundary reveals that it is also a standing wave with most of its energy confined in the BARC stripes. Mode profiles for q = 1.4π/a displayed in Figure  2c indicate that at this see more wavevector, the first branch has the characteristics of the RW. In contrast, the higher two SAWs leak energy PXD101 into the Si substrate as their dispersion curves extend beyond

the transverse bulk wave threshold [16, 22–24]. The dispersion relations of the RW and Sezawa wave (SW), modeled by treating the Py/BARC array as a homogeneous effective medium [25] on a Si substrate, are presented in Figure  2a. It can be seen that the gap opening arises from the zone folding of the RW dispersions and avoided crossings at the BZ boundary. A prominent feature of the phonon dispersion spectrum is the large hybridization bandgap. For a structure, such as ours, Levetiracetam comprising a ‘slow’ film on a ‘fast’ substrate, Sezawa waves will exist only below the transverse bulk wave threshold, and over a restricted range of qh, where h is the film thickness [23, 26]. As shown in Figure  2a, within the first BZ, the SW and zone-folded RW do not cross, indicating that the measured bandgap does not originate from the hybridization of these waves. Instead, within the bandgap, the zone-folded RW crosses the transverse bulk wave threshold. Additionally, above but close to this threshold, attenuated SAWs called pseudo-Sezawa waves which exist as resonances with the substrate continuum of modes have been observed [23, 26, 27]. We thus attribute the origin of the bandgap to the hybridization and avoided crossing of the zone-folded RW and pseudo-Sezawa waves.