Figure 1 shows the band structure of the CdS/MEH-PPV inorganic–organic hybrid system. Figure 1 Schematic energy level diagram for the CdS/MEH-PPV hybrid nanocomposite. With energy levels in eV relative to vacuum. Efficient photoconductivity learn more requires not only efficient charge separation but also efficient transport of the carriers to the electrodes without recombination, in that sense, the morphology of nanocomposite being crucial in providing suitable paths for both electron

and hole towards the appropriate electrode [7]. The NC network must be homogeneous so that each negative charge can efficiently hop to another NC in the direction of the internal field, this requirement being a complex issue when NCs are dispersed in polymeric matrices. The main difficulty

is due to the high surface-to-volume ratio of NCs that tend to form agglomerate to lower their surface energy. Furthermore, the addition of a dense network of NCs to polymers can significantly alter the mechanical properties of the resulting nanocomposite material compromising the advantageous properties of organic semiconductor such as the easy processability [9]. The nanocomposite is frequently gained by solution blending, i.e. dispersion of NCs in polymer solutions that can be dried under vacuum or can be used to obtain thin films by spin-casting (solvent evaporation) [10]. During these procedures, the NCs form microsized Tyrosine Kinase Inhibitor Library Edoxaban aggregates and cannot be separated from each other. As a consequence, nanocomposites have been commonly prepared by synthesis of the inorganic NCs in situ, for instance in solution,

where the solvent is a monomer and the nanocomposite is then prepared through in situ polymerization [11, 12]. Alternatively, the inorganic NCs can be synthesized inside polymer matrices through the thermolysis of suitable precursors. Recent works of our research group have demonstrated that cadmium thiolates are promising materials for the in situ synthesis of nanocrystalline CdS [13]–[18]. Using unimolecular precursors, as cadmium thiolates, it is possible to overcome any problem, occurring in the other chemical methods, such as the low temporal stability of reagents, the inhomogeneity of multicomponent mixing and the intrinsic high reactivity and toxicity of the precursor used. Furthermore, unimolecular precursors guarantee the stoichiometry control of thermolytic process. Unfortunately, cadmium thiolates, having a polymeric structure, are insoluble in typical organic solvents; so, it is not possible to homogeneously disperse them in polymeric matrices, and the thermolysis process induces the growth of CdS NCs with a disordered distribution.

J Natl Cancer Inst 1959, 22:719–748.PubMed 13. DerSimonian R, Laird N: Meta-analysis in clinical trials. Control

Proteasome cleavage Clin Trials 1986, 7:177–188.PubMedCrossRef 14. Tobias A: Assessing the influence of a single study in the meta-analysis estimate. Stata Tech Bull 1999, 8:15–17. 15. Egger M, Davey Smith G, Schneider M, Minder C: Bias in metaanalysis detected by a simple, graphical test. BMJ 1997, 315:629–634.PubMedCrossRef 16. David-Beabes GL, Lunn RM, London SJ: No association between the XPD(Lys751G1n) polymorphism or the XRCC3 (Thr241Met) polymorphism and lung cancer risk. Cancer Epidemiol Biomarkers Prev 2001, 10:911–912.PubMed 17. Misra RR, Ratnasinghe D, Tangrea JA, et al.: Polymorphisms in the DNA repair genes XPD, XRCC1, XRCC3, and APE /ref-1, and the risk of lung cancer among male smokers in Finland. Cancer Lett 2003, 191:171–178.PubMedCrossRef 18. Wang Y, Liang D, Spitz MR, et al.: XRCC3 genetic polymorphism, smoking, and lung carcinoma risk in minority

populations. Cancer 2003, 98:1701–1706.PubMedCrossRef 19. Popanda O, Schattenberg T, Phong CT, et al.: Specific combinations of DNA repair gene variants and increased risk for non-small cell lung cancer. Carcinogenesis 2004, 25:2433–2441.PubMedCrossRef 20. Jacobsen NR, Raaschou-Nielsen O, Nexo B, et al.: GSK458 chemical structure XRCC3 polymorphisms and risk of lung cancer. Cancer Lett 2004, 213:67–72.PubMedCrossRef 21. Harms C, Salama SA, Sierra-Torres CH, Cajas-Salazar N, Au WW: Polymorphisms in DNA repair genes, chromosome aberrations, and lung cancer. Environ Mol Mutagen

2004, 44:74–82.PubMedCrossRef 22. Matullo G, Dunning AM, Guarrera S, et al.: DNA repair polymorphisms and cancer risk in non-smokers in a cohort study. Carcinogenesis 2006, 27:997–1007.PubMedCrossRef 23. Zienolddiny S, Campa D, Lind H, et al.: Polymorphisms Astemizole of DNA repair genes and risk of non-small cell lung cancer. Carcinogenesis 2006, 27:560–567.PubMedCrossRef 24. Ryk C, Kumar R, Thirumaran RK, Hou SM: Polymorphisms in the DNA repair genes XRCC1, APEX1, XRCC3 and NBS1, and the risk for lung cancer in never- and ever-smokers. Lung Canc 2006, 54:285–292.CrossRef 25. Lopez-Cima MF, Gonzalez-Arriaga P, Garcia-Castro L, et al.: Polymorphisms in XPC, XPD, XRCC1, and XRCC3 DNA repair genes and lung cancer risk in a population of northern Spain. BMC Cancer 2007, 7:162.PubMedCrossRef 26. Zhang ZL, Zhou CC, Zhang J, Tang L, Su B: Relationship between polymorphisms of DNA repair gene XRCC3 and susceptibility to lung cancer. Zhonghua Jie He He Hu Xi Za Zhi 2007, 30:936–940.PubMed 27. Improta G, Sgambato A, Bianchino G, et al.: Polymorphisms of the DNA repair genes XRCC1 and XRCC3 and risk of lung and colorectal cancer: a case–control study in a Southern Italian population. Anticancer Res 2008, 28:2941–2946.PubMed 28. Xia W, Zhang Y, Su D, Shi F: Association of single nucleotide polymorphisms of DNA repair gene XRCC3–241 with non-small cell lung cancer. Zhejiang Med J 2008, 30:1291–1293. 29.

Here we first examine the importance of the mitochondrial genome to drug sensitivity Atezolizumab using ρ 0 petite strains deleted of mitochondrial DNA. We then examine the value to elucidating the mechanism of action of dhMotC of combining screening of ρ 0 cells with 3 genome-wide screening approaches: drug-induced haploinsufficiency, chemical-genetic synthetic lethality and suppression of drug sensitivity by increased gene expression. We find that despite their similar conceptual basis, namely altering drug sensitivity by modifying gene dosage, the 3 approaches can provide distinct sets of information that, when integrated, reveal a much more complete picture of the spectrum of effects of a

drug on cells. Results and discussion Screen for mitochondria-dependent inhibitors of yeast growth Halo assays, traditionally used in antibacterial screens, can be used to assess cytotoxic properties of chemicals in yeast [12]. Fungistatic and fungicidal chemicals spotted onto plates containing a lawn of S. cerevisiae growing in soft agar cause

zones of growth inhibition (halos) that are easily detected by visual inspection. Robotic pinning enables high-density arraying of compounds for increased throughput. We used the halo assay to screen approximately 3,500 FDA-approved drugs and bioactive chemicals [13] as well as in-house chemicals for inhibition of yeast growth. Chemicals were pin-transferred onto agar containing selleckchem the wild type yeast strain BY4741 [14] or strain FY1679-28C/TDEC [15] with deletion of 2 transcription factors, PDR1 and PDR3, that regulate a wide range of multidrug resistance genes, to increase click here the likelihood of identifying active compounds. To determine the effect of functional mitochondria

on drug sensitivity, the screen was also carried out on respiratory-deficient ρ 0 petite mutants of the 2 strains. The strains lacking functional mitochondria were generated by propagating cells in the presence of ethidium bromide, resulting in the selective loss of the mitochondrial genome, including several essential components of the electron-transport chain, which renders cells respiratory-deficient [16]. The ρ 0 petite strains were unable to grow on glycerol, a nonfermentable carbon source, confirming their inability to generate ATP by mitochondrial oxidative phosphorylation (data not shown). Plates were inspected after 48 h incubation at 30°C and halos > 2 mm in diameter were scored. 51 chemicals inhibiting the growth of FY1679-28C/TDEC were identified (Table 1), 39 of which also inhibited the growth of BY4741. Only 4 chemicals affected the growth of wild type and ρ 0 cells differently. Suloctidil, myriocin, dhMotC and antimycin A inhibited respiratory-competent strains but failed to inhibit the growth of the ρ 0 strains (Figure 1A and 1B).

J Plankton Res 19:1637–1670CrossRef Samson G, Prášil O,

Yaakoubd B (1999) Photochemical and thermal phases of chlorophyll a fluorescence. Photosynthetica 37(2):163–182CrossRef Schreiber U (1986) Detection of rapid induction kinetics with a new type of high-frequency modulated chlorophyll fluorometer. Photosynth Res 9:261–272CrossRef Schreiber U (2004) Pulse-amplitude (PAM) fluorometry and saturation pulse method. In: Papageorgiou G, Govindjee (eds) Chlorophyll fluorescence: a signature of Photosynthesis. Kluwer, Dordrecht, pp 279–319 Schreiber U, Krieger A (1996) Hypothesis: two fundamentally different types of variable chlorophyll fluorescence in vivo. FEBS Lett 397:131–135PubMedCrossRef Schreiber U, Bilger W, Schliwa U (1986) Continuous recording of photochemical and non-photochemical chlorophyll fluorescence quenching with a new type of modulation fluorometer. Photosynth Res 10:51–62CrossRef Schreiber U, Neubauer C, Schliwa U (1993) PAM fluorometer based Palbociclib supplier on medium-frequency pulsed Xe-flash measuring light: a highly sensitive new tool in basic and applied photosynthesis

research. Photosynth Res 36:65–72CrossRef Schreiber U, Bilger W, Neubauer C (1994) Kinase Inhibitor Library Chlorophyll fluorescence as a non-intrusive indicator for rapid assessment of in vivo photosynthesis. In: Schulze E-D, Caldwell MM (eds) Ecological studies, vol 100. Springer, Heidelberg, pp 49–70 Schreiber U, Hormann H, Neubauer C, Klughammer C (1995) Assessment Sodium butyrate of photosystem II photochemical quantum yield by chlorophyll fluorescence quenching analysis. Aust J Plant Physiol 22:209–220CrossRef Schreiber U, Kühl M, Klimant I, Reising H (1996) Measurement of chlorophyll fluorescence within leaves using a modified PAM fluorometer with a fiber-optic microprobe. Photosynth Res 47:103–109CrossRef Schreiber U, Gademann R, Ralph PJ, Larkum AWD (1997) Assessment of photosynthetic performance of prochloron in Lissoclinum-Patella in hospite by chlorophyll fluorescence measurements. Plant Cell Physiol 38:945–951CrossRef Schreiber U, Klughammer C, Kolbowski J (2011) High-end chlorophyll fluorescence analysis with the MULTI-COLOR-PAM. I. Various light qualities and their applications. PAM Application

Notes, vol 1, pp 1–19. http://​www.​walz.​com/​downloads/​pan/​PAN11001.​pdf Siebke K, von Caemmerer S, Badger M, Furbank RT (1997) Expressing an RbcS antisense gene in transgenic Flaveria bidentis leads to an increased quantum requirement for CO2 fixed in Photosystems I and II. Plant Physiol 115:1163–1174PubMed Stirbet A, Govindjee (2011) On the relation between the Kautsky effect (chlorophyll a fluorescence induction) and Photosystem II: basics and applications of the OJIP fluorescence transient. J Photochem Photobiol B 104:236–257PubMedCrossRef Strasser RJ, Tsimilli-Michael M, Srivastava A (2004) Analysis of the chlorophyll a fluorescence transient. In: Papageorgiou G, Govindjee (eds) Chlorophyll fluorescence: a signature of photosynthesis.

13 ± 6.67 years) and 34 were coaches (33 males and 1 female; 37.01 ± 11.70 years). All were members of the Croatian National Sailing Team. Thirty-one athletes sailed in Olympic sailing classes, while 13 sailed in the intermediate sailing classes (i.e., sailing classes that are preliminary to the physically and technically more demanding Olympic classes). At the time of the study, 28 athletes sailed single-crew, while 16 sailed in double-crew boats. All of the subjects were directly under the patronage of the Croatian Sailing Tyrosine Kinase Inhibitor Library Association and the Croatian Olympic Committee as potential Olympic candidates or future Olympic hopefuls, and more

than two-thirds of the athletes and 45% of the coaches achieved International competitive results. The IRB approved the investigation, and all participants consented prior to participation in the study. Instruments The testing was undertaken using the Questionnaire of Substance Use (QSU), an instrument that was previously developed and validated with regard to reliability (89 – 93% of subjects responded equivalently within the test-retest design), while the validity was evidenced by an appropriate level of discriminative validity

for different groups of subjects [40–43]. The basic QSU includes questions about attitudes toward DSs, doping factors, sociodemographics, and sport-specific factors. The sport-specific factors were modified specifically for sailing as a sport (see Results for Edoxaban more details). The sociodemographic data CB-839 included age, sex, and educational level. Sports-related factors (sport-factors) included sports experience (in terms of years involved in sailing), crew number (one or two), current sailing class (Olympic or non-Olympic), and sports achievement (sports results achieved on a 6-point scale from “local competition” to

“medal won at European/World championship in Olympic classes”). DSs and doping factors were studied through questions about the subject’s self determined knowledge about DSs and doping (two separate questions, self-assessed on a five-point scale ranging from “I have no knowledge at all” to “Excellent”), the athlete’s opinion about doping practices in sailing (4-point scale from “I do not think doping is used” to “Doping is often used”), potential doping habits (4-point scale from “I do not intend to use doping” to “I’ll use it if assured it will help me”), trust in coaches regarding doping and trust in physicians regarding doping (both “Yes-No” questions), the number of times the participant has undergone doping testing (four-point scale from “Never” to “More than five times”), and personal opinion regarding penalties for doping offenses (five point scale from “Doping should be allowed” to “Lifelong suspension”).

Constructs shRNAlentiviral selleck chemicals constructs in pLKO.1 against human LAMP1 was purchased from Sigma Aldrich, and following verification of knockdown, clone ID NM_005561.2-1183s1c1 used to compromise lysosomal integrity. Packaging vectors were obtained through Addgene, Inc. (Cambridge, MA). Lentivirus particles were prepared by transfection of 293 T cells in T75 flasks with 3 μg construct, 2.8 μgpRSV-Rev, 2.4 μgpMDLg/pRRE, and 0.6 μg pMD2.G utilizing FuGENE® 6 Transfection Reagent from F. Hoffmann-La Roche Ltd. (Basel, Switzerland).

Forty-eight and 72 hours following transfection, supernatant was transferred to Bxpc3 cells in the presence of polybrene (8 μg/mL). Transformed cells were selected with puromycin (1 μg/mL) and assayed accordingly. Antibody staining Cells were washed once with PBS prior to fixation with IC

Fixation Buffer (eBiosciences) for 15 minutes at 37°C. Fixed cells were washed with PBS, resuspended in Permeabilization Buffer (eBiosciences), and incubated for 30 minutes at room temperature. Intracellular antigen staining was performed with FITC-antibody selleck inhibitor dilution of 1:100 in Permeabilization Buffer for 60 minutes at room temperature. Mean fluorescence in FL1 was quantified with a FACSCalibur flow cytometer. Cell viability Cell lines maintained at optimal culture conditions were seeded into 96-well white, clear-bottom plates and following treatment, viability determined with CellTiter-Glo Luminescent Viability Assay from Promega (Madison, WI). Luminescence was quantified with a SpectraMax Gemini microplate spectrofluorometer from Molecular Devices (Silicon Valley, CA). Viability relative to vehicle was fit by non-linear regression and plotted against concentration. Cellular protease

assay Cells were treated in the presence of inhibitors and cytosolic extracts prepared using the digitonin extraction Thalidomide method as previously described [43]. Washed cells were resuspended at 1×106 cells/mL in extraction buffer consisting of sucrose (250 mM), HEPES (20 mM), KCl (10 mM), MgCl2 (1.5 mM), EDTA (1 mM), and digitonin (30 μM). Cells were placed on ice on an orbital shaker for 10 minutes prior to centrifugation for 1 min at 14,000 rpm at 4°C. Supernatants were collected and 20 μL used to detect cleavage of Z-RR-AMC in and equal volume of reaction buffer consisting of sodium acetate (100 mM), NaCl (200 mM), EDTA (4 mM), DTT (10 mM), and Z-RR-AMC (10 μM). Plates were read following incubation at 37 ° for 60 minutes with SpectraMax Gemini microplate spectrofluorometer, Molecular Devices (Silicon Valley, CA) (ex 355 nm, em 450 nm).

Patients with intermediate risk underwent LRP or

RALP . Anesthetic protocol The patients did not receive premedication. In the TIVA-TCI group, anaesthesia was induced with propofol (DiprivanTM, ASTRA-Zeneca, Milano, Italy) 6 μg ml−1 and remifentanyl (UltivaTM, GlaxoSmith-Kline AB, Verona, Italy) 0.4-1 μg kg−1 min, simultaneously BGB324 clinical trial administered using two separate modules of a continuous computer-assisted TCI system. Anaesthesia was maintained with propofol 4 μg ml−1 and remifentanil 0.25 μg Kg−1 min. This infusion was modified by 0.05 μg kg−1 min steps according to analgesic needs. In the BAL group, anaesthesia was induced with midazolam (Hameln pharmaceuticals Gmbh, Hameln, Germany) 0.1 mg kg−1 and fentanyl (FentanestTM, Pftzer, Latina, Italy) 1.5 μg kg−1 Anaesthesia was maintained with sevoflurane (SevoraneTM, Abbott, Latina, Italy) 2.0% , oxygen 40% and air 70% with positive pressure ventilation in a circle system, in order to achieve normocapnia. In both groups, cisatracurium besylate (NimbexTM, Glaxo Smith Kline) 0.1-0.5 mg kg−1 was given to facilitate orotracheal intubation with a cuffed tube, followed by the continuous application of 0.06-0.12 mg kg−1 h−1

via infusion pumps. Pneumoperitoneum was created by intraperitoneal insufflation of CO2 with an insufflation pressure of 13–15 mmHg and patient in the supine position. Patients Luminespib nmr were then placed in the steep Trendelenburg position (30° from horizontal). Intraperitoneal

pressure was maintained at 15 mmHg during the induced pneumoperitoneum. A routine anaesthesia monitoring was performed on all patients (Table 1). Table 1 Clinical characteristics and peri-operative data of patients with prostate cancer DOCK10 who underwent surgery with TIVA-TCI or BAL anaesthesia   TIVA-TCI (n. 54) BAL (n. 48) P Clinical data          Age (yrs) 60.66 (5.91) 62.16 (6.23) 0.31    Venous thromboembolism risk          Highest risk 54 (100%) 48 (100%) 1    Prostate cancer risk*          Intermediate-risk 26 (48.1%) 30 (62.5%)      High-risk 28 (51.8%) 18 (37.5%) 0.17    ASA, n (%):          I 4 (7.4%) 6 (12.5%)      II 50 (92.6%) 42 (87.5%) 0.39    Histological grade of cancer          G2 (Gleason 5–6) 15 (27.8%) 14 (29.2)      G3 (Gleason 7–10) 39 (72.2%) 34 (70.8%) 0.88    pT, n (%)          2 30 (55.6%) 32 (66.7%) 0.25    3 24 (44.4%) 16 (33.3%)      pN, n (%) #          0 17 (85.0%) 24 (96.0%) 0.20    1 3 (15.0%) 1 (4.0%)   Peri-operative data          Type of surgery          LRP 36 (66.7%) 34 (70.8%) 0.65    RALP 18 (33.3%) 14 (29.2%)      Time of anaesthesia (min) 107.5 (16.8) 101.4 (26.2) 0.26    Blood loss (ml) 123.3 (131.1) 121.4 (110.6) 0.81    Total amount of crystalloid received (ml) 468.5 (110.21) 496.8 (198.5) 0.27    Intra-operative body temperature 36.2 (0.3) 36.1 (0.2) 0.83    Intra-operative MAP (mmHg) 104.6 (10.5) 106.2 (10.2) 0.61    Intra-operative SpO2 (%) 96.7 (0.9) 97.8 (1.8) 0.

In this study, comparative computational methods were applied to determine the maturation pathway regulating the assembly of functional c-type cytochrome holoforms in four genera of anammox bacteria, using key protein constituents of maturation Systems I-III as biomarkers. Our analysis showed that all anammox genome assemblies contain at least one full set of System II (Ccs) genes. Methods All anammox bacteria belong to the order Brocadiales that branches deeply into the phylum Planctomycetes

and includes five genera (Kuenenia, Scalindua, Brocadia, Jettenia, and Anammoxoglobus)[10]. In this study draft genomes representative of four anammox genera were check details analyzed. Kuenenia stuttgartiensis [NCBI bioproject: PRJNA16685 [5]], Scalindua profunda [JGI: 2017108002 and 2022004002 [6]], and strain KSU-1 (representing Jettenia genus) [NCBI bioprojects: PRJDA163683 and PRJDB68 [7]] obtained as described elsewhere. Genomic data for Brocadia fulgida were obtained as described here below. Brocadia fulgida genomic data Library preparation and sequencing All kits used in this section were obtained from Life technologies (Life technologies,

Carlsbad, CA, USA). Genomic DNA, isolated using a CTAB phenol/chloroform based method, was sheared for 5 minutes using many the Ion Xpress™ Plus Fragment Ibrutinib clinical trial Library Kit following the manufacturer’s instructions. Further library preparation was performed using the Ion Plus Fragment Library Kit following manufacturer’s

instructions. Size selection of the library was performed using an E-gel 2% agarose gel. Emulsion PCR was performed using the Onetouch 200 bp kit and sequencing was performed on an IonTorrent PGM using the Ion PGM 200 bp sequencing kit and an Ion 318 chip, resulting in 5.25 million reads with an average length of 179 bp. Assembly and annotation The obtained 5.25 million reads were quality trimmed and all reads below 200 bp were discarded. The remaining 2,22 million reads were assembled using the CLC genomics workbench (v6.5.1, CLCbio, Aarhus, Denmark) with word size 35 and bubble size 5000. Brocadia fulgida accounted for 91% of the assembled reads. Contigs were assigned to Brocadia fulgida based on coverage (>30 fold). The obtained 411 contigs were annotated using Prokka 1.7.2 (Prokka: Prokaryotic Genome Annotation System – http://​vicbioinformatic​s.​com/​). After annotation, a round of manual curation was performed to correct detected frame shifts. Raw reads and assembled data are available under NCBI bioproject PRJEB4876.

Conflicts of interest Jean-Yves Reginster on behalf of the Department of Public Health, Epidemiology and Health Economics of the University of Liège, Liège, Belgium. Consulting fees or paid advisory boards: Servier, Novartis, Negma, Lilly, Wyeth, Amgen, GlaxoSmithKline, selleck kinase inhibitor Roche, Merckle, Nycomed, NPS, and Theramex. Lecture fees when speaking at the invitation of

a commercial sponsor: Merck Sharp and Dohme, Lilly, Rottapharm, IBSA, Genevrier, Novartis, Servier, Roche, GlaxoSmithKline, Teijin, Teva, Ebewee Pharma, Zodiac, Analis, Theramex, Nycomed, and Novo-Nordisk. Grant support from industry: Bristol Myers Squibb, Merck Sharp & Dohme, Rottapharm, Teva, Lilly, Novartis, Roche, GlaxoSmithKline, Amgen, and Servier. Jean-Jacques Body has received speakers and BYL719 cell line consultant fees from Amgen and Novartis, and

research support from Merck Sharp & Dohme, Novartis, Procter & Gamble, Servier, and Roche. Yves Boutsen has received speakers and/or consultant fees and/or research support from Procter & Gamble, Eli-Lilly, Daiichi-Sankyo, Merck Sharp & Dohme, Novartis, Servier, and Roche. Jean-Marc Kaufman has received speakers and/or consultant fees and/or research support from Amgen, Daiichi-Sankyo, Glaxo Smith Kline, Meck Sharp & Dohme, Novartis, Nycomed, Servier, and Roche. Stephan Goemaere has received speakers fees and/or research support from Amgen, Eli Lilly, Glaxo Smith Kline, Merck Sharp & Dohme, Novartis, Nycomed, Proctor & Gamble, Sanofi-Aventis, Servier,

and Roche. Steven Boonen has received consulting fees and/or research support from Amgen, Merck, Novartis, Nycomed, Procter & Gamble Pharmaceuticals, and Sanofi-Aventis. Pierre Bergmann has no conflict of interest. Jean-Pierre Devogelaer participated in most of trials with antiosteoporotic drugs. Serge Rozenberg has no conflict of interest. Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. References 1. Cummings SR, Black DM, Rubin SM (1989) Lifetime risks of hip, Colles’, or vertebral fracture PDK4 and coronary heart disease among white postmenopausal women. Arch Intern Med 149:2445–2448PubMedCrossRef 2. Autier P, Haentjens P, Bentin J, Baillon JM, Grivegnee AR, Closon MC, Boonen S (2000) Costs induced by hip fractures: a prospective controlled study in Belgium. Belgian Hip Fracture Study Group Osteoporos Int 11:373–380 3. Cranney A, Tugwell P, Wells G, Guyatt G (2002) Meta-analyses of therapies for postmenopausal osteoporosis. I. Systematic reviews of randomized trials in osteoporosis: introduction and methodology. Endocr Rev 23:496–507PubMedCrossRef 4.

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 PS-341 research buy 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 wavevector, the first branch has the characteristics of the RW. In contrast, the higher two SAWs leak energy SCH772984 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, 3-oxoacyl-(acyl-carrier-protein) reductase 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.