Thus, it has been widely used in the fields of renewable energy and ecological environmental protection [2–4]. However, as a wide band gap oxide semiconductor (E g = 3.23 eV), anatase TiO2 can only show photocatalytic activity under UV light irradiation (λ < 387.5 nm) that accounts for only a small portion of solar energy (approximately 5%), in contrast to visible light for a major part of solar energy (approximately 45%). Therefore, how to effectively utilize sunlight is the most challenging subject for the extensive application of TiO2 as a photocatalyst. In the past decades, many efforts have been devoted to extending the spectral response of TiO2 to visible light,

including energy band modulation by doping with elements [5–11], the

construction of heterojunctions BVD-523 ic50 by combining TiO2 with metals such as Pt or Pd [12, 13] and other semiconductors (such as MnO2[14], RuO2[15], and WO3[16]), and the addition of quantum dots [17] or dyes [18] on the surface of TiO2 for better light sensitization. Because of RXDX-106 molecular weight the unique d electronic configuration and spectral characteristics of transition metals, transition metal doping is one of the most effective approaches to extend the absorption edge of TiO2 to visible light region, which either inserts a new band into the original band gap or modifies the conduction band (CB) or valence band (VB), improving the photocatalytic activity of TiO2 to some degree [19–24]. For example, Umebayashi et al. [5] showed that the localized energy level due to Co doping was sufficiently low to lie at the top of the valence band, while the dopants such as V, Mn, Fe, Cr, and Ni produced the mid-gap states. Thalidomide Yu et al. [21] reported that the density functional theory (DFT) calculation further confirmed the red shift of absorption edges and the narrowing of the band gap of Fe-TiO2 nanorods. Hou et al. [22] showed that new occupied bands were found in the band gap of Ag-doped anatase TiO2. The formation of these new bands results from the hybridization

of Ag 4d and Ti 3d states, and they were supposed to contribute to visible light absorption. Guo and Du [23] showed that Cu could lead to the enhancement of d states near the uppermost part of the valence band of TiO2 and the Ag or Au doping caused some new electronic states in the band gap. Even though the effects of the transition metal-doped TiO2 have been investigated frequently, it remains difficult to make direct comparisons and draw conclusions due to the various experimental conditions and different methods for sample preparation and photoreactivity testing. At the same time, because of the lack of the detailed information about the effects of metal doping on crystal structures and electronic structures, there is still much dispute about these issues.

Histologically, 26 (96.3%) of 27 type Ge tumor and all 47 type G tumors were adenocarcinoma. Patients with Type G tumors tended to have earlier stage diseases than the other tumor groups. Table 2 Comparison of clinicopathological characteristics Variable Type E (SQ) (n = 12) Type E (AD) (n = 6) Type Ge (n = 27) Type G (n = 47) P-value Sex         0.906  Male 10 5 20 37    Female 2 1 7 10   Age (mean ± SD) 64.4 ± 6.84 66.3 ± 7.97 65.2 ± 10.6 66.5 ± 9.67 0.728 Extent of surgical resection         < 0.001**  Subtotal esophagectomy with partial gastrectomy 11 3 0 0    Proximal gastrectomy with partial esophagectomy 1 1 8 20    Total gastrectomy

with partial click here esophagectomy 0 2 19 27   Extent of lymph node dissection         < 0.001**  Abdominal, mediastinal and cervical 9 2 0 0    Abdominal and mediastinal 2 3 4 0    Abdominal and lower mediastinal† 1 1 17 8    Abdominal 0 0 6 39   Number of dissected lymph nodes (mean ± SD) 28.1 ± 12.1 28.7 ± 18.1 46.4 ± 34.6 35.3 ± 26.8 0.295 Pathological tumor size (mm, mean ± SD) 46.3 ± 22.4

41.5 ± 36.4 62.2 ± 18.6 37.9 ± 20.5 < 0.001** Main histological type check details         < 0.001**  Squamous cell carcinoma 12 0 1 0    Adenocarcinoma 0 6 26 47   Esophagogastric junctional invasion         < 0.001**  Yes 6 3 27 0    No 6 3 0 47   Siewert classification         < 0.001**  Type I 2 0 0 0    Type II 1 0 15 0    Type III 0 0 11 0    Not applicable 3 12 1 47   Depth of tumor invasion         0.025*  pT1 3 3 4 23    pT2 0 1 3 7    pT3 9 2 14 10    pT4 0 0 6 7   Lymph node metastasis         0.005**  pN0 3 3 8 33    pN1 6 2 6 5    pN2 2 1 5 6    pN3 1 0 8 3   Distant metastasis         < 0.001**  M0 8 5 12 47    M1 4 1 15 0   TNM Stage         < 0.001**  pStage I 2 3 4 27    pStage II 2 0 6 11    pStage III 4 2 2 9    pStage IV 4 1 15 0   * P < 0.05, ** P < 0.01. † Including lower thoracic paraesophageal, diaphragmatic and posterior mediastinal lymph node. Incidence of lymph node metastases were summarized in Table 3. Seven (58.3%) of 12 type E (SQ) tumors, 3 (50.0%) of 6 type E (AD) tumors, 19 (70.4%) of 27 type

Ge tumors and 14 (29.8%) of 47 type unless G tumors had lymph nodes metastases (P = 0.003). Although incidence of nodal metastasis in pT1 tumor was significantly lower in the type G tumor group than the other type tumor groups, there was no significant difference in pT2, pT3 and pT4 tumors among 4 tumor groups. With regard to lymph node location, no nodal metastasis in the cervical and mediastinal lymph nodes was seen in the type G tumor group. Although nodal metastases in perigastric lymph nodes were seen in all tumor types, only one nodal metastasis in intra-abdominal lymph nodes, except for perigastric lymph nodes, was recognized in type E tumor group. Nodal metastasis at the splenic hilum was seen in only in the Ge tumor group.

Comments: Trichoderma solani is phenotypically anomalous in the Longibrachiatum Clade because its growth rate is much slower at all temperatures, barely growing at 35°C, and for its small, broadly ellipsoidal to subglobose conidia. Druzhinina et al. (2012) found this species to be phylogenetically

associated with T. effusum, T. citrinoviride and T. pseudokoningii. Acknowledgments Over several years cultures for this project were provided by Toru Okuda (formerly Nippon Roche) Japan; Giovanni Vanacci, University of Pisa; Harry Evans, CABI UK; Le Dinh Don, Long Nam University, Vietnam; Enrique Arevalo, ICT Peru; Andrews Akrofi, CRIG, Ghana; Sunday Agbeniyi, CRIN, Nigeria; Pierre Tondje, IRAD, Cameroon; G. Gilles and Françoise Candoussau, Pau, France; V. Doyle, The New York Botanical Garden, and V.S. Lopez, Universidad del Papaloapan, Oaxaca, Selleck Dasatinib México; Tomas Melgarejo, Universidad Nacional Agrararia La Molina, Lima, Peru. Orlando Petrini corrected several of the Latin descriptions. Collecting in Sri Lanka was supported by NSF grant DEB 0089474 to the Dept. of Plant Pathology, The Pennsylvania State University. Work in the lab of C.P.K. was supported by the Austrian Science Foundation (grant FWF P-19340-MOB). The financial support of W.M.J. by the

Austrian Science Fund (FWF; project P22081-B17) is acknowledged. Mention of trade names or commercial products in this publication is solely for the purpose of providing specific information and does not imply recommendation or endorsement by the U.S. Department of Agriculture. The U.S. Department of Agriculture is an equal opportunity employer. Open Access This article is distributed under the terms of the Creative Staurosporine molecular weight 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 Atanasova L, Jaklitsch WM, Komoń-Zelazowska M, Kubicek CP, Druzhinina IS (2010) Clonal species Trichoderma parareesei sp. acetylcholine nov. likely resembles the ancestor of the cellulase producer Hypocrea jecorina/T. reesei.

Appl Environ Microbiol 76:7259–7267PubMedCrossRef Birky CW Jr, Adams J, Gemmel M, Perry J (2010) Using population genetic theory and DNA sequences for species detection and identification in asexual organisms. PLoS One 5(5):e10609. doi:10.​1371/​journal.​pone.​001060 PubMedCrossRef Bisby GR (1939) Trichoderma viride Pers. ex Fries, and notes on Hypocrea. Trans Br Mycol Soc 23:149–168CrossRef Bissett J (1984) A revision of the genus Trichoderma. I. Section Longibrachiatum sect. nov. Can J Bot 62:924–931CrossRef Bissett J (1991a) A revision of the genus Trichoderma. II. Infrageneric classification. Can J Bot 69:2357–2372CrossRef Bissett J (1991b) A revision of the genus Trichoderma. III. Section Pachybasium. Can J Bot 69:2373–2417CrossRef Bissett J (1991c) A revision of the genus Trichoderma. IV. Additional notes on Section Longibrachiatum.

Primary antibodies (mouse anti-human PLK-1 and β-actin monoclonal antibody, 1:2,000) (Santa Cruz Biotechnology, Santa Cruz, CA) were used, followed by incubation with horseradish peroxidase-linked secondary antibody (goat anti-mouse IgG, 1:1,000). Blots were visualized using an Enhanced Chemiluminescence kit (Cell Signaling, Danvers, MA). Therelative band density of PLK-1 to β-actin was quantified with check details Bio-Rad Quantity One 1-D Analysis Software (Bio-Rad, Hercules, CA). The experiment was performed in triplicate. Cell cycle and apoptosis analysis by flow cytometry Cell cycle and apoptosis status of HeLa cells after treatment were determined by flow cytometry. In brief, treated

cells were harvested and washed once with ice-cold 0.1 M PBS, fixed with 70% ethanol and stained with PI solution (50 μg/ml propidium iodide,

1 mg/ml RNase). Cells were then analyzed for cell cycle status by flow cytometry (FACScan, Becton Dickinson, Ixazomib concentration USA). To quantify apoptosis, cells were stained with annexin-V and PI using a Vybrant Apoptosis Assay Kit (Invitrogen) according to the manufacturer’s instructions. Hoechst 33258 staining and activity analysis of caspase-3 The morphological alterations associated with apoptosis were observed in transfected HeLa cells by microscopy using the Hoechst 33258 staining approach. At 36 h post-transfection, cells were fixed (methanol/glacial acetic acid at 3:1) for 15 min at 4°C. Hoechst others 33258 (Santa Cruz Biotechnology, Santa Cruz, CA) was added to the well at a concentration of 10 μg/ml, and cells were then incubated for 20 min at 37°C. Before observation, cells were washed three times with PBS. Caspase-3 activation was also tested with the Caspase-3 Fluorescent Assay Kit (R&D, Minneapolis, MN). Transfected cells were harvested for the assay 36 h after transfection, according to the manual. Statistical analyses Immunostaining of tissue sections was analyzed with the Chi-square test. Differences between groups in terms of mRNA analysis, cell proliferation,

and apoptosis were analyzed using a two-tailed t -test or analysis of variance (ANOVA) using SPSS 13.0 software. The significance level was set at P < 0.05. Results Expression of PLK-1 in human cervical carcinoma tissues To investigate the presence of aberrant PLK-1 expression in human cervical carcinoma tissues, we examined PLK-1 expression by immunohistochemical staining. The clinical pathologic characteristics of specimens, including tumor size, lymph node status, tumor grade, distant metastasis and biomarker expression are listed in Table 1. Of the 36 tumor sections, 32 showed positive immunostaining for PLK-1, with a positive rate of 88.9%. Examples of immunostained slides are shown in Fig. 1. Cytoplasmic and some brown nuclear staining in tumor cells served as an index of PLK-1 expression.

9 0.001 ≥10 9 45     <10 24 24     Serum albumin,g/L     20.05 0.001 ≥35 24 18     <35 9 51     TNM stage Roxadustat ic50     13.33 0.001 I-II 21 18     III-IV 12 51     Figure 1 The level

of TRAF6 protein in muscle of cancer patients and control. The expression of ubiquitin in muscle of control and cancer patients We assessed the expression of ubiquitin in 29 control muscles and 102 patient muscles. Ubiquitin was significantly upregulated in muscle of gastric cancer compared with the control muscles (P < 0.05). Ubiquitin was upregulated in 58.82% (60/102) muscles of gastric cancer. Over expression of ubiquitin in muscles of gastric cancer were associated with TNM stage and weight loss (P > 0.05) (Table 3). In order to analyze the expression of ubiquitin protein with quantitation, 8 muscle of control and cancer patients were detectec by western blotting, the study indicated the expression of ubiquitin in 5 muscle of cancer patients were higher than control (Figure 2). Table 3 The expression of ubiquitin

in muscle of cancer patients   low high χ 2 P Value Percent weight loss     11.78 0.001 ≥10 15 42     <10 27 18     Serum albumin,g/L     15.74 0.001 ≥35 27 15     <35 15 45     TNM stage     20.52 0.001 I-II 27 12     III-IV 15 48     Figure 2 The level of ubiquitin protein in muscle of cancer patients and control. Association between expression of TRAF6 and ubiquitin Seventeen cases of gastric cancer had high expression of both TRAF6 Selleck AZD6244 and ubiquitin, and eight cases of gastric cancer had low

expression of both TRAF6 and ubiquitin. There was significant between Ergoloid TRAF6 and ubiquitin expression (χ 2 =6.68; P = 0.01) (Table 4, Figure 3). Table 4 Association between expression of TRAF6 and ubiquitin Clinical parameters TRAF6   high low χ2 P ubiquitin     20.05 0.001 high 51(85.0%) 9(15.0%)     low 18(42.9%) 24(57.1%)     Figure 3 Association between expression of TRAF6 and ubiquitin. Discussion In healthy individuals, skeletal muscle metabolism requires a balance of anabolic and catabolic processes, resulting in a continuous renewal of muscle proteins without a net change in overall muscle mass. However, in cancer cachexia and other chronic illnesses, the muscle wasting were associated with the reduced rate of protein synthesis, increased protein degradation, or a combination of both contributes [13]. One common mechanism associated with skeletal muscle protein degradation in cancer cachexia is the activation of the adenosine triphosphate-dependent ubiquitin-proteasome proteolytic path way, this system plays a major role in muscle wasting [5, 6]. The study showed muscle ubiquitin mRNA was hyper expressed in gastric cancer patients compared to controls [14], the ubiquitin-proteasome proteolytic system play important role in the pathogenesis of muscle protein hyper catabolism in cancer cachexia. To investigate the role of ubiquitin expression in the skeletal muscle of gastric cancer patients.

PageRuler Prestained Protein Ladder #SM0671 marker (Fermentas) and low range molecular weight markers

RPN 755 (Amersham Biosciences) were used as molecular weight markers of proteins and LPS in the SDS-PAGE silver stained gels. Western immunoblot analysis The isolated vesicles and the different sub-cellular extracts (see below) were subjected to polyacrylamide gel electrophoresis and then blotted onto a PVDF membrane. Proteins were identified using different primary polyclonal antisera at a final dilution of 1:5000 against CdtA, CdtB, CdtC [20], an anti-Omp50 antiserum at a final dilution of 1:5000 [37], an anti-HtrA (E. coli) antiserum at a final dilution of 1:7500 [38], and anti-CRP antiserum at a final dilution of 1:3000 [39]. For CRP detection,

we used E. coli anti-CRP antiserum since the CRP proteins from C. jejuni and E. coli have 80% identity at protein level. Anti-rabbit horseradish selleck peroxidase-conjugate was used as a secondary antiserum at a final dilution of 1:20,000. SB203580 order The ECL+ chemiluminescence system was used to detect the level of chemiluminescence that was then monitored using a Flour-S MultiImager (BioRad) and by autoradiography. Lipooligosaccharide analysis and staining Lipooligosaccharide (LOS) samples were prepared from whole-cell lysates (0.1 ml samples) and OMVs (50 μl samples of the OMV preparations). The samples were subjected to complete digestion with proteinase K as described earlier [40]. The isolated LOS samples (2.5 μl of the whole cell extracts and 10

μl of the OMV extracts, respectively) were separated on 16% Tricine gels (Invitrogen, Carlsbad, CA, USA) and then silver stained [41]. Dissociation assay Vesicle samples (60 μg/ml total protein) in 50 mM HEPES (pH 7.3) were incubated on ice for 1 hour in the absence or presence of either NaCl (1 M), Na2CO3 (0.1 M) pH 10.0, Urea (8 M) or 1% SDS [28]. Samples were then centrifuged at 100,000 × g for 2 hours at 4°C and both pellet and supernatant fractions were analyzed by SDS-PAGE and immunoblot analyses using anti-CdtA, anti-CdtB, anti-CdtC polyclonal antiserum and anti-GroEL Clomifene polyclonal antiserum against E. coli GroEL protein. Before loading, the soluble proteins in the supernatant were concentrated by TCA-precipitation. Electron microscopy and immunogold labeling Samples from vesicle preparations were negatively stained with a solution of 0.1% uranyl acetate on carbon coated Formvar grids and examined under the electron microscope. Micrographs were taken with a JEOL 2000EX electron microscope (JEOL Co., Ltd., Akishima, Japan) operated at an accelerating voltage of 100 kV. For immunoelectron microscopy, a colloidal gold probe (Wako Pure Chemical Industries Ltd., Osaka, Japan) was used to label the specific reaction sites of anti-CDT sera in the specimens of OMVs from C. jejuni.

Figure 4 Phagosomal escape of F. tularensis. Colocalization of GFP-expressing F. tularensis strains and LAMP- 1. J774 cells were infected for 2 h with FK228 supplier F. tularensis strains expressing GFP (Green fluorescent protein) and, after washing, incubated for indicated time points. Fixed specimens were labeled for the late endosomal and lysosomal marker LAMP-1. 100 bacteria were scored per sample and time point. Results from a representative experiment are shown. Bars represent mean values and error bars are used to indicate standard deviations. Asterisks indicate that the colocalization differs significantly from that of LVS (*: P < 0.05; **: P < 0.01). Figure 5 Colocalization of GFP- expressing

F. tularensis strains and LAMP- 1. J774 cells were infected with the LVS, the ΔpdpC mutant, or the ΔiglC mutant expressing GFP (Green fluorescent protein) at an MOI of 200 and, after washing, incubated for 6 h. Colocalization of GFP-labeled F. tularensis and LAMP-1 on fixed and labeled specimens was analyzed SCH727965 nmr using a confocal microscope (Nikon Eclipse 90i, Nikon, Japan). Scale bar 10 μm. Figure 6 Subcellular colocalization in J774 cells of F. tularensis bacteria. J774 cells were infected for 2 h with F. tularensis strains and, after washing, incubated for 6 h. Bacteria were examined using transmission electron microscopy (TEM) and categorized into one of four categories

depending on the preservation of the phagosomal membrane. At least 100 bacteria per sample were scored. Results from a representative experiment are shown. Figure 7 Electron micrographs of J774 macrophages infected with F. tularensis. (A) Cells infected with LVS, the ΔpdpC mutant, or the ΔiglC mutant. (B) A close-up of the

ΔpdpC micrograph from A. Black arrows indicate the borders of the remaining vacuolar membranes surrounding the intracellular bacterium. These findings appeared to be contradictory, since the LAMP-1 colocalization data suggested that Vildagliptin the degree of phagosomal escape of ΔpdpC was similar to the ΔiglA and ΔiglC mutants, prototypes for the phagosomally located mutants, whereas the TEM data indicated distinct differences between the ΔiglC and ΔpdpC mutants. We believe that the findings can be reconciled, however, since the TEM data indicated that essentially no ΔpdpC bacteria were free in the cytoplasm, whereas ~ 80% were surrounded by slightly or highly damaged membranes. This unusual phenotype demonstrated that a majority of the ΔpdpC bacteria was closely adjacent to membrane parts, in agreement with the confocal microscopy data indicating that 60-75% of the bacteria colocalized with LAMP-1. Therefore, the mutant will show a high percentage of colocalization although not being confined to an intact phagosome. Thus, we conclude that PdpC directly or indirectly plays a very important role for the normal phagosomal escape.

, 2008). Thiazolidinone derivatives have been further reported to possess diverse pharmacological properties, such as antibacterial, antifungal, anticonvulsant, anticancer, antituberculosis, and antihuman immunodeficiency virus type 1 (HIV-1) activities. Thiazolidinones are AZD1152-HQPA supplier novel inhibitors of the bacterial enzyme MurB, a precursor acting during the biosynthesis of peptidoglycan as an essential component of the cell wall of both gram-positive and gram-negative bacteria. (Bonde and Gaikwad, 2004; Aridoss et al., 2007; Küçükgüzel et al., 2002; Capan et al., 1999; Barreca et al., 2001; Andres

et al., 2000; El-Gaby et al., 2009) The identification and synthesis of combinational chemotherapeutic drugs with different mechanisms of action and with few side effects are an important part of the efforts to overcome antimicrobial resistance (Bayrak et al., 2010a, b). A recent survey of novel small-molecule therapeutics has revealed that the majority of the drugs results from an analog-based approach and that their market

share check details represents two-thirds of all drug sales (Vicini et al., 2008). In the present study, as a part of our ongoing study on the synthesis of bioactive hybrid molecules, we aimed to obtain the far derivatives of linezolid. It was reported that SAR studies of linezolid demonstrated a high tolerance for structural variation at the 4-position of the phenyl ring (Weidner-Wells et al., 2002). In the structures of the newly synthesized compounds, the phenyl ring substituted by pyridine and oxazolidinone scaffold by other azole rings such as 1,3-thiazole, 1,3-thiazolidinone,

1,2,4-triazole, 1,3,4-thiadiazole, and 1,3,4-oxadiazole nucleus. Results and discussion The synthetic route for the newly synthesized compounds (3–13) is illustrated and outlined in Schemes 1 and 2. Scheme 1 Synthetic pathway for the preparation of compounds 1–6. i morpholine, ii Pd/C catalyst, H2NNH2, iii BrCH2CO2Et, iv H2NNH2, v BrC6H4CHO, vi C6H5CH=CHCHO Scheme 2 Synthetic pathway for the preparation of compounds 7–13. i CS2/KOH, ii phenyl piperazine, iii PhNCS, iv BrCH2COC6H4(4-), v NaOH, vi H2SO4, vii BrCH2CO2Et The synthesis of compound 3 was performed from the reaction of ethyl bromoacetate with compound 2 that is available commercially. Temsirolimus Then, compound 3 was converted to the corresponding hydrazide (4) by the treatment with hydrazine hydrate. The FT-IR and 1H NMR spectra of compound 4 displayed signals pointing the presence of hydrazide function, whereas the signals due to ester group disappeared in the NMR spectrum. The treatment of hydrazide, 4 with aromatic aldehydes, namely, 4-bromobenzaldehyde and cinnamaldehyde produced the corresponding Schiff bases, compounds 5 and 6. In the 1H NMR spectra of these compounds, the signal derived from NH2 group disappeared; instead, new signals originated from aldehyde moiety were recorded at the related chemical shift values in the 1H NMR and 13C NMR spectra.

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antistaphylococcal agent. Appl Microbiol Biotechnol 2008, 80:555–561.PubMedCrossRef 15. Kokai-Kun JF, Chanturiya T, Mond JJ: Lysostaphin eradicates established Staphylococcus aureus biofilms in jugular vein catheterized mice. J Antimicrob Chemother 2009, 64:94–100.PubMedCrossRef 16. Deresinski S: Bacteriophage Therapy: Exploiting Smaller Fleas. Clin Infect Dis 2009, 48:1096–1101.PubMedCrossRef 17. Soothill JS, Hawkins C, Anggard EA, Harper DR: Therapeutic use of bacteriophages. Lancet Infect Dis 2004, 4:544–545.PubMedCrossRef 18. Lang L: FDA approves use of bacteriophages to be added to meat and poultry products. Gastroenterology 2006,131(5):1370.PubMed 19. Loessner MJ: Bacteriophage endolysins-current state of research and applications. Amobarbital Curr Opin Microbiol 2005, 8:480–487.PubMedCrossRef 20. Fischetti VA: Bacteriophage lytic enzymes: novel anti-infectives. Trends Microbiol 2005, 13:491–496.PubMedCrossRef 21. Donovan DM, Lardeo M, Foster-Frey J: Lysis of Staphylococcal mastitis pathogens by bacteriophage phi11 endolysin. FEMS Microbiol Lett 2006,265(1):133–139.PubMedCrossRef 22. Paul VD, Rajagopalan SS, Sundarrajan S, George SE, Asrani JY, Pillai R, Chikkamadaiah R, Durgaiah M, Sriram B, Padmanabhan S: A novel Bacteriophage Tail Associated Muralytic Enzyme (TAME) from Phage K and its development into a potent antistaphylococcal protein. BMC Microbiol 2011, 11:226.PubMedCrossRef 23.

After that, the AsH3 flow was removed from the chamber, while TMSb (6.75×10−5) and TMIn (4.5×10−6) flows were simultaneously introduced into the reactor chamber to initiate the growth of InSb NWs. The

InSb NWs were grown for 40 min and then cooled down with the protection of only hydrogen flow (TMIn and TMSb flows were removed from the reactor chamber during cooling). For comparison, InSb layers were also grown directly on Si (111) under the same growth conditions but without InAs seed layer. The morphology of InSb structures was characterized with field-emission scanning electron microscopy (FE-SEM; JSM-6700 F, JEOL, Akishima-shi, Japan)and transmission electron microscopy (TEM; Tecnai G20, 200 keV, FEI, Hillsboro, OR, USA). Raman scattering measurements were performed in a backscattering geometry at room temperature with a Jobin Yvon HR800 confocal micro-Raman spectrometer (HORIBA, selleck chemicals llc Proteases inhibitor Kyoto, Japan), in which a 514.5-nm line of an Ar-ion laser was used as the excitation source with the focus size around 1 μm and excitation power of 0.5 mW. Results and discussion Figure 1 shows the SEM images of InSb structures with and without InAs seed layer. Clearly, InSb NWs are formed in the sample

with InAs seed layer, while no InSb NWs are observed in the sample without InAs seed layer. For the latter case, as shown in Figure 1b, only particle-like morphology is observed, instead of NWs. This indicates that InAs seed layer plays an important role in growing InSb NWs. Epitaxial growth of InSb is not trivial due to its large lattice constant (a 0 =

0.648 nm) compared to other III-V-semiconductor materials. As reported in our previous work [11], vertical InAs NWs can be directly heteroepitaxially grown on Si substrates at about 550°C (Additional file 1: Figure S1 and Additional file 2: Figure S2). Therefore, the InAs seed layer deposited at 550°C can form InAs NWs, which provide a template for the subsequent growth Lepirudin of InSb NWs. With the growth temperature being reduced to 440°C, TMIn and TMSb are introduced into the reactor chamber, and the InSb growth is initiated on the template provided by the InAs seed layer, which facilitates the formation of InSb NWs. This growth mechanism is confirmed by the chemical composition distribution along the InSb NWs, which will be discussed later. It should be noted that the parasitic growth of non-wire-like InSb material is also observed in the form of InSb structures with non-well-developed crystal faces [12]. All vertical InSb NWs are grown along the (111) direction perpendicular to Si substrate, as shown in Figure 1a. Figure 1 SEM images of InSb NWs grown on Si substrate. SEM image of the InSb NWs grown with (a) and without (b) InAs-seed-layer (tilt 45°); (c) side view of the InSb NWs showing a clear metallic droplet on their top.