J Clin

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Mexico. Can J Microbiol 2005, 51:996–1000.PubMedCrossRef 49. Cousins D, Williams S, Liebana E, Aranaz A, Bunschoten A, Van Embden J, Ellis T: Evaluation of four DNA typing techniques in epidemiological investigations of bovine tuberculosis. J Clin Microbiol 1998, 36:168–178.PubMed 50. Zumarraga MJ, Martin C, Samper S, Alito A, Latini O, Bigi F, Roxo E, Cicuta ME, Errico F, Ramos MC, Cataldi A, van Soolingen D, Romano MI: Usefulness of spoligotyping in molecular epidemiology Capmatinib molecular weight of Mycobacterium bovis -related infections in South America. J Clin Microbiol 1999, 37:296–303.PubMed 51. Gibson AL, Hewinson G, Goodchild T, Watt B, Story A, Inwald J, Drobniewski FA: Molecular epidemiology of disease due to Mycobacterium bovis in humans in the United Kingdom. J Clin Microbiol 2004, 42:431–434.PubMedCrossRef 52. Haddad N, Ostyn A, Karoui C, Masselot M, Thorel

IKBKE MF, Hughes SL, Inwald J, Hewinson RG, Durand B: Spoligotype diversity of Mycobacterium bovis strains isolated in France from 1979 to 2000. J Clin Microbiol 2001, 39:3623–3632.PubMedCrossRef 53. Mocetinostat Costello E, O’Grady D, Flynn O, O’Brien R, Rogers M, Quigley F, Egan J, Griffin J: Study of restriction fragment length polymorphism analysis and spoligotyping for epidemiological investigation of Mycobacterium bovis infection. J Clin Microbiol 1999, 37:3217–3222.PubMed 54. Sun YJ, Bellamy R, Lee AS, Ng ST, Ravindran S, Wong SY, Locht C, Supply P, Paton NI: Use of mycobacterial interspersed repetitive unit-variable-number tandem repeat typing to examine genetic diversity of Mycobacterium tuberculosis in Singapore. J Clin Microbiol 2004, 42:1986–1993.PubMedCrossRef 55.

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PubMedCrossRef 17. Collazo find more CM, Galan JE: The invasion-associated type III system of Salmonella typhimurium directs the translocation of Sip proteins into the host cell. Mol Microbiol 1997, 24:747–756.PubMedCrossRef 18. Mashburn-Warren LM, Whiteley M: Special delivery: vesicle trafficking in prokaryotes. Mol Microbiol 2006, 61:839–846.PubMedCrossRef 19. Kesty NC, Mason KM, Reedy M, Miller SE, Kuehn MJ: Enterotoxigenic Escherichia

coli vesicles target toxin delivery into mammalian cells. Embo J 2004, 23:4538–4549.PubMedCrossRef 20. Mashburn LM, Whiteley M: Membrane vesicles traffic signals and facilitate group activities in a prokaryote. Nature 2005, 437:422–425.PubMedCrossRef 21. McBroom AJ, Kuehn MJ: Release of outer membrane vesicles by Gram-negative bacteria is a novel envelope stress response. Mol Microbiol 2007, 63:545–558.PubMedCrossRef 22. Fernandez-Moreira E, Helbig JH, Swanson MS: Membrane vesicles shed by Legionella pneumophila inhibit fusion of phagosomes with lysosomes. Infect Immun 2006, 74:3285–3295.PubMedCrossRef 23. Schooling SR, Beveridge TJ: Membrane vesicles: an overlooked component of the matrices of biofilms. J Bacteriol 2006, 188:5945–5957.PubMedCrossRef

24. Deatherage BL, Lara JC, Bergsbaken T, Rassoulian Barrett SL, Lara S, Cookson BT: Biogenesis of bacterial membrane vesicles. Mol Microbiol 2009, 72:1395–1407.PubMedCrossRef 25. Kadurugamuwa JL, Beveridge TJ: Delivery of the non-membrane-permeative antibiotic gentamicin into mammalian cells by using Shigella flexneri membrane vesicles. Antimicrob Agents Chemother 1998, 42:1476–1483.PubMed 26. Hume PJ, McGhie EJ, Hayward RD, Koronakis V: The purified Shigella IpaB and Salmonella SipB translocators CA-4948 share biochemical

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33% later apoptosis The treatment with etoposide led to 13 41% e

33% later apoptosis. The treatment with etoposide led to 13.41% early apoptosis

and 7.80% later apoptosis (Figure 8b). The results clearly reveal that the early apoptosis increased to 42.72% and later apoptosis increased to 9.90% (Figure 8c) when the cells were treated with ECCNSs. It is now well established that etoposide-induced cleavage of DNA by topoisomerase II can mediate the formation of chromosomal translocation breakpoints, leading to the expression of oncogenic factors responsible [44]. Etoposide can cause apoptosis cascade in gastric cancer cells by coupling DNA damage to p53 phosphorylation through the action of DNA-dependent protein kinase [45]. The percentage of both early apoptosis and later apoptosis in the ECCNSs-treated group remarkably increased compared click here with free etoposide alone and untreated control, which indicated that ECCNSs were able to accelerate the apoptosis processes of tumor cells. The result also revealed that etoposide entrapped in CCNSs could enhance the efficient antitumor effect. Figure 8 FACS analysis of VX770 SGC-7901 cells stained with Annexin V- FITC and PI. (a) Cells did not treat with any agents as blank control, (b) cells apoptosis induced by VP-16, (c) cells treated with the ECCNSs. In all panels, LR represents early apoptosis and UR represents late apoptosis. The CLSM image of the etoposide/ECCNSs is shown in Figure 9.

The high therapeutic SRT2104 price effect by ECCNSs was investigated by the uptake behavior in SGC-7901 cells. Thus, the effective therapy may result from the enhanced intracellular delivery, the pH-sensitive release, and protection of etoposide by ECCNSs. Etoposide (rows a, b, c) and ECCNSs (rows d, e, f) passed through the cell membrane of SGC-7901 cells and assembled in nucleus at the predetermined point of 1, 2, and 4 h. These results demonstrated that cellular uptake of SGC-7901

cell was time-dependent, and the efficient cellular uptake of ECCNSs was higher than that of the free etoposide. From the CLSM image, it could also be seen that the CCNS carriers could aggregate around the nucleus (blue fluorescence) and even directly intrude into the nucleus. Figure 9 Confocal laser scanning microscopy images of the etoposide. (Rows a, b, and c) and ECCNSs (rows d, e, f) on SGC-7901 cells. At the predetermined point of 1, 2, and 4 h. In each case, 1, 2, and 3 indicate DAPI, FITC, nearly and Merge, respectively. The scale bar represents 25 μm. Kinetic assessment of ECCNSs (Figure 10b, c, d) uptake and void etoposide (Figure 10f, g, h) in SGC-7901 cell was conducted by plotting the fluorescence peak of each sample against the different incubation times of 1 h (b, f), 2 h (c, g), and 4 h (d, h). The number of events with high intensity for 30 μg/mL etoposide increased when the incubation time continued to 4 h, pretending its uptake into cells. At the same time, etoposide did not show any significant change in fluorescence intensity compared with ECCNSs.

2004), making compilation of all species distributions a daunting

2004), making compilation of all species distributions a daunting task. Amazonia, the largest and least accessible part of the Neotropics, still harbors many regions where no plants have been collected at all; Schulman et al. (2007) reported 43% of Amazonia as devoid of botanical collections and an additional 28% as poorly collected. Species with limited or low occurrence are more likely to remain undiscovered, thus impeding the assessment of the distribution of narrow BEZ235 concentration endemic species. Given the fact that large areas generally are under-sampled, different techniques have been applied to map distribution patterns at large scale. The

first essential steps toward estimating plant biodiversity at the global scale have been made by Davis et al. (1997) and Barthlott et al. (1999, 2005) selleck inhibitor using inventory-based

data. These inventories are summary data for geographic units of varying size, mainly based on floras, regional species accounts, local checklists and plot-based data. Whereas Davis et al. (1997) collected information on all of their 234 priority sites and created sub-maps centered on these sites, Barthlott et al. (1999; 2005) estimated plant species richness for standardized units of area (10,000 km2) to derive global maps of plant species richness. In both studies, the Neotropics were indicated to be species-rich, VX-680 order but it was also noted that underlying collection data are lacking for vast parts of Amazonia (Kier et al. 2005; Kreft and Jetz 2007). As an alternative to inventory-based analyses of species richness, distribution patterns can also be obtained by overlaying maps of geographic ranges of individual species, henceforth referred to as species ranges. Basically, species ranges correspond to regions where occurrences of individuals of the species have been recorded (Gaston 1991), but various more sophisticated concepts of deriving species ranges from occurrence data

exist (Lomolino et al. 2006). For the Neotropics, two approaches to estimate angiosperm species ranges and species richness patterns have been applied. These are exclusively based on species occurrence records and do not rely on a summary of different data sources. Hopkins (2007) studied ranges Selleck Enzalutamide of 1,584 Amazonian species at 1° grid resolution. Here, species ranges were generated by extrapolating from point occurrence data sets, if neighbor occurrences were positioned within the maximum distance of roughly 500 km. The superposition of the thus derived species ranges yielded a species richness map of known species that recognized large parts of the Amazon basin as species-rich. At the same time it displayed a bias for better collected areas. In addition to this approach based on species ranges, Hopkins (2007) modeled species richness based on species numbers, using the same maximum distance of roughly 500 km. In both approaches, this predefined limit can lead to overestimation of species ranges and of species numbers.

J Clin Microbiol 2012,50(7):2299–2304 PubMedCrossRef 35 Liu H, R

J Clin Microbiol 2012,50(7):2299–2304.PubMedCrossRef 35. Liu H, Rodes B, George R, Steiner B: Molecular characterization and analysis of a gene encoding the acidic repeat protein (Arp) of Treponema pallidum . J Med Microbiol 2007,56(Pt6):715–721.PubMedCrossRef 36. Harper KN, Liu H, Ocampo PS, Steiner BM, Martin A, Levert K, Wang D, Sutton M, Armelagos GJ: The sequence of the acidic repeat protein ( arp ) gene differentiates venereal

from nonvenereal Treponema pallidum subspecies, and the gene has evolved Blasticidin S cell line under positive selection in the subspecies that cause syphilis. FEMS Immunol Med Microbiol 2008,53(3):322–332.PubMedCrossRef 37. Centurion-Lara A, Tozasertib order Castro C, Barrett L, Cameron C, Mostowfi M, Van Voorhis WC, Lukehart SA: Treponema pallidum major sheath protein homologue Tpr K is a target of opsonic antibody

and protective immune response. J Exp Med 1999, 189:647–656.PubMedCrossRef 38. Stamm LV, Greene SR, Bergen HL, Hardham JM, Barnes NY: Identification and sequence analysis of Treponema pallidum tprJ , a member of a polymorphic multigene family. Palbociclib cell line FEMS Microbiol Lett 1998,169(1):155–163.PubMedCrossRef 39. Giacani L, Molini B, Godornes C, Barrett L, Van Voorhis W, Centurion-Lara A, Lukehart SA: Quantitative analysis of tpr gene expression in Treponema pallidum isolates: Differences among isolates and correlation with T-cell responsiveness in experimental syphilis. Infect Immun 2007,75(1):104–112.PubMedCrossRef 40. Giacani L, Centurion-Lara A, Lukehart SA: Length of guanosine homopolymeric repeats modulates promotor activity of subfamily II tpr genes Aldehyde dehydrogenase of Treponema pallidum ssp. pallidum . FEMS Immunol Med Microbiol 2007,51(2):289–301.PubMedCrossRef 41. Cox DL, Luthra A, Dunha-Ems S, Desrosiers DC, Salazar JC, Caimano MJ, Radolf JD: Surface immunolabeling and consensus computational framework to identify candidate rare outer membrane proteins of Treponema pallidum . Infect Immun 2010, 78:5178–5194.PubMedCrossRef 42. Giacani L, Godornes C, Puray-Chavez M, Guerra-Giraldez C, Tompa M, Lukehart SA, Centurion-Lara A: TP0262 is a modulator of promotor activity of the tpr Subfamily II genes

of Treponema pallidum ssp. pallidum . Mol Microbiol 2009,72(5):1087–1099.PubMedCrossRef 43. Leader BT, Godornes C, Van Voorhis WC, Lukehart SA: CD4+ lymphocytes and gamma interferon predominate in local immune responses in early experimental syphilis. Infect Immun 2007,75(6):3021–3026.PubMedCrossRef 44. Van Voorhis WC, Barrett LK, Koelle DM, Nasio JM, Plummer FA: Primary and secondary syphilis lesions contain mRNA for Th1 cytokines. J Infect Dis 1996,173(2):491–495.PubMedCrossRef 45. Cruz AR, Ramirez LG, Zuluaga AV, Pillay A, Abreu C, Valencia CA, La Vake C, Cervantes JL, Dunham-Ems S, Cartun R, Mavilio D, Radolf JD, Salazar JC: Immune evasion and recognition of the syphilis spirochete in blood and skin of secondary syphilis patients: two immunologically distinct compartments. PLoS Negl Trop Dis 2012,6(7):e1717.

The cardiovascular effects of NHD, as assessed by transthoracic

The cardiovascular effects of NHD, as assessed by transthoracic

echocardiography (TTE) and cardiac magnetic resonance (CMR) imaging, have been click here a subject of recent interest. Chan et al. [6] first reported an improvement in left ventricular mass by TTE in an observational study of 28 patients on NHD over a mean follow-up of 3.4 years. A subsequent randomized controlled trial of 52 patients in Alberta also demonstrated a decrease in LV mass by CMR over a 6-month follow-up [4]. However, a more recent study randomizing 87 patients to conventional hemodialysis vs. NHD did not demonstrate any difference in LV mass as assessed by CMR in NHD patients after 1 year [7]. Little is known, however, about the effects of NHD on both atrial and ventricular remodeling as assessed by TTE and CMR in an incident NHD population… The primary objective of the study was to determine the effects of NHD on cardiovascular remodeling over a one-year follow-up using both TTE and CMR. Methods Study population All patients enrolled in the NHD training program at a single tertiary care center were asked to participate in the study from January 2009 to December 2011 inclusive. For inclusion into the training

Pexidartinib program, patients were required to be able to perform NHD, have a life expectancy greater than 12 months, and have no reliable expectation of receiving a kidney transplant within 12 months. The study protocol was approved by the University of Manitoba research ethics board GNE-0877 (REB protocol number H2008:279). Study protocol Upon enrollment into the NHD training program, patients underwent 6–10 weeks of one-on-one training with a nurse. The patients went on to perform daytime home hemodialysis for 1–4 weeks, followed by overnight extended hours hemodialysis. All patients had TTE and CMR studies performed at baseline and after 1 year of NHD. All cardiac imaging parameters were performed the day following an overnight

hemodialysis run when patients are closest to their prescribed dry weight. Demographic, clinical, and laboratory data were collected at baseline. Hematology and chemistry laboratory values were obtained monthly both pre- and post-dialysis. Parathyroid hormone and lipid profiles were measured every 3 months. Echocardiography Transthoracic echocardiography was performed using a standard echocardiography machine (GE Vivid 7, Milwaukee, WI, USA) at baseline and 12-month follow-up. Cardiac chamber dimensions and function were determined according to the American Society of Echocardiography guidelines [16]. TransLY2835219 price mitral left ventricular (LV) filling velocities were measured at the tips of the mitral valve leaflets using the apical four-chamber view and pulsed-wave Doppler. Manual tracing of the transmitral LV filling signal was performed to obtain peak early (E) and late (A) transmitral velocities, E/A ratio, and E wave deceleration time.

t Erythromycin 0 5 0 5 638 27 Tetracycline 0 25 0 25 330 27 Cipr

t. Erythromycin 0.5 0.5 638 27 Tetracycline 0.25 0.25 330 27 Ciprofloxacin 0.5 0.5 1097 17 (almost o. t.) t delay and P max show the values of the curves determined at one concentration below the MIC value. a n. d.: not determinable using the tested concentrations. b o. t.: Outside measuring time. MICs for E. coli ATCC25922 We evaluated the MICs of 12

different antibiotics for E. coli. For brevity, we present here the results for 7 antibiotics grouped by mode of action. The antibiotics used and their concentrations can be found in the corresponding LY411575 in vitro figures. All evaluations were also performed in parallel using the standard method – visual detection of turbidity at 24 hours. Unless otherwise stated, the results for the MIC determination were the same for this website calorimetry and the standard visual method. In Figs. 1, 2, 3, 4, 5 and 6, Column A shows the recorded heat flow rate data (μW = μJ/s vs. time in min.). Any time delay (t delay ) before a heat signal was recorded was the time required until there Torin 2 were sufficient numbers of active bacteria to produce a heat flow signal above the instrument’s detection limit. The highest peak in a μW vs. time curve indicates the maximum rate of heat production observed (P max ). Column B presents the results of integrating the data in Column A to show the cumulative amount of heat produced over time (J vs. time in min.).

As explained later, the Column B curves are somewhat analogous to conventional growth curves showing the increase in the number of bacteria over time. Mean slopes (ΔQ/Δt) for a given portion of an aggregate heat curve are aggregate rates of heat production and indicative of their rate of bacterial growth. Maximum values (Q max ) are related to the total numbers of cells produced by

time t. E. coli and cephalosporines of the 1st and 2nd generation. (Fig. 1). The 1st generation cephalosporine used in this study was cefazolin and its MIC for E. coli was correctly determined using IMC as 2 mg l-1 based on the recommendations of the CLSI [15]. At the MIC and higher concentrations there was essentially no growth. However, there was a slight temporary increase in heatflow at the beginning of the experiments. This suggests a slight transitory increase in metabolic activity of the bacteria present, followed by no subsequent growth. At all subinhibitory concentrations, Etofibrate heat production of E. coli was the same (same t delay , P max , ΔQ/Δt, and Q max ). Cefoxitin was used as an antibiotic representing the 2nd generation of cephalosporines although it is a member of a subgroup of this generation and also active for anaerobic bacteria. The cefoxitin MIC could also be determined correctly using IMC as 8 mg l-1. In contrast to cefazolin, there was no transient initial increase in heatflow at the MIC (Fig. 1A). Also, the profiles of the curves at subinhibitory concentrations differed markedly between cefazolin and cefoxitin (Fig. 1). For cefoxitin, t delay (Fig.

​sanger ​ac ​uk The entire nucleotide sequence, Pbsp, and the pr

​sanger.​ac.​uk. The entire nucleotide sequence, Pbsp, and the predicted amino acid sequence, PbSP, have been submitted to the GenBank database under accession number AY319300. The National Center for Biotechnology Information (NCBI) BLASTp algorithm http://​www.​ncbi.​nlm.​nih.​gov

was used to search in the non-redundant database for proteins with sequence similarities to the translated full-length PbSP cDNA. The ScanProsite algorithms http://​ca.​expasy.​org/​tools/​scanprosite/​ were used to search for motifs and conserved domains in the deduced find more protein. The presence of signal peptide was identified by using the SignalP program http://​www.​cbs.​dtu.​dk/​services/​SignalP/​, while the prediction of cellular localization was performed by using the PSORT II algorithm http://​psort.​ims.​u-tokyo.​ac.​jp/​form2.​html. this website The complete genomic sequence of Pbsp was obtained in the P. brasiliensis genomic database http://​www.​broad.​mit.​edu/​science/​projects/​msc/​data-release-summary and the promotor region was analyzed by using the Promotor scan algorithms http://​www-bimas.​cit.​nih.​gov/​cgi-bin/​molbio/​proscan. Cloning of PbSP cDNA into expression Selleckchem BLZ945 vector Oligonucleotide primers were designed to amplify the complete cDNA encoding the PbSP. The nucleotide sequence

of the sense and antisense primers were 5′-TCTGGATCCATGAAAGGCCTCTTCGC-3′ and 5′-ACACTCGAGTCCAGAGATGAAAGCGTT-3′, containing BamHI and XhoI restriction sites, respectively (underlined). The amplification parameters were as following: 94°C for 2 min, followed by 30 cycles of denaturation at 94°C for 20 s, annealing at 50°C for 20 s, and extension at 72°C for 2 min; final extension was at 72°C for 5 min. The PCR product was electrophoresed and a 1491 bp amplicon was gel excised and cloned into the pGEX-4T-3 expression vector (GE Healthcare). The recombinant plasmid was used to transform the E. coli strain C43(DE3) competent cells by using the heat shock method [29]. Ampicilin-resistant transformants were cultured, and plasmid SSR128129E DNA was analyzed by PCR and DNA sequencing, as described above. Heterologous expression of PbSP and antibody production The protein heterologous

expression was performed as described [30] with modifications. Cultures of transformed E. coli containing pGEX-4T-3 cloned with Pbsp were grown in Luria-Bertani (LB) medium supplemented with 100 μg/ml of ampicillin, at 37°C. As the cells reach the log phase (A600 0.6), IPTG (isopropyl-β-D-thiogalactopyranoside) was added to the growing culture to a final concentration of 0.5 mM to induce protein expression. After 2 h incubation, the bacterial cells were harvested by centrifugation at 5.000 g and ressuspended in phosphate saline buffer (PBS) 1×. E. coli cells transformed with pGEX-4T-3 and E. coli were used as controls. The cell extracts ressuspended in PBS 1× were electrophoresed on a 10% SDS-PAGE, followed by Coomassie brilliant blue staining.

Stickiness and clumping of the chromosomes were some of the most

Stickiness and clumping of the chromosomes were some of the most common effects

of these tested compounds on the treated root tips. Stickiness usually leads to the formation of anaphase and telophase bridges, and this ends up inhibiting post-telophase, metaphase and cytokinesis, CB-5083 manufacturer respectively, and thus hampering cell division. In vitro cytotoxicity activity by MTT assay method All the synthesized compounds prepared by Scheme I and previously reported (Chhajed et al., 2007, 2013) compounds were subjected to anticancer activity. CTC50 (cytotoxic concentration at which 50 % of the cells are dead after drug exposure) determined for test and standard compound with the help of MTT assay HEK 293 (epidermal kidney cell line), BT474 (breast cancer cell line) and Crenigacestat research buy NCI-H226 (lung cancer) cell lines by MTT method (Freshney, 2000; Edmondson et al., 1988; Prasad et al., 2005; Chiruvella et al., 2008). The viability of control cells was designated as 100 %, and the others were expressed as percentage compared to the control.

The results were compared with standard drug indisulam (ISL). The results demonstrated a strong dose-dependent growth inhibition in treated cell lines. It showed that different cells had a different sensitivity to the inhibition effect of tested compounds. The results are given in Tables 3, 4 and 5 for HEK 293, BT474 and NCI-H226. Thus, from the data, it can be concluded that all test compounds are potent Selleck Mocetinostat cytotoxic agents because of higher CTC50 at lower concentrations, and moreover, the compound (4b) (CTC50 = 0.922) and compound (7f) (CTC50 = 0.754) were found to be most potent agent among all the compounds tested against HEK 293. While compounds

(9c) (CTC50 = 0.751) and (9j) (CTC50 = 0.913) were found to be most potent agent among all the compounds G protein-coupled receptor kinase tested against BT474 and NCI-H226 cell lines, respectively. But none of tested compound was found to be potent compared to standard drug indisulam. From above all cell lines such as HEK 293, M468 and NCI-H226, it has been concluded that compounds (7f), (6f), (9b), (9c) and (9j) are more potent than all synthesized compounds. Compounds (6e) and (6b) have moderate activity than all synthesized compounds. Compounds (4a) and (9 g) have less activity than all synthesized compounds on all cell lines. Structure activity relationship of compounds showed that the presence of NH linker between aryl moiety which is substituted by electron-withdrawing group and 1,3,4-thiadiazole ring has been recognized as potent anticancer agent. Substitution on phenyl ring with chloro, methoxy and nitro group gives better anticancer activity.

It

can be seen that two series of films are only composed

It

can be seen that two series of films are only composed of TiN or TiAlN phase, while AZD8931 chemical structure no SiN x phase is detected. Veprek had attributed the absence of SiN x phase to its amorphous characteristic [4]. buy SC79 Actually, it can also be explained by low content of SiN x phase. Figure 1a,b indicates that TiN/SiN x and TiAlN/SiN x nanocomposite films both present (200) preferred orientation. With the increase of Si content, the intensities of TiN and TiAlN (200) diffraction peaks firstly increase and then decrease, suggesting that the crystallinity for TiN and TiAlN phases initially improves and then deteriorates. The TiN/SiN x and TiAlN/SiN x films exhibit the highest crystallinity when Si/Ti (or Si/Ti0.7Al0.3) ratio is 4:21 and 3:22, respectively. Figure 1 XRD patterns of (a) TiN/SiN x and (b) TiAlN/SiN x nanocomposite films with different Si content. The influence of Si content on crystallinity throws doubt upon the nc-TiN/a-SiN x model proposed by Veprek [3, 4]. If SiN x phase exists as amorphous state, the increase of Si/Ti ratio from 1:24 to 5:20 (SiN x fraction

accordingly rises from 4 to 20 at.%) only leads to thickening of amorphous SiN x interface, which cannot improve the crystallization degree of film, but lowers it due to the increasing impeditive effect AICAR manufacturer on TiN growth. In addition, as amorphous SiN x interfacial phase thickens, TiN and TiAlN phases cannot only present (200) orientation, but may also grow along other directions owing to the randomicity of isothipendyl crystallite growth [10]. Therefore, whether SiN x interfacial phase

is amorphous deserves to be further deliberated. In fact, the effect of Si content on crystallinity of TiN/SiN x and TiAlN/SiN x films brings into our mind the influence of amorphous modulation layer thickness on the crystallization degree of nanomultilayered films, such as TiN/SiC [11], TiAlN/SiO2[12], and CrAlN/SiN x [13]. In these nanomultilayered film systems, with the increase of amorphous layer thickness, the crystallization degree of films firstly increases and then decreases, which can be attributed to two facts. On one hand, the initial increase of amorphous layer thickness could not only crystallize the amorphous layer and grew epitaxially with crystal layer, but also the newly deposited crystal layer could grow epitaxially on crystallized amorphous layer, leading to the ‘mutual promotion effect’ of growth in nanomultilayers and improvement of crystallization integrity. The thicker the crystallized amorphous layer thickness is, the higher the crystallization degree of the nanomultilayered film. On the other hand, with further increase of amorphous layer thickness, the amorphous layers cannot keep the crystallization state and change back into the amorphous state, which destructs epitaxial growth structure and decreases the crystallization integrity of the nanomultilayer.