Furthermore, Ni foam also provides a highly conductive network for electron transport during the charge and discharge processes. The endurance test was conducted using galvanostatic charging-discharging cycles at 1 A · g-1 (insert of Figure 4d). The discharge capacitance loss after 2,000 consecutive cycles is about

20%. The specific capacitance degradation is estimated to be from 263 to 205 F · g-1 (Figure 4d). Although the Ni foam serves as a conductive matrix to promote fast Faradaic charging and discharging of the Mn3O4 nanorods, its loose structure leads to the flaking off of the nanorods from the Ni foam substrate. Time-dependent mTOR inhibitor Mn3O4/Ni foam composite properties To shed light on the formation process, temporal evolution of the Mn3O4 nanostructures was studied by examining the products obtained under different reaction times of 1, 4, and 8 h. XRD patterns and Raman spectra LY2603618 were measured to identify the components of the different samples. The XRD patterns of the composite obtained under 1 h can be indexed to MnO2 and Mn3O4 crystal structures (Figure 5a). For the composites obtained under 4 and 8 h, the intense XRD peak at 2θ ≈ 19°disappeared corresponding to the MnO2 (200) crystal structures and the left peaks attribute to the Mn3O4 crystal structures. Figure 5b shows the Raman spectra of the powder scratched from composite electrodes. The peak MK-0457 cost position of composites

obtained under 4 and 8 h are red shifted compared with that of the composite obtained under 1 h. As is known, the Raman spectra for the MnO2 DCLK1 phase and the Mn3O4 phase are located at 638.5 cm-1 and 652.5 cm-1, respectively [31]. Therefore, this red shift of Raman spectra indicates the component variation from the MnO2 phase to Mn3O4, which is in excellent agreement with the result obtained from the XRD study. The SEM images of products obtained under different reaction times of 1, 4, and 8 h are shown in Figure 6. The products collected after 1 h consisted of nanosheets with a thickness of about 30 nm (Figure 6a,b). When the reaction

time increases to 4 h, some nanorods accompanied with nanoparticles begin to appear (Figure 6c,d). As the reaction proceeds to 8 h, the nanosheets disappeared and all of the products are nanorods with few nanoparticles (Figure 6e,f). After 10 h of the hydrothermal reaction, well-defined nanorods are obtained (Figure 3c,d). Based on the time-dependent morphology evolution described above, the formation mechanism of Mn3O4 nanorods can be proposed. At the initial stage, a large number of nanocrystallites nucleate and grow into nanosheets to minimize the overall energy of the system. However, the nanosheets are just intermediate products and not stable. After the reaction for 4 h, some of the nanosheets dissolve with the emergence of nanorods with some nanoparticles. When the reaction proceeds for 8 h, all of the nanosheets have transformed into nanorods with nanoparticles.

PubMedCentralPubMedCrossRef 23. Bomfim MR, Barbosa-Stancioli EF, Koury MC: Detection of pathogenic leptospires in urine from naturally infected cattle by nested PCR. Vet J 2008,178(2):251–256.PubMedCrossRef 24. Suwimonteerabutr J, Chaicumpa W, Saengjaruk P, Tapchaisri P, Chongsa-nguan M, Kalambaheti T, Ramasoota P, Sakolvaree Y, Virakul P: Evaluation

of a monoclonal selleck screening library antibody-based dot-blot ELISA for detection of Leptospira spp in bovine urine samples. Am J Vet Res 2005,66(5):762–766.PubMedCrossRef 25. Bal AE, Gravekamp C, Hartskeerl RA, De Meza-Brewster J, Korver H, Terpstra WJ: Detection of leptospires in urine by PCR for early diagnosis of leptospirosis. J Clin Microbiol 1994,32(8):1894–1898.PubMedCentralPubMed 26. Bolin CA, Zuerner RL, Trueba G: Comparison of three techniques to detect Leptospira interrogans serovar Hardjo type hardjo-bovis in bovine urine. Am J Vet Res 1989,50(7):1001–1003.PubMed 27. Rai AJ: The urinary proteome. 2010, 641:361. https://​library.​plantandfood.​co.​nz/​cgi-bin/​koha/​opac-detail.​pl?​biblionumber=​18633.CrossRef 28. Haake DA: Hamster model of leptospirosis. Curr Protoc Microbiol 2006,Chapter

12(Unit 12E):2.PubMed 29. Sigdel TK, Kaushal A, Gritsenko M, Norbeck AD, Qian WJ, Xiao W, Camp DG 2nd, Smith RD, Sarwal MM: Shotgun proteomics identifies proteins specific for acute renal transplant rejection. Proteomics Clin Appl 2010,4(1):32–47.PubMedCentralPubMedCrossRef check details 30. Loftheim H, Midtvedt K, Hartmann A, Reisaeter AV, Falck P, Holdaas H, Jenssen T, Reubsaet L, Asberg A: Urinary proteomic shotgun ICG-001 molecular weight approach for identification of potential acute rejection biomarkers in renal transplant recipients. Transplant Res 2012,1(1):9. http://​www.​transplantationr​esearch.​com/​content/​1/​1/​9

PubMedCentralPubMedCrossRef 31. Burtis CA, Ashwood ER, Tietz NW: Tietz Textbook of Clinical Chemistry. 3rd edition. Philadelphia: W.B. Saunders; 1999. 32. Varghese SA, Powell TB, Budisavljevic MN, Oates JC, Raymond JR, Almeida JS, Arthur JM: Urine biomarkers predict the cause of glomerular disease. J Am Soc Nephrol 2007,18(3):913–922.PubMedCentralPubMedCrossRef Teicoplanin 33. Riaz S, Skinner V, Srai SK: Effect of high dose thiamine on the levels of urinary protein biomarkers in diabetes mellitus type 2. J Pharm Biomed Anal 2011,54(4):817–825.PubMedCrossRef 34. Burns KD, Hiremath S: Urinary angiotensinogen as a biomarker of chronic kidney disease: ready for prime time? Nephrol Dial Transplant 2012,27(8):3010–3013.PubMedCrossRef 35. Penders J, Delanghe JR: Alpha 1-microglobulin: clinical laboratory aspects and applications. Clin Chim Acta 2004,346(2):107–118.PubMedCrossRef 36. Short CD, Durrington PN, Mallick NP, Hunt LP, Tetlow L, Ishola M: Serum and urinary high density lipoproteins in glomerular disease with proteinuria. Kidney Int 1986,29(6):1224–1228.PubMedCrossRef 37.

avium [34, 52]. The GPL produced by this serotype is not well characterised, but the presented results indicate that they may be able to produce biofilm despite the apparent lack of some genes involved in production of the most common nsGPL. As stated above, GPL has been associated

with biofilm forming abilities. In the present study, presence of the GPL genes tested was not correlated with biofilm formation, but an association might be due to expression and not presence of the genes. The significant differences in biofilm forming abilities observed between porcine and human TGF-beta family isolates are surprising since these isolates were very similar when tested for other characteristics. BI 2536 purchase Other studies have reported that isolates of human origin may form biofilm [30,

33], so although a significant difference in biofilm formation was observed between human and porcine isolates of M. avium subsp. hominissuis in the present study, this is not a consistent difference. The ability to invade bronchial epithelial cells has been demonstrated to be impaired in biofilm deficient mutants of CB-839 the M. avium strain A5, and the same mutants had an impaired ability to cause infection in mice [53]. It has thus been suggested that the ability of an isolate to form biofilm is linked to virulence. Biofilm forming isolates may also reach their hosts in large numbers if loosening in clusters from a naturally occurring biofilm. The condition of the host may differ between humans and swine. Human hosts are often immunocompromised or have predisposing lung conditions [6, 54], while porcine hosts probably

are not. Swine rarely present with clinical disease caused by M. DNA ligase avium subsp.hominissuis [4]. It could be speculated that swine get infected only when exposed to a large infective dose of the bacterium, for instance originating from naturally occurring biofilms, or that these biofilm related isolates are more virulent. This may lead to a selection for biofilm forming isolates in swine, explaining the differences observed in the present study. Conclusion An optimised method to screen isolates of Mycobacterium avium for biofilm formation was established, and this method was used to examine 97 isolates retrieved from humans, swine and birds. Nine isolates, all of porcine origin, formed biofilm. No correlation was found between the ability of the isolates to form biofilm with the presence of selected GPL genes. The biofilm forming isolates were not related by RFLP or hsp65 sequencing. The differences observed between the porcine and human isolates raises questions regarding their biofilm forming abilities and the importance of biofilm production for their infectious potential. Acknowledgements We would like to thank Prof. Tone Tønjum (Rikshospitalet University Hospital, Norway) and Dr. Ulf R.

Urology 1999,54(3):567–72.PubMedCrossRef 10. Weidner N, Carroll PR, Flax J, Blumenfeld W, Folkman J: Tumor angiogenesis correlates with metastasis in invasive prostate carcinoma. Am. J. Pathol. 1993,143(2):401–9.PubMed 11. Gerber HP, Vu TH, Ryan AM, Kowalski J, Werb Z, Ferrara N: VEGF couples hypertrophic cartilage remodeling, ossification and angiogenesis during endochondral bone formation. Nat Med 1999,5(6):623–8.PubMedCrossRef 12. ldfarb SB, Hudis C, Dickler MN: Bevacizumab in metastatic breast cancer:

when may it be used? Ther Adv Med Oncol 2011,3(2):85–93. 13. Di Costanzo F, Mazzoni F, Micol Mela M, Antonuzzo L, Checcacci D, Saggese M, Di Costanzo F: Bevacizumab in non-small cell lung cancer. Drugs 2008,68(6):737–46.PubMedCrossRef 14. deGramont A, Van Cutsem E: Investigating the potential of bevacizumab in other indications: metastatic IDO inhibitor renal cell, non-small cell lung, pancreatic and breast cancer. Oncology 2005,69(suppl 3):46–56.CrossRef 15. Amselem L, Cervera E, Díaz-Llopis M, Montero J, Garcia-Pous M, Udaondo P, García-Delpech S, Salom D: Intravitreal bevacizumab

(Avastin) for choroidal metastasis secondary to breast carcinoma: short-term follow-up. Eye 2007,21(4):566–567.PubMed 16. Zondor SD, Medina PJ: see more Bevacizumab: an angiogenesis inhibitor with efficacy in colorectal and other malignancies. Ann. Pharmacother. 2004,38(7–8):1258–1264.PubMed 17. Brekken R, Overholser J, Stastny V, Waltenberger J, Minna JD, Thorpe PE: Selective inhibition of vascular endothelial growth factor (VEGF) receptor 2 (KDR/Flk-2) activity by a monoclonal anti-VEGF antibody blocks tumor growth in mice. Cancer Res. 2000,60(18):5117–5124.PubMed 18. Yang H, Jager MJ, Grossniklaus HE: Bevacizumab suppression of establishment of micrometastases in experimental ocular melanoma.

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Similarly, Student 6 indicated that she can not ever think of herself as marrying a non-Turkish person because she does not feel comfortable expressing her feelings in English. She said, How am I supposed to talk about my problems with my partner in my second language? It takes away from the whole interaction. This is why I have not changed at all. I think that all of my interactions with Americans are superficial because of language barriers. How am I supposed to TH-302 datasheet say “I love you” to the person I love in English? I can’t just say ‘I love you’. Discussion In this study we aimed at getting a better understanding about how international students’

expectations and attitudes changed vis-à-vis Buparlisib mw romantic relationships. Given that the US, characterized as an individualistic culture, is very different than the collectivistic Turkish culture, we expected that participants would experience a significant amount of change in their expectations and attitudes toward romantic relationships.

Using a grounded theory approach, we wanted to capture their experiences. CB-5083 When exploring the topics in which participants experienced ‘change’, we came across five different themes: frequent occurrence and acceptance in the host country, accepting of others but not of self, less social control in the host country, increased sense of individualism, and feeling more strongly and protective of the values of the home country. On the other hand, when exploring the topics in which participants experienced ‘no change’, we identified three main themes: no change because of religious beliefs, no change because

of cultural and societal values, and no change because of social isolation stemming from language barriers. Overall, for those who have changed, it seems that living in the US made them more accepting of certain topics whereas for others who have not changed, maintaining their cultural heritage was more important. This is in line with eltoprazine the two main dynamics underlined in Berry’s (1997) acculturation strategies of immigrants: acceptance (or not) of the dominant culture and maintenance of cultural heritage. Berry suggests that people who become accepting of the host culture’s values either get assimilated or integrated depending on their level of maintenance of cultural heritage. In other words, an immigrant who embraces both the values of the host and the home culture becomes integrated into the host society, which is ideal, whereas those who lose touch with their home culture’s values become assimilated (Berry et al. 2002). Although international students are technically not immigrants, most of them stay in the country for at least 2 or 3 years and experience the American life to the fullest, with limited access to their home country.

In cervical cancer, although the prognostic relevance of micrometastases has not yet been established, Juretzka et al recommend adjuvant radiotherapy in the event of detection VEGFR inhibitor of micrometastases [69]. Marchiolè et al found that the relative risk of recurrence in presence of true micrometastases (focus of metastatic disease ranging from 0.2 mm to no more

than 2 mm) was 2.30 (CI: 1.65-3.20, p < 0.01) and 2.22 (CI: 1.30-3.80, p = 0.09) in the presence of submicrometastases (focus of metastatic disease no more than 0.2 mm including the presence of single non cohesive tumour cells) [13]. These authors addressed the issue of adjuvant therapy in patients with both lymphovascular space involvement and micrometastases [13]. However, despite a high incidence of micrometastases in cervical cancer, Coutant et al PR 171 failed to demonstrate a relation between the presence of micrometastases or submicrometastases and the recurrence rate, probably due to the small sample size and a relative short follow-up [29]. In early stage endometrial cancer, Yabushita et al. [22] analyzed the relation between disease recurrence and presence of micrometastases by IHC in pelvic lymph nodes. Although in their report, the term micrometastases is used to refer to metastases in which tumor cells were detected

only by the IHC method and the term occult metastasis refers to the presence of tumor cell fragments, the authors found that micrometastases in lymph node was associated with recurrence of disease in univariate (p < 0.0001) and multivariate analysis (p = 0.009). However, as for cervical cancer, the debate on whether the detection of micrometastases could be an indicator of adjuvant therapy continues. Conclusion Although accumulating data emphasize the contribution of serial sectioning and IHC to detect micrometastases, the clinical implications of ultrastaging on adjuvant therapy remains a matter of debate in uterine cancers. References

1. Cote RJ, Peterson HF, Chaiwun B, Gelber RD, Goldhirsch A, Castiglione-Gertsch M, Gusterson B, Neville AM: Role of immunohistochemical detection of lymph-node metastases in management of breast cancer. International Breast SB431542 order cancer Study Group. Lancet 1999,354(9182):896–900.PubMedCrossRef 2. Reich Cediranib (AZD2171) O, Winter R, iegl B, Tamussino K, Hass J, Petru E: Does the size of pelvic lymph nodes predict metastatic involvment in patient with endometrial cancer? Int j Gynecol Cancer 1996, 6:4.CrossRef 3. Joseph E, Messina J, Glass FL, Cruse CW, Rapaport DP, Berman C, Reintgen DS: Cancer J Sci Am. 1997,3(6):341–345.PubMed 4. Saha S, Bilchik A, Wiese D, Espinosa M, Badin J, Ganatra BK, Desai D, Kaushal S, Singh T, Arora M: Ultrastaging of colorectal cancer by sentinel lymph node mapping technique–a multicenter trial. Ann Surg Oncol 2001, 8:94S-98S.PubMed 5. Cserni G: Axillary staging of breast cancer and the sentinel node.

Robust MLPA Akt cancer clusters of strains with identical STs or belonging to CCs were identified among the population, mainly among the 3 main clades this study. Each of these clusters LY3039478 in vivo included a limited number of strains (2 to 6 strains) that were further shown to be unrelated based on epidemiological data and/or PFGE results, and 52 out of the 191 fully analyzed strains (27.2%) were involved in these clusters. Twelve clusters grouped

strains from a unique host, i.e., a fish-associated subset within A. salmonicida and 11 human-associated subsets within the A. veronii (n = 6), A. caviae (n = 3) and A. hydrophila (n = 2) clades. Nine of these subsets included only disease-associated strains. Notably, all of the A. veronii human-associated clusters were disease associated. Among these clusters, ST13, which was shared by 6 strains of human origin and was mainly recovered during wound infections, may reflect a host (niche)-adapted pathogenic cluster among the A. veronii clade, which was otherwise characterized by high genetic diversity. The striking, unique PFGE pattern and ST may reflect the adaptation of this cluster to a niche in which genetic and genomic variability is not permitted due to strong constraints. However, because of the small number of strains included in these clusters, an increased number of strains should be studied to confirm whether specific lineages or CCs are more likely to contain

clinical isolates or be associated with a specific illness. The present this website study showed a relatively low frequency of recombination events compared to previous studies [15, 28]. This result may originate in the differences between these studies in the genes evaluated and the population sampling strategies employed. The population sample studied by Martino et al. differed significantly from ours, as most of their isolates were obtained from fish, crustaceans

or mollusks [15]. Silver et al. deliberately included a very small number of isolates (n = 12) of host-associated strains (e.g., only strains isolated from leeches, human wounds or human feces), which may constitute a recruitment bias because these strains may be host Tideglusib adapted [28]. Interestingly, the recombination events encountered in our study were predominantly observed within clonal complexes (e.g., CC “D”, grouping A. veronii strains recovered during human diarrhea episodes), which supported the previous hypothesis of the study by Silver et al. [28]. Taxonomic considerations MLPA may be helpful for identification purposes. Indeed, strains that have previously rarely been reported in the literature were recognized among the study population, among which an A. jandaei isolate from a human urinary tract infection and an A. allosaccharophila strain recovered during human bacteremia were particularly remarkable. Moreover, MLPA may allow the correct identification of strains deposited in strain collections under erroneous or incomplete nomenclature, as observed for A.

In CKD-MBD, serum Ca and P concentrations are measured at every visit. Serum Ca concentration needs to be corrected if hypoalbuminemia exists. In CKD stages 3–5, serum PTH is measured at least once a year. If it is found out of an optimal range, consultation with nephrologists is recommended. In CKD stages 3–5, administration of active vitamin D and calcium regimens used for osteoporosis may be reduced in dose. Abnormal mineral and bone metabolism in CKD Hypocalcemia, hyperphosphatemia, and disordered vitamin D metabolism in the kidney

are intricately involved in the pathophysiology of abnormal bone and www.selleckchem.com/products/Romidepsin-FK228.html mineral metabolism in CKD. Furthermore, CKD-MBD may be associated with osteoporosis related to aging or menopause or

with corticosteroids used for underlying diseases, such as glomerulonephritis and nephrotic syndrome. In case of abnormal bone and mineral metabolism related to CKD, consultation with nephrologists is recommended. Diagnosis Secondary hyperparathyroidism appears in CKD stages 3–5. According to the K/DOQI guidelines, an intact PTH (i-PTH) level ≥70 pg/mL is suggestive of secondary hyperparathyroidism. Osteoporosis is diagnosed if there is a history of bone fracture or bone mineral SN-38 density measurement is less than 70% of the mean value of young adults (YAM). If the bone mineral density is between 70 and Avelestat (AZD9668) 80% of YAM, a diagnosis of suspected SC79 manufacturer osteoporosis is made. Therapy and follow-up (Tables 22-1, 22-2) Table 22-1 Calcium and phosphate in CKD 1. Under steroid treatment

(CKD stage 1, 2) Give bisphosphonate if persistent use of steroid for more than 3 months. If it is impossible due to adverse reactions, such as gastrointestinal symptoms or pregnancy, give active vitamin D or vitamin K (Japanese Society for Bone and Mineral Research). In CKD stage 3, bisphosphonate can be used; however, it may not be safe. There is a report that PTH may rise with bisphosphonate, therefore, use it with professional acumen 2. Treatment of mineral and bone disorder (CKD-MBD)  (1) CKD stage 3, 4   In case of GFR < 60 mL/min/1.73 m2, PTH will increase. Start controlling serum level of phosphate. Restrict protein intake; if not sufficient, give phosphate binders such as CaCO3. If high PTH continues, start low dose of active vitamin D. With progress of CKD stage, control of serum phosphate becomes difficult. If hyperphosphatemia is present, vascular calcification may occur with vitamin D. Vitamin D may need to be decreased or stopped  (2) CKD stage 5   Should be treated by nephrologists Quoted, with modification, from: K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease, edited by the National Kidney Foundation.

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waste water treatment. J Lumin 2012,132(7):1668–1677. doi: 10.​1016/​j.​jlumin.​2012.​02.​031 CrossRef 23. Patterson A: The Scherrer formula for X-ray particle size determination. Phys Rev 1939,56(10):978.CrossRef 24. Rahim A, Abdel Hameed R, Khalil M: Nickel as a catalyst for the electro-oxidation of methanol in alkaline medium. J Power Sources 2004,134(2):160–169.CrossRef 25. Fan C, Piron D, Sleb A, Paradis P: Study of electrodeposited nickel-molybdenum, nickel-tungsten, cobalt-molybdenum, and cobalt-tungsten as hydrogen electrodes in alkaline water electrolysis. J Electrochem Soc 1994,141(2):382–387.CrossRef 26. Raj IA, Vasu K: Transition metal-based hydrogen electrodes in alkaline solution – electrocatalysis on nickel based binary alloy coatings. J Appl Electrochem 1990,20(1):32–38.CrossRef 27. Fleischmann M, Korinek K, Pletcher D: The oxidation of organic compounds at a nickel anode in alkaline solution. J Electroanal Chem

Interfacial Electrochem 1971,31(1):39–49.CrossRef 28. Vuković M: Voltammetry and anodic stability of a hydrous oxide film on a nickel electrode in alkaline solution. J Appl Electrochem 1994,24(9):878–882.CrossRef Phosphoprotein phosphatase 29. Enea O: Molecular structure effects in electrocatalysis – II. oxidation of d-glucose and of linear polyols on Ni electrodes. Electrochim Acta 1990,35(2):375–378.CrossRef 30. Geng D, Lu G: Dependence of onset potential for methanol electrocatalytic oxidation on steric location of the active center in multicomponent electrocatalysts. J Phys Chem C 2007,111(32):11897–11902.CrossRef 31. Shukla A, Christensen P, Hamnett A, Hogarth M: A vapour-feed direct-methanol fuel cell with proton-exchange membrane electrolyte. J Power Sources 1995,55(1):87–91.

Nevertheless, this deduction needs to be verified from HRTEM observations. Figure 2 presents the typical cross-sectional HRTEM images of TiN/SiN x film with Si/Ti selleckchem ratio of 4:21 and TiAlN/SiN x film with Si/Ti0.7Al0.3 ratio of 3:22. From Figure 2a,c, it is clear that similar with TiN and TiAlN monolithic films, both nanocomposite films show obvious columnar growth structure, in agreement with results from Zhang et al. [7] and Kauffmann et al. [8]. This columnar growth structure

cannot be explained by the nc-TiN/a-SiN x model. According to the model [4, 14], with the addition of Si AZD8931 element, the amorphous SiN x interfacial phase interrupted the columnar growth of TiN and divided into many equiaxed TiN nanocrystallites. In this case, the columnar cross-sectional morphology should not be observed, but the amorphous fracture morphology as presented in [15]. However, the columnar cross-sectional structure is obviously observed in both TiN/SiN x and TiAlN/SiN x films, which brings further question to nc-TiN/a-SiN x model. Figure 2 Cross-sectional HRTEM images of TiN/SiN x and TiAlN/SiN x nanocomposite films.

(a) Low magnification, (b) medium magnification, (d) high magnification for TiN/SiN x nanocomposite Dinaciclib ic50 film (Si/Ti = 4:21), and (c) low magnification, (e) high magnification for TiAlN/SiN x nanocomposite film (Si/Ti0.7Al0.3 = 3:22). The SiN x interfacial PLEKHB2 phase is observed to exist as crystallized state, rather than amorphous state, such as E zone between A and C crystals, F zone between A and B crystals, H zone between B and D crystals, and G zone between C and D crystals. From Figure 2a, it can also be seen that many small equiaxed nanocrystallites exist within the TiN/SiN x film in the cross-sectional morphology. In the medium-magnification

image of Figure 2b, it is obvious that many equiaxed nanocrystallites with dark contrast are surrounded by the interfacial phase with bright contrast. According to the nanocomposite structure of TiN/SiN x film, it is not difficult to conclude that the equiaxed nanocrystallites with dark contrast and interfacial phase with bright contrast correspond to TiN and SiN x phases, respectively, indicating that the film constituted of equiaxed TiN nanocrystallites encapsulated with SiN x interfacial phase, rather than columnar-like TiN nanocrystals proposed by Kong et al. [5]. The average size of TiN crystallite is about 6 to 10 nm, with average SiN x interfacial thickness of 0.5 to 0.7 nm. In the high-magnification image of Figure 2d, the TiN crystallites basically grow along with the same direction and present the epitaxial growth structure.