Buhr DL, Acca FE, Holland EG, Johnson K, Maksymiuk GM, Vaill A, K

Buhr DL, Acca FE, Holland EG, Johnson K, Maksymiuk GM, Vaill A, Kay BK, Weitz DA, Weiner MP, Kiss MM: Use of micro-emulsion technology for the directed evolution of antibodies. Methods 2012, 58:28–33.PubMedCrossRef 61. Kiss MM, Babineau EG, Bonatsakis M, Buhr DL, Maksymiuk GM, Wang D, Alderman D, Gelperin DM, Weiner MP: Phage ESCape:

an emulsion-based approach for the selection of recombinant phage display antibodies. J Immunol Methods 2010, 367:17–26.PubMedCrossRef 62. Liu Y, Adams JD, Turner K, Cochran FV, Gambhir SS, Soh HT: Controlling the selection TEW-7197 in vitro stringency of phage display using a microfluidic device. Lab Chip 2009, 9:1033–1036.PubMedCrossRef 63. Persson J, Augustsson P, Laurell T, Ohlin M: Acoustic microfluidic chip technology to facilitate automation of phage display selection. selleck chemicals llc FEBS J 2008, 275:5657–5666.PubMedCrossRef 64. Wang J, Liu Y, Teesalu T, Sugahara KN, Kotamrajua VR, Adams JD, Ferguson BS, Gong Q, Oh SS, Csordas AT, et al.: Selection of phage-displayed peptides on live adherent cells in microfluidic channels. Proc Natl Acad Sci USA 2011, 108:6909–6914.PubMedCrossRef 65. Sorensen MD, Kristensen P: Selection of antibodies against a single rare cell present in a heterogeneous population using phage display. Nat Protoc 2011, 6:509–522.PubMedCrossRef 66. Sorensen MD, Agerholm IE, Christensen B, Kolvraa S, Kristensen P: Microselection–affinity

selecting antibodies against a single rare cell in a heterogeneous population. J Cell Mol Med 2010, 14:1953–1961.PubMedCrossRef 67. Kalyuzhnaya MG, Zabinsky R, Bowerman S,

Baker DR, Lidstrom ME, Chistoserdova L: Fluorescence in situ hybridization-flow cytometry-cell sorting-based method for separation and enrichment of type I and type II methanotroph populations. Appl Environ Microbiol 2006, 72:4293–4301.PubMedCrossRef 68. Koser CU, Ellington MJ, Cartwright EJ, Gillespie SH, Brown NM, Farrington M, Holden MT, Dougan G, Bentley SD, Parkhill J, Peacock SJ: Routine use of microbial whole genome sequencing in diagnostic and public health microbiology. PLoS Pathog 2012, 8:e1002824.PubMedCrossRef Rapamycin 69. Chan JZ, Pallen MJ, Oppenheim B, Constantinidou C: Genome sequencing in clinical microbiology. Nat Biotechnol 2012, 30:1068–1071.PubMedCrossRef 70. Studier FW: Protein production by auto-induction in high density shaking cultures. Protein Expr Purif 2005, 41:207–234.PubMedCrossRef 71. Wang Q, Garrity GM, Tiedje JM, Cole JR: Naive bayesian classifier for rapid assignment of rRNA sequences into the new bacterial taxonomy. Appl Environ Microbiol 2007, 73:5261–5267.PubMedCrossRef Competing interests The authors declare no competing financial interests. Authors’ contributions DC and FF planned the OICR-9429 nmr experiments, carried out the phage selection and the molecular studies, participated in sorting experiments, and drafted the paper. NV and SK participated in the phage selection. AEKD carried out the sorting experiment with KR and supervised the genomic analysis conducted by ARD.

Effects of heat-stress in isolated chloroplasts Photosynth Res 2

Effects of heat-stress in isolated chloroplasts. Photosynth Res 25:161–171CrossRef Cruz JA, Sacksteder CA, Kanazawa A, Kramer DM (2001) Contribution of electric field (ΔΨ) to steady-state transthylakoid proton

motive force in vitro and in vivo. Control of pmf parsing into ΔΨ and ΔpH by counterion fluxes. Biochemistry 40:1226–1237PubMedCrossRef Cruz JA, Avenson TJ, Kanazawa A, Takizawa K, Edwards GE, Kramer DA (2004) Plasticity in light reactions Cytoskeletal Signaling inhibitor of photosynthesis for energy production and photoprotection. J Exp Bot 56:395–406PubMedCrossRef Cruz JA, Avenson TJ, Kanazawa A, Takizawa K, Edwards GE, Kramer DM (2005) Plasticity in light reactions of photosynthesis for energy production and photoprotection. J Exp Bot 56:395–406PubMedCrossRef Demmig-Adams B (1992) Photoprotection and other responses of plants to high light stress. Annu Rev Plant Physiol Plant Mol Biol 43:599–626CrossRef Furbank RT, Foyer CH (1986) Oscillations in levels of metabolites from the photosynthetic carbon reduction cycle in spinach leaf disks generated by the transition from air to 5 % CO2. Arch Biochem

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We note that, due to thermal fluctuations, the curvature profile

We note that, due to thermal fluctuations, the curvature profile of the rings are constantly changing; calculating the bending strain energy for a particular case may result in a more accurate description for a single instance. Thus, we consider limiting cases only. The maximal case can be determined considering the upper bound of α = 1, wherein the entire loop may unfurl, and the minimum β. In the three-loop configuration, κ = 6π/L, while completely unfolded, κ = 2π/L, such VX-680 concentration that, for this particular structure, the lower bound of β is 1/3. With these two assumptions, (4b) Moreover, noting again that κ = 6π/L, (4c) Note that here D represents the effective

bending stiffness. We also presume that carbyne behaves as a flexible molecular chain with a temperature-dependent flexibility and finite rigidity at zero temperature. A common property of molecular chains in polymer science is the persistence length, P, defined as the characteristic length over which direction can be correlated [71], related to both temperature (T) and bending rigidity (D). For flexible molecules, the persistence length can be approximated

as P = D/k B T, where k B is the Boltzmann constant [72]. In a similar manner, persistence length is this website formulated here as a proxy for rigidity, assuming some finite persistence independent of temperature. As a consequence, the bending MRT67307 cell line stiffness, D, can be directly represented as a function of temperature: (5) where P 0 is considered the temperature-independent persistence length. In effect, the apparent bending rigidity increases with temperature,

also supported by previous theoretical results; a recent ab initio (temperature-free) investigation reports the bending stiffness to be in the order of 5.3(10-2) nN-nm2[23], while a finite temperature (300 K) molecular dynamics study reports a stiffness of approximately 13 to 20(10-2) nN-nm2[21]. Here, D 0 is the rigidity at zero temperature (as carbyne is not ideally flexible) SPTBN5 and thus is approximated as 5.3(10-2) nN-nm2. At the critical condition for unfolding, the gained strain energy (Equation 4) must be sufficient to overcome a local energy barrier, Ω, where Ω is a combination of adhesion energy and required strain energy to unfold (e.g., local increase in curvature as depicted in Figure 7 and torsional and adhesion contributions) such that ΔU b = Ω. Substituting (4) into (3c) and rearranging to solve for temperature results in (6) Using Equation 6 with the simulation results, the approximate unfolding temperature, T unfolding, can be predicted. The key assumption is that the unfolding process does not imply a constant decrease in energy (i.e., release of bending strain energy), and thus some energetic input, Ω, is required to allow deviation from the high-energy folded or looped state, which can be considered a temperature-dependent state of quasi-equilibrium.

Int J Clin Pract 60:896–905CrossRefPubMed 23 Gold DT, Safi W, Tr

Int J Clin Pract 60:896–905CrossRefPubMed 23. Gold DT, Safi W, Trinh H (2006) Patient preference and adherence: comparative US studies between two bisphosphonates, weekly risedronate selleck screening library and monthly ibandronate. Curr Med Res Opin 22:2383–2391CrossRefPubMed 24. Bouee S, Charlemagne

A, Fagnani F, Le Jeunne P, Sermet C, Naudin F, Lancry PJ (2004) Changes in osteoarthritis management by general practitioners in the COX2-inhibitor era-concomitant gastroprotective therapy. Joint Bone Spine 71:214–220CrossRefPubMed 25. Rosen CJ, Hochberg MC, Bonnick SL, McClung M, Miller P, Broy S, Kagan R, Chen E, Petruschke RA, Thompson DE, de Papp AE (2005) Treatment with once-weekly alendronate 70 mg compared with once-weekly risedronate 35 mg in women with selleck kinase inhibitor postmenopausal osteoporosis: a randomized double-blind study. J Bone Miner Res 20:141–151CrossRefPubMed 26. McCombs JS, Thiebaud P, McLaughlin-Miley C, Shi J (2004) Compliance with drug therapies for the treatment and prevention of osteoporosis. Maturitas 48:271–287CrossRefPubMed 27. Brankin E, Walker M, Lynch N, Aspray T, Lis Y, Cowell W (2006) The impact

of dosing frequency on compliance and persistence with bisphosphonates among postmenopausal women in the UK: evidence from three databases. Curr Med Res Opin 22:1249–1256CrossRefPubMed 28. Lynch N, Walker M, Cowell W, Suppapanya N, Hammerschmidt T, Rigney U (2005) An international comparison of the learn more impact of dosing frequency on adherence with bisphosphonate therapy among postmenopausal women in the UK and Germany. J Bone Miner Res 21:S180 29. Silverman S, Chesnut C, Amonkar M, Cziraky M, Barr C (2006) Improved persistence in women treated with once-monthly ibandronate versus weekly biphosphonates: a first look. J Bone Miner Res 22:SU355 30. Rosenbaum P, Rubin D (1983) The central role of the propensity score in observational studied for causal effects. Biometrika 70:41–55CrossRef 31. Cotte FE, Mercier F, De Pouvourville G (2008) Relationship between compliance and persistence with osteoporosis medications and fracture risk in primary health care in France: a retrospective case–control analysis. Clin Ther

30:2410–2422CrossRefPubMed 32. Adachi J, Lynch N, Middelhoven H, Hunjan M, Cowell W (2007) The association between compliance and persistence with bisphosphonate Selleck Ixazomib therapy and fracture risk: a review. BMC Musculoskelet Disord 8:97CrossRefPubMed 33. Siris ES, Harris ST, Rosen CJ, Barr CE, Arvesen JN, Abbott TA, Silverman S (2006) Adherence to bisphosphonate therapy and fracture rates in osteoporotic women: relationship to vertebral and nonvertebral fractures from 2 US claims databases. Mayo Clin Proc 81:1013–1022CrossRefPubMed 34. Blouin J, Dragomir A, Moride Y, Ste-Marie LG, Fernandes JC, Perreault S (2008) Impact of noncompliance with alendronate and risedronate on the incidence of nonvertebral osteoporotic fractures in elderly women. Br J Clin Pharmacol 66:117–127CrossRefPubMed 35.

0 g, 8 3 mmol) and ethylendiamine (4 2 g, 70 mmol) were dissolved

An aqueous NaOH solution (1 M) was added carefully to the solution with magnetic stirring. The precipitate was recovered by PF-02341066 chemical structure filtration, washed thoroughly with water, and then dried under vacuum, yielding (1) as a pink fluffy powder (3.21 g, 80%); 1H NMR (CDCl3): δ (ppm) 7.85

(d, 1H, VEGFR inhibitor J = 2.5 Hz), 7.44 (t, 2H, J = 6.7 Hz), 7.06 (s, 1H), 6.42 to 6.37 (m, 6H), 3.33 (q, 10H, J = 7.1 Hz), 2.91 (t, 2H, J = 6.7 Hz), 1.16 (t, 12H, J = 6.7 Hz); 13C NMR (CDCl3): δ (ppm) 170.5, 153.7, 153.3, 149.1, 133.2, 130.0, 128.4, 128.3, 123.9, 123.2, 108.6, 103.6, 97.8, 66.4, 44.4, 41.1, 39.5, 12.66. Figure 1 shows the synthesis to obtain derivative (1). Figure 1 Synthesis to obtain derivative (1). The Rh-UTES

derivative was obtained by following the next procedure (Figure 2): In a 10-mL round-bottom flask fitted with magnetic stirrer, m-xylenediisocyanate (0.05 g, 0.26 mmol) and 3-aminopropyltriethoxysilane (APTES) (0.04 g, 0.18 mmol) were refluxed in 5 mL of toluene under N2 for 12 h. Derivative (2) was used without isolation, the Rh-amine derivative (1) was added (0.1 g, 0.21 mmol) under N2, and the reaction was refluxed for 3 h. The solvent https://www.selleckchem.com/products/i-bet151-gsk1210151a.html was evaporated under reduced pressure to give a beige powder (0.22 g, 96%); 13C NMR (DMSO-d 6): δ (ppm) 168.0, 158.1, 154.2, 153.0, 148.1, 141.0, 133.2, 130.5, 128.6, 128.5, 126.2, 126.1, 126.0, 125.9, 125.7, 124.0, 122.8, 108.3, 105.3, 97.8, 64.6, 60.2, 44.1, 43.4, 40.6, 38.4, 21.2, 15.1, 14.5, 12.8; IR data: ν max (cm-1): 3331, 2970 to 2890, 1695, 1624, 1574, 1513, 1082, 962, 771. Figure 2 Synthesis of Rh-UTES (3). PSi device functionalization The binding of Rh-UTES derivative within the PSi nanostructured devices was performed following one-step method through silane chemistry by reacting the methoxy groups (-OCH3)3 of the fluorescent molecule with the siloxane (-Si-O) groups of the thermally oxidized PSi surface [18]. Briefly, the PSi samples were dipped in 2 mL of Rh-UTES derivative solution

(1.16 μM Epothilone B (EPO906, Patupilone) in ACN) at room temperature, and all of the reaction system was kept under inert atmosphere with magnetic stirring. The reaction time was fixed at 3 h to obtain the final PSiMc/Rh-UTES sensors. Metal capture Once obtained, the PSiMc/Rh-UTES sensors were exposed to 2.0 mL of mercury aqueous solutions. To assure the presence of the free Hg2+ ions, the solutions were adjusted at pH 3.0 using HNO3 0.1 M (based in the Hg speciation diagram). The complexation reactions were carried out at room temperature for 12 h under magnetic stirring. Results and discussion Rh-UTES derivative was successfully synthesized from a rhodamine base in a relatively good yield. To evaluate the metal ion binding capability of this new compound, a colorimetric evaluation was performed in a liquid phase.

Hereby we investigated the role of sgcR3 in C-1027 biosynthesis,

Hereby we investigated the role of sgcR3 in C-1027 biosynthesis, and provided an initial understanding of pathway-specific regulatory network of sgcR1, sgcR2 and sgcR3 Anlotinib supplier in S. globisporus C-1027. Results Overexpression of sgcR3 increased the production of C-1027 Computer-assisted analysis

of the sgcR3 gene product (395 aa) showed a high sequence similarity (33% identities and 47% positives) within the whole length of protein TylR of S. fradiae (Fig. 2B), a pathway-specific global activator of tyl cluster [20, 23]. To investigate the function of sgcR3, the expression plasmid of sgcR3 associated with its native promoter, named pKCR3 (see Methods), was constructed based on the multi-copy pKC1139 [30] and then introduced into S. globisporus C-1027 by conjugation. Thereafter, the resultant sgcR3 overexpression strains were fermented by incubation in liquid medium FMC-1027-1 (see Methods). The antibacterial bioassay this website against Bacillus subtilis CMCC(B) 63501 (data not shown) and the HPLC analysis indicated that the pKCR3 led to a 30–40% increase in C-1027 production (Fig. 3c)

in comparison to that in wild type strain (Fig. 3b), whereas C-1027 production level detected in the wild type strain with the parental vector pKC1139 had no difference. Therefore, the result suggested that the function of sgcR3 could be positive for C-1027 biosynthesis in selleck S. globisporus C-1027. Figure 3 Determination of C-1027 production in sgcR3 overexpression strain and disruption strain R3KO. HPLC analysis of C-1027 chromophore standard (a), C-1027 produced by wild type strain (b), one of sgcR3 overexpression strains (c) and R3KO mutant (d) are shown. Inactivation and complementation of sgcR3 In order to ascertain the contribution of sgcR3 to

the regulation of C-1027 biosynthesis, a part of coding region of sgcR3 (507 bp) was replaced PARP inhibitor with a thiostrepton resistant gene (tsr) to create the sgcR3 disrupted strain S. globisporus R3KO (Fig. 4A). Successful disruption of the intended target was confirmed by PCR using primers complementary to one end of tsr and to untouched DNA outside the disruption constructs (data not shown). Southern blot analyses authenticated the site-specific disruptions of sgcR3 using left arm for crossover and deleted part of sgcR3 gene as probes respectively (Fig. 4B, 4C). The antibacterial bioassay against B. subtilis (Fig. 4D, b) and HPLC analysis (Fig. 3d) showed that disruption of sgcR3 completely abolished C-1027 production. Figure 4 Inactivation and complementation of sgcR3. A, The plasmid pOJR3KO, constructed for sgcR3 inactivation as described in Methods, was used for gene disruption. Predicted restriction enzyme polymorphism caused by gene replacement is shown. B, BamHI; Bc, BclI; E, EcoRV. B, Southern blot hybridization of BamHI-digested chromosomal DNA of wild type strain (lane 1) and R3KO mutant (lane 2). Left arm for crossover is used as hybridization probe.

Immunity 2008, 29:319–324 PubMedCrossRef 25 von Specht BU, Knapp

Immunity 2008, 29:319–324.GSK2118436 cost PubMedCrossRef 25. von Specht BU, Knapp B, Muth G, Broker M, Hungerer KD, Diehl KD, Massarrat K, Seemann A, Domdey H: Protection of immunocompromised mice against lethal infection Nirogacestat purchase with Pseudomonas aeruginosa by active or passive immunization with recombinant P. aeruginosa outer membrane protein F and outer membrane protein I fusion proteins. Infect Immun 1995, 63:1855–1862.PubMed 26. Zuercher AW, Imboden MA, Jampen S, Bosse D, Ulrich M, Chtioui H, Lauterburg BH, Lang AB: Cellular immunity in healthy volunteers treated with an octavalent conjugate Pseudomonas aeruginosa vaccine. Clin Exp Immunol 2006, 143:132–138.PubMedCrossRef

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Pseudomonas aeruginosa in cystic fibrosis lung infection. Science 2000, 288:1251–1254.PubMedCrossRef 30. Govan JR, Harris GS: Pseudomonas aeruginosa and cystic fibrosis: unusual bacterial adaptation and pathogenesis. Microbiol Sci 1986, 3:302–308.PubMed 31. Pier GB, Meluleni G, Goldberg JB: Clearance of Pseudomonas aeruginosa from the murine gastrointestinal tract is effectively mediated by O-antigen-specific circulating antibodies. Infect Immun 1995, 63:2818–2825.PubMed 32. Belkaid Y: Regulatory T cells and infection: a dangerous necessity. Nat

Rev Immunol 2007, 7:875–888.PubMedCrossRef 33. Ueno K, Koga T, Kato K, Golenbock DT, Gendler SJ, Kai H, Kim KC: MUC1 mucin is a negative regulator of toll-like receptor signaling. Am J Respir Cell Mol Biol 2008, 38:263–268.PubMedCrossRef 34. Machen TE: Innate immune response Dapagliflozin in CF airway epithelia: hyperinflammatory? Am J Physiol Cell Physiol 2006, 291:C218–230.PubMedCrossRef 35. Skerrett SJ, Wilson CB, Liggitt HD, Hajjar AM: Redundant Toll-like receptor signaling in the pulmonary host response to Pseudomonas aeruginosa . Am J Physiol Lung Cell Mol Physiol 2007, 292:L312–322.PubMedCrossRef 36. De Luca A, Montagnoli C, Zelante T, Bonifazi P, Bozza S, Moretti S, D’Angelo C, Vacca C, Boon L, Bistoni F, Puccetti P, Fallarino F, Romani L: Functional yet balanced reactivity to Candida albicans requires TRIF, MyD88, and IDO-dependent inhibition of Rorc. J Immunol 2007, 179:5999–6008.PubMed 37. Rawling EG, Martin NL, Hancock REW: Epitope mapping of the Pseudomonas aeruginosa major outer membrane porin protein OprF. Infect Immun 1995, 63:38–42.PubMed 38.

Distribution of molecular function Gene Ontology terms associated

Distribution of molecular function Gene Ontology terms associated with HBV-human protein interactions Additional file 1, Table S8. Functional analysis of the HHBV distribution and enrichment in cellular pathways using KEGG annotations. (XLS 460 KB) MEK inhibitor review References 1. Kao JH, Chen DS: Global control of hepatitis B virus infection. Lancet Infect Dis 2002, 2: 395–403.PubMedCrossRef 2. Park NH, Song IH, Chung YH: Chronic hepatitis B in hepatocarcinogenesis. Postgrad Med J 2006, 82: 507–515.PubMedCrossRef 3. Huang TJ, Lu CC, Tsai JC, Yao WJ, Lu X, Lai MD, Liu HS, Shiau AL: Novel autoregulatory function of hepatitis B virus M protein on surface gene expression. J Biol Chem 2005, 280: 27742–27754.PubMedCrossRef

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K, Xing L, Chase MR, Vazquez A, Holthaus AM, Ewence AE, Li N, Hirozane-Kishikawa T, Hill DE, et al.: Epstein-Barr virus and virus human protein interaction maps. Proc Natl Acad Sci USA 2007, 104: 7606–7611.PubMedCrossRef 8. Wang N, Zheng Y, Yu X, Lin W, Chen Y, Jiang Q: Sex-modified effect of hepatitis B virus infection on mortality from primary liver cancer. Am J Epidemiol 2009, 169: 990–995.PubMedCrossRef 9. Settles B: ABNER: an open source tool for automatically tagging genes, proteins and other entity names in text. Bioinformatics 2005, 21: 3191–3192.PubMedCrossRef 10. Rebholz-Schuhmann D, Arregui M, Gaudan S, Kirsch H, Jimeno A: Text processing through Web services: calling Whatizit. Bioinformatics heptaminol 2008, 24: 296–298.PubMedCrossRef 11. von Mering

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One may argue that these data reflect the fact that starved bacte

One may argue that these data reflect the fact that starved bacteria do not have the resources necessary

to alter their protein expression patterns in Epigenetics inhibitor response to further stress (amoeba killing machinery) so that the kinetics of killing are altered. A resulting faster intracellular killing occurring during the 1 h-long gentamicin treatment could explain the apparent lower uptake values. However, ~20% of starved bacteria recovered at T0 after gentamicin treatment were recovered at 5 h. This is greater than observed for the heat-stressed bacteria for which the 5 h recovery was only 10% of the bacteria recovered at T0, and for which no effect on uptake was detected at T0. Therefore, the lower recoveries

observed after nutrient stress immediately after gentamicin treatment indicate decreased uptake and not enhanced initial killing. For the three other stresses tested, we did not observe any clear correlation between gene transcription and uptake by amoeba. This could indicate that the genes may be more important for intracellular survival than for uptake, which we demonstrated with the htrA mutant. Effect of pre-exposure to stress on intracellular survival in amoeba The novelty of this study is that we investigated if pre-exposure to stressful conditions may prime the bacteria for resistance to further intracellular stress. https://www.selleckchem.com/products/LY2603618-IC-83.html The bacteria that had been pre-exposed to low nutrient, heat and osmotic stress were more sensitive to intracellular killing than control C. jejuni as seen at 5 h post gentamicin treatment. These results indicate that exposure

of C. jejuni to these stresses Orotidine 5′-phosphate decarboxylase prior to interactions with amoebae not only did not prime the bacteria to fight off the amoebae killing machinery, but also strongly compromised their ability to survive within the amoebae. These findings are consistent with previous data showing that pre-exposure of C. jejuni to environmental stresses (except oxidative stress) did not promote its survival within Caco-2 cells or macrophages [45, 47]. Heat-stressed bacteria were taken up at non-stressed levels but did not survive any better than starved or osmotically-stressed bacteria that had decreased uptake. This suggests that uptake and intracellular survival rely on distinct properties of the bacteria and that the impact of each stress on either step (uptake or survival) is likely dependent on the repertoire of genes targeted by the transcriptional regulation response elicited by each stress. Conclusions The data presented indicate that environmental stresses such as nutrient starvation, heat exposure and hyper-osmolarity click here reduced the survival of C. jejuni in the absence of amoeba and also reduced its intra-amoeba survival. Starvation and, to a lower extent, osmotic stress also reduced bacterial uptake by amoebae.

Al2O3 peaks observed even for the untreated sample may originate

Al2O3 peaks observed even for the untreated sample may originate from the surface oxidation of Al film at ambient condition. Figure 4 XRD patterns of a 90-nm-thick Al film on Si substrate before and after annealing. Samples annealed for 9 h at 550°C. Figure 5 shows the variation of sheet www.selleckchem.com/products/netarsudil-ar-13324.html resistance against annealing time for a 40-nm-thick Al film on Si substrate. For comparison, the sheet resistances of an untreated and a 9-h annealed 90-nm-thick Al films are also plotted. The distribution of sheet resistances at each data CBL0137 mouse point was less than 3% around the average value, leading to the overlap of

error bars with the symbols representing the average. The sheet resistance of the sample increases by approximately

25 times after 3 h annealing at 550°C. This is an indicator that spontaneous granulation has significantly progressed and the initial Al film was substantially consumed in the middle of the process (see the particles of a variety of sizes in Figure 2b). Although the sheet resistance selleck kinase inhibitor of the sample is determined by the combined effects of particles and residual film, it is reasonable to think that the residual film is a dominant player due to the small size of the particles. Raising the annealing time further, the sheet resistance slightly increases, then almost saturates at about 260 Ω/sq, which corresponds to a 27-fold increase from the initial value. The slight increase of the sheet resistance may be caused by the further granulation and Al-Si alloying. The sheet resistances of a 40-nm-thick and a 90-nm-thick Al films after 9 h annealing are close to each other, reflecting that microparticle formation accompanying Al film consumption has maturely taken

place in both samples. The resistivity (ρ) of the untreated Al films was (3.8 to 4.1) × 10−7 Ω m when calculated using a simple relation, ρ = R s × t, where R s and t are the sheet resistance and the thickness of the film, respectively. This calculated value is more than an order of magnitude larger than the literature value [(2.65 to 2.82) × 10−8 Ω m] [16, 26], PLEKHM2 which is attributable to the presence of Al2O3 layer on the surface of Al films. The surface-oxidized microparticles of Al-Si alloys and the channel network structures of the surface-oxidized Al films are expected to cooperatively suppress the thermal conduction through the heterogeneous systems, resulting in the improved thermoelectric performance. Figure 5 Sheet resistance of a 40-nm-thick Al film on Si substrate as a function of annealing time. Annealing temperature was fixed at 550°C. The sheet resistance rapidly increases after 3 h annealing and then almost saturates. For comparison, sheet resistances of a 90-nm-thick Al film before and after 9 h annealing are also plotted.