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Oral Dis 2009,15(6):388–399.PubMedCrossRef

4. Altekruse SF KC, Krapcho M, Neyman N, Aminou R, Waldron W, Ruhl J, Howlader N, Tatalovich Z, Cho H (Eds): SEER Cancer Statistics Review, 1975–2008. Bethesda, MD: National Cancer Institute; 1975–2008. posted to the SEER web site, 2011, based on November 2010 SEER data submission 5. Johnson NW, Jayasekara P, Amarasinghe AAHK: Squamous cell carcinoma and Momelotinib precursor lesions of the oral cavity: epidemiology and aetiology. Periodontol 2011,57(1):19–37.CrossRef 6. Tanaka T, Tanaka M, Tanaka T: Oral carcinogenesis and oral cancer chemoprevention: learn more a review. Pathol Res Int 2011 2011, 10 pages. Article ID 431246 7. Tsantoulis PK, Kastrinakis NG, Tourvas AD, Laskaris G, Gorgoulis VG: Advances in the biology of oral cancer. Oral Oncol 2007,43(6):523–534.PubMedCrossRef 8. Lax AJ, Thomas W: How bacteria could cause cancer: one step at a time. Trends Microbiol 2002,10(6):293–299.PubMedCrossRef

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End points of interest were objective response rate (ORR), overall survival (OS), and event-free survival (EFS). Statistical analysis To estimated ORR, the patients were divided into responders and non-responders. The responders were defined as complete response (CR) and partial response (PR) and the non-responders including stable disease

(SD) and progressive disease (PD). The pooled odds ratio (OR) and its 95% confidence intervals (CIs) were calculated by the methods proposed by Mantel and Haenszel [11], or by DerSimonian R and Laird N [12]. For time-to-event data-OS and EFS, the hazard ratios (HRs) and associated 95% confidence interval (CI) were Nocodazole mouse estimated using the methods reported by Parmar [13]. The between study heterogeneity

was determined by Q test and I 2 metric (I 2 = 0–25%: no heterogeneity; I 2 = 25–50%: moderate heterogeneity; I 2 = 50–75%: large heterogeneity; I 2 = 75–100%: extreme heterogeneity) [14]. The fixed-effect model was applied in the initial analysis, and if the significant selleck chemicals llc heterogeneity existed, then the confirmed random-effect model was used. Begg’s test was click here used to evaluate the publication bias. P < 0.05 indicated significant publication bias [15]. All P value was two-tailed, and STATA version 11.1 (Stata Corporation, USA) was used to perform the most of data analysis. Results Eligible studies 188 potentially relevant studies were identified HAS1 through the search strategy. After checking the title and abstract, 134 studies excluded because it was very clear that their design didn’t meet our inclusion criteria. Then the full texts of 54 articles were carefully screened, 29 studies were excluded as data insufficiency that we could not extract the data for analysis, 2 studies were excluded for potential data overlap

as the same institute conducted the research and their patients recruitment time may exist overlap. Finally, a total of 23 studies were eligible for the final analysis. Among them, 19 studies estimated the relationship between BRCA1 and platinum-based chemotherapy outcome [10, 16–33], 3 were toxal-based [34–37]. Additional one studies evaluated the toxal-based in fist-line chemotherapy and a part of patients received platinum-based treatment [36]. The study selection process was showed in Figure 1. Figure 1 The flow chart of study selection and exclusion. Study characteristics Our meta-analysis composed 23 studies [10, 16–37] including 2606 NSCLC patients. The sample size variant from 34 to 769, 17 studies were about East-Asian population [16–25, 27, 28, 30, 32–34, 37], 5 studies were about Caucasian [10, 26, 29, 35, 36] and 1 studies may contain different races as the samples were from the prospective randomized clinical trial International Adjuvant Lung Trial (IALT) [31].

Mol Microbiol 2008,69(4):784–793.PubMedCrossRef 34. White R, Chiba S, Pang T, Dewey JS, Savva CG, Holzenburg A, Pogliano K, Young R: Holin triggering in real time. Proc Natl Acad Sci U S A 2011,108(2):798–803.PubMedCrossRef 35. Ranjit DK, Endres JL, Bayles KW: Staphylococcus aureus CidA and LrgA proteins exhibit holin-like properties. J Bacteriol 2011,193(10):2468–2476.PubMedCrossRef 36. Bayles KW: Are the molecular strategies that control apoptosis conserved in bacteria? Trends Microbiol 2003, 11:306–311.PubMedCrossRef 37. Ahn SJ, Rice KC, Oleas J, Bayles KW, Burne RA: The Streptococcus mutans Cid and Lrg systems modulate virulence traits in response to multiple environmental INCB018424 cost signals. Microbiology 2010,156(Pt 10):3136–3147.PubMedCrossRef

38. Sharma-Kuinkel BK, Mann EE, Ahn JS, Kuechenmeister LJ, Dunman PM, Bayles KW: The Staphylococcus aureus LytSR two-component regulatory system affects biofilm CHIR98014 formation. J Bacteriol 2009,191(15):4767–4775.PubMedCrossRef 39. Brunskill EW, Bayles KW: Identification of LytSR-regulated genes from Staphylococcus aureus. J Bacteriol 1996,178(19):5810–5812.PubMed 40. Zhu T, Lou Q, Wu Y, Hu J, Yu F, Qu SCH727965 clinical trial D: Impact of the Staphylococcus epidermidis LytSR two-component regulatory system on murein hydrolase activity, pyruvate utilization and global transcriptional profile. BMC Microbiol 2010, 10:287.PubMedCrossRef 41. Chandramohan L, Ahn JS, Weaver KE, Bayles KW: An overlap between the control of programmed

cell death in Bacillus anthracis and sporulation. J Bacteriol 2009,191(13):4103–4110.PubMedCrossRef 42. Kobayashi K,

Ogura M, Yamaguchi H, Yoshida K, Ogasawara N, Tanaka T, Fujita Y: Comprehensive DNA microarray analysis of Bacillus subtilis two-component regulatory systems. J Bacteriol 2001,183(24):7365–7370.PubMedCrossRef PLEKHB2 43. Brunskill EW, Bayles KW: Identification and molecular characterization of a putative regulatory locus that affects autolysis in Staphylococcus aureus. J Bacteriol 1996,178(3):611–618.PubMed 44. Patton TG, Yang SJ, Bayles KW: The role of proton motive force in expression of the Staphylococcus aureus cid and lrg operons. Mol Microbiol 2006,59(5):1395–1404.PubMedCrossRef 45. Wu C, Cichewicz R, Li Y, Liu J, Roe B, Ferretti J, Merritt J, Qi F: Genomic island TnSmu2 of Streptococcus mutans harbors a nonribosomal peptide synthetase-polyketide synthase gene cluster responsible for the biosynthesis of pigments involved in oxygen and H2O2 tolerance. Appl Environ Microbiol 2010,76(17):5815–5826.PubMedCrossRef 46. Merritt J, Qi F, Shi W: A unique nine-gene comY operon in Streptococcus mutans. Microbiology 2005,151(Pt 1):157–166.PubMedCrossRef 47. Petersen FC, Tao L, Scheie AA: DNA binding-uptake system: a link between cell-to-cell communication and biofilm formation. J Bacteriol 2005,187(13):4392–4400.PubMedCrossRef 48. Dubbs JM, Mongkolsuk S: Peroxiredoxins in bacterial antioxidant defense. Subcell Biochem 2007, 44:143–193.PubMedCrossRef 49.

Figure 4 The catalytic performance of the Au/HNTs catalyst as a function of reaction time. Conclusions In conclusion, we have demonstrated that HNTs are an attractive support for gold nanoparticles, which results in an excellent catalytic activity www.selleckchem.com/products/epz-5676.html in solvent-free oxidation of benzyl alcohol. The high catalytic activity is found to be related to the tubular structure of the HNTs and the oxidized gold species. This process is promising in the development of a truly heterogeneous

catalyst for alcohol oxidation. Acknowledgements The authors would like to thank the supports from the National Natural Science Foundation of China (No. 21306061), Key Project of Educational Commission of Guangdong Province (No. 2012B091100296), and Project of Base of Production, Education and Research (No. cxzd1148). References 1. Mallat T, Baiker A: Oxidation of alcohols with molecular oxygen on solid catalysts. Chem Rev 2004, 104:3037–3058.CrossRef 2. Haruta M, Tsubota S, Kobayashi T, Kageyama H, Genet MJ, Delmon B: Low-temperature oxidation of CO over gold supported on TiO 2 , alpha-Fe check details 2 O 3 , and Co 3 O 4 . J Catal 1993, 144:175–192.CrossRef 3. Guo X, Ye W, Sun

HY, Zhanga Q, Yang J: A dealloying process of core-shell Au@AuAg nanorods for Lenvatinib porous nanorods with enhanced catalytic activity. Nanoscale 2013, 5:12582–12588.CrossRef 4. Guo X, Zhang Q, Sun YH, Zhao Q, Yang J: Lateral etching of core-shell Au@metal nanorods to metal-tipped Au nanorods with improved catalytic activity. ACS Nano 2012, 6:1165–1175.CrossRef 5. Ye W, Guo X, Xie F, Zhu R, Zhao Q, Yang J: Kinetics-controlled growth of bimetallic RhAg on Au nanorods and their catalytic properties. Nanoscale not 2014, 6:4258–4263.CrossRef 6. Chretien S, Buratto SK, Metiu H: Catalysis by very small Au clusters. Curr Opin Solid State Mat Sci 2007, 11:62–75.CrossRef 7. Bamwenda GR, Tsubota S, Nakamura T, Haruta M: The influence of the preparation methods on the catalytic activity of platinum

and gold supported on TiO 2 for CO oxidation. Catal Lett 1997, 44:83–87.CrossRef 8. Guzman J, Carrettin S, Corma A: Spectroscopic evidence for the supply of reactive oxygen during CO oxidation catalyzed by gold supported on nanocrystalline CeO 2 . J Am Chem Soc 2005, 127:3286–3287.CrossRef 9. Yang J, Guan YJ, Verhoeven T, van Santen R, Li C, Hensen EJM: Basic metal carbonate supported gold nanoparticles: enhanced performance in aerobic alcohol oxidation. Green Chem 2009, 11:322–325.CrossRef 10. Joussein E, Petit S, Churchman J, Theng B, Righi D, Delvaux B: Halloysite clay minerals—a review. Clay Min 2005, 40:383–426.CrossRef 11. Zhang Y, He X, Ouyang J, Yang HM: Palladium nanoparticles deposited on silanized halloysite nanotubes: synthesis, characterization and enhanced catalytic property. Sci Rep 2013, 3:2948–2953. 12. Fan L, Ichikuni N, Shimazu S, Uematsu T: Preparation of Au/TiO 2 catalysts by suspension spray reaction method and their catalytic property for CO oxidation.

J Bacteriol 1989,171(1):392–401.PubMed 13. Wang SP, Sharma PL, Schoenlein PV, Ely B: A histidine protein kinase is involved in polar organelle development in Caulobacter crescentus . Proc Natl Acad Sci USA 1993,90(2):630–634.PubMedCrossRef 14. Hinz AJ, Larson DE, Smith CS, Brun YV: The Caulobacter crescentus polar organelle development protein PodJ is differentially localized and is required for polar targeting of the PleC development regulator. Mol Microbiol 2003,47(4):929–941.PubMedCrossRef 15. Viollier PH, Sternheim N, Shapiro L: Identification of a localization factor for the polar positioning of bacterial

structural and regulatory proteins. Proc Natl Acad Sci USA 2002,99(21):13831–13836.PubMedCrossRef CP673451 cell line 16. Ouimet MC, Marczynski GT: Analysis of Peptide 17 a cell-cycle promoter bound by a response regulator. J Mol Biol 2000,302(4):761–775.PubMedCrossRef 17. Quon KC, Marczynski GT, Shapiro L: Cell cycle control by an essential bacterial two-component signal transduction protein. Cell 1996, 84:83–93.PubMedCrossRef 18. Kelly AJ, Sackett MJ, Din N, Quardokus E, Brun YV: Cell cycle-dependent transcriptional and proteolytic regulation of FtsZ in Caulobacter . Genes Dev 1998,12(6):880–893.PubMedCrossRef 19. Sackett

MJ, Kelly AJ, Brun YV: Ordered expression of ftsQA and ftsZ during the Caulobacter crescentus cell cycle. Mol Microbiol 1998,28(3):421–434.PubMedCrossRef 20. Stephens C, Zweiger G, Shapiro L: Cooridinate cell cycle control of a Caulobacter DNA methyltransferase and the flagellar

Temsirolimus supplier genetic hierarchy. J Bacteriol 1995, 177:1662–1669.PubMed 21. Zhuang WY, Shapiro L: Caulobacter FliQ and FliR membrane proteins, required for flagellar biogenesis and cell division, belong to a family of virulence factor export proteins. J Bacteriol 1995,177(2):343–356.PubMed 22. Skerker JM, Shapiro L: Identification and cell cycle control of a novel pilus system in Caulobacter crescentus . EMBO J 2000,19(13):3223–3234.PubMedCrossRef 23. Meisenzahl AC, Shapiro L, Jenal U: Isolation and characterization of a xylose-dependent promoter from Caulobacter crescentus . J Bacteriol 1997,179(3):592–600.PubMed 24. Gora KG, Tsokos CG, Chen YE, Srinivasan BS, Perchuk BS, Laub MT: A cell-type-specific protein-protein interaction modulates transcriptional activity of a master regulator in Caulobacter crescentus . Mol Cell 2010,39(3):455–467.PubMedCrossRef 25. selleck screening library Schredl AT, Perez Mora YG, Herrera A, Cuajungco MP, Murray SR: The Caulobacter crescentus ctrA P1 promoter is essential for the coordination of cell cycle events that prevent the over-initiation of DNA replication. Microbiology 2012,158(Pt 10):2492–2503.PubMedCrossRef 26. Reisenauer A, Quon K, Shapiro L: The CtrA response regulator mediates temporal control of gene expression during the Caulobacter cell cycle. J Bacteriol 1999,181(8):2430–2439.PubMed 27.

(A) ECC-1 cells grown in normal FCS supplemented cell culture. Typical RB forms are present at 24 hours post infection (B) No

hormone supplemented stripped FCS media. Once again normal RB morphology was observed under this condition; RBs appeared similar to normal FCS supplemented cell culture. (C) Estradiol supplemented, RBs were distinctly different, appearing as large aberrant form. Estradiol supplementation of infected cells, resulting in BIIB057 cost smaller inclusions containing enlarged, atypical RB forms (arrows). (D) Progesterone supplemented, shape and morphology of RBs were normal including binary fission. Morphological examination of progesterone exposed cultures with TEM did not show any evidence of aberrant, persistent forms. Magnification: × 20K, marker represent 200 nm. Progesterone exposure induces an up-regulated energy utilising chlamydial response Overall, 85 chlamydial genes were observed to have two-fold or greater up-regulated gene expression levels in the presence of progesterone. The five top genes that were observed with this mRNA expression profile encode for proton or sodium-glutamate symport Selleckchem A1155463 protein (gltT) [33.4 fold], the putative glycerol-3-phosphate acyltransferase

(plsX) [16.17 fold], glucose inhibited division protein (lplA_2) [11.9 fold], NADH-quinone reductase complex (nqr2) [10.95 fold] and polynucleotide adenylyltransferase (pcnB_1) [10.75 fold]. In addition to these 85 genes, 135 chlamydial genes were observed to have a reduced gene expression profile in response to the presence of progesterone. The five top down AZD5363 order regulated Histamine H2 receptor genes include

exoribonuclease II (vacB) [67.96 fold], isopentenylpyrophosphate transferase (miaA) [33.91 fold], cysteinyl-tRNA synthetase (cysS) [33.64 fold], thioredoxin reductase (trxB) [33.44fold], and ribonucleotide-diphosphate reductase subunit alpha (nrdA) [29.25 fold]. 103 genes had unknown annotated functions (hypothetical genes). By comparison to the estradiol response, which resulted in a down-regulation of fatty acid and nucleotide metabolism pathways, progesterone exposure had no or little effect on these pathways but did result in a significant up-regulation of the TCA cycle and glycolysis pathways (Table 3). In some aspects the progesterone response was opposite or counter-balancing to the estradiol response. Progesterone resulted in a general up-regulation of carbohydrate metabolism pathways as well as an up-regulation of amino acid metabolism pathways. The progesterone-mediated response mounted by Chlamydia reflects the host’s flux of metabolites. Progesterone has been reported to have a suppressive effect in general on estradiol [25], and after prolonged exposure, it appears that Chlamydia is diverting specific pathways to compensate.

Cloning of fnbB gene fragments Generic primers, corresponding to conserved DNA encoding the signal sequence and fibronectin binding domain 2, were designed from conserved sequences in fnbB genes from publicly available S. aureus genomes. PCR products were cleaved with BamHI restriction sites incorporated into the primers, ligated to BamHI-cleaved pBluescript DNA and transformed into E. coli. The cloned fnbB gene fragments were sequenced using T3 and T7 primers by GATC Biotech AG (Germany).

DNA hybridisation using fnbB type-specific probes DIG-labelled isotype-specific probes were synthesised by PCR. Primers were designed to amplify a small region of DNA (~300 bp) in the N3 sub-domain of isotypes I-VII. The PCR products were labelled by incorporating DIG-labelled dNTPs (Roche). Five ng of DNA encoding the A domain of FnBPB from clinical Vorinostat chemical structure isolates was spotted onto positively charged nylon membranes (Roche) and allowed to air-dry. Membranes were incubated for 5 min on blotting paper soaked in denaturation solution (1.5 M NaCl, 0.5 M

NaOH), 5 min in neutralization solution (1.5 M NaCl, 1 M Tris-HCl, pH 7.4), and finally Tucidinostat molecular weight for 15 min on blotting paper soaked with 2× SSC solution (300 mM NaCl, 30 mM tri-sodium VS-4718 mouse citrate). DNA was fixed on the membranes by incubation at 120°C for 30 min. Membranes were incubated for 2 h at 68°C in pre-hybridization solution (5× SSC, 0.1% w/v N-lauroylsarcosine, 0.02% w/v SDS and 1× Blocking Reagent (Roche). DIG-labelled probes were denatured by heating at 95°C for 10 min, diluted in pre-hybridization solution and incubated with nylon membranes for 18 h at 68°C. mafosfamide Following hybridization, the membranes were washed twice with 2× SSC/0.1% w/v SDS at room temperature followed by two washes with 0.5× SSC/0.1% w/v SDS at 68°C for 20 min. Membranes were equilibrated for 30 min in maleic acid buffer (100 mM maleic acid, 150 mM NaCl, pH 7.5), and

bound DIG-labelled probes were detected by incubation for 30 min with alkaline phosphatase-conjugated anti-DIG antibody (Roche) diluted 1:10,000 in maleic acid buffer. After washing twice with maleic acid buffer containing 0.3% v/v Tween 20, the chemiluminescence substrate CSPD (Roche) was used to detect bound anti-DIG antibodies and membranes were exposed to X-OMAT UV Plus Film (Kodak). Bioinformatic and phylogenetic analysis of FnBPB A domain isotypes Protein sequences were aligned in pairwise combinations to calculate amino acid identity using the ExPASY SIM alignment tool http://​www.​expasy.​org/​tools/​sim-prot.​html. The concatenated MLST allele sequences of S. aureus strains were downloaded from the MLST database http://​saureus.​mlst.​net/​.

coli BL21. Growth temperature were 37°C, except where indicated and growth rates were estimated by measuring the increase in OD600. Origin of the immunoreactive MS2/28 DNA fragment Isolation and characterization of the M. synoviae DNA fragment MS2/28 [GenBank: MSU66315] was previously described [18]. MS2/28 contains two partial ORFs, referred to as MS2/28.1 (5′ end) and MS2/28.2 (3′ end). Reverse transcription and polymerase chain reaction (RT-PCR) The total RNA of M. synoviae strain WVU 1853 was isolated from a

24-h culture, using a protocol recommended for Gram-positive bacteria [23]. Genomic M. synoviae DNA was eliminated from the RNA preparation using DNAse I (2,5 mg/ml) digestion for a 1-h period at 37°C. DNAse I-treated Momelotinib cost total RNA of M. synoviae was prepared as described above. Reverse transcription was performed at 55°C in a 20 μl reaction mixture containing 2 μg of total RNA, 4 μl of dNTP at 20 mM each, 12.5 μM of the reverse primer 2/28.1Rev (5′-GGGCGGCCGCCTACACTTGCAGTACTTGGCG-3′), 20 units of AMV reverse transcriptase and 2 μl of 10 × buffer reaction (50 mM Tris-Cl, 8 mM MgCl2, 30 mM KCl, 1 mM dithiotreitol, pH = 8). The first strand cDNA synthesis was allowed to proceed

for 1 h followed by inactivation at 65°C during 10 min. PCR amplification was next performed using 2/28.1Rev coupled to the PromF primer (5′-GTCGACGAAATTAAGTAAATTATTAAAG-3′) which anneals to the 5′ end region (-120 to -98) of the expected vlhA1-derived transcript. The amplification check details reaction consisted of 30 cycles of 94°C for 120 s, 55°C for 120 s and 72°C for 120 s, followed by an extension of 72°C for 7 min. Cloning and sequencing of the RT-PCR

product The 1.934 kb RT-PCR product was purified and ligated into NotI/SalI-digested pBluescript II KS+ plasmid. The ligation product was used to transform E. coli HB101 cells and recombinant clones were screened using restriction analysis. Determination Astemizole of the nucleotide sequence was performed with the Prism Ready Reaction Dye Deoxy Terminator Cycle sequencing Kit on an ABI PRISM 377 DNA sequencer (Applied Biosystems). The cloned amplicon was sequenced in both orientations from two different plasmid clones using sequence-specific internal and plasmid-anchored primers. The sequence data were edited and aligned using the software programs BioEdit [24] and ClustalW [25]. Confirmation of the position of the completed MS2/28.1 gene sequence relative to the unique vlhA1 promoter Using genomic DNA extracted from selleck inhibitor single colonies as template, PCR amplifications were performed, combining EXpro (5′-CAAATTTAGTTAATTCACTTA-3′), a sense primer placed in the vlhA1 promoter region (-213 to -193), with either vlhA1 R (5′-TATTGTTTTCGGCATTATTTGCTACGTC-3′), a vlhA1-specific reverse primer, or ORF5.1R (5′-GCCTCCACTTCCATCTCCGCTTTCACT-3′), the MS2/28.1-specific reverse primer. To ensure that the full-length MS2/28.

7 NWs and the islands see more grown on the Si(110) surface. It can be seen that the NWs and 3D islands have sharply different contrast. The 3D islands are much brighter than the NWs, while the NWs are just a little brighter than the Si(110) substrate. This result indicates that the average atomic weight of the 3D islands is much greater than that of the NWs, while the average atomic weight of the NWs is slightly larger than that of the Si substrate. Therefore, the 3D islands

and NWs have different chemical compositions. The 3D islands correspond to the Mn-rich silicide such as Mn5Si3, and the NWs correspond to the Si-rich phase MnSi~1.7. This conclusion is consistent with that reported for the Mn silicides formed on the Si(111) SGC-CBP30 in vivo surface [20, 21]. Figure 6 Atomically resolved STM image of the manganese silicide NW and its tunneling current-voltage properties. (a) Atomically resolved STM image (10 × 10 nm2) of an ultrafine manganese silicide NW grown on the Si(110) surface and (b) the scanning tunneling spectra measured on top of the NW showing semiconducting characteristics with a bandgap of approximately 0.8 eV. The red and blue curves were obtained on two different positions on the NW. Figure 7 Ex situ BE-SEM image of the manganese silicide NWs and 3D islands grown on Si(110) surface. Conclusions In summary, the influence of growth

conditions such as growth temperature, deposition rate, and deposition time on the formation of MnSi~1.7 NWs on a Si(110) surface has been investigated by STM. High growth temperature and low Mn deposition rate are found to be favorable for the formation of NWs with a large aspect ratio, indicating

that the supply of free Si atoms per unit time plays a crucial role in the growth of the NWs. The NWs orient solely with the long axis along the Si direction. The I-V curves measured on top of the NWs, and the BE-SEM image reveal that the NWs consist of MnSi~1.7. The growth of the parallel MnSi~1.7 NWs on the Si substrate provides an opportunity for the study of electronic properties of NWs and the fabrication of nanoelectronic devices with novel functions. Acknowledgements This work was supported by the National Natural Science Foundation of China under grant no. 61176017 and the Innovation Program ADAMTS5 of Shanghai Municipal Education Commission under grant no. 12ZZ025. References 1. Liang S, Islam R, Smith DJ, selleck chemical Bennett PA, O’Brien JR, Taylor B: Magnetic iron silicide nanowires on Si(110). Appl Phys Lett 2006, 88:113111.CrossRef 2. He Z, Smith DJ, Bennett PA: Epitaxial DySi2 nanowire formation on stepped Si(111). Appl Phys Lett 2005, 86:143110.CrossRef 3. He Z, Smith DJ, Bennett PA: Endotaxial silicide nanowires. Phys Rev Lett 2004, 93:256102.CrossRef 4. Preinesberger C, Becker SK, Vandré S, Kalka T, Dähne M: Structure of DySi2 nanowires on Si(001). J Appl Phys 2002, 91:1695.CrossRef 5.