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a cheese factory. Appl Environ Microbiol 1997, 63:3144–3150.PubMed 9. Hardie JM, Whiley RA: The Genus Streptococcus–Oral. The Prokaryotes Third Edition (Edited by: Dworkin M, Falkow S, Rosenberg E, Schleifer K-H, Stackebrandt E). Springer 2006, 76–107. 10. Doyuk E, Ormerod OJ, Bowler IC:

Native valve endocarditis due to Streptococcus vestibularis and Streptococcus oralis. J Infect 2002, 45:39–41.CrossRefPubMed 11. Partridge SM: Prosthetic valve endocarditis due to Streptococcus PI3K Inhibitor Library mouse vestibularis. J Infect 2000, 41:284–285.CrossRefPubMed 12. Corredoira JC, Alonso MP, Garcia JF, Casariego E, Coira A, et al.: Clinical characteristics and significance of Streptococcus salivarius bacteremia and Streptococcus bovis bacteremia: a prospective 16-year study. Eur J Clin Microbiol Infect Dis 2005, 24:250–255.CrossRefPubMed 13. Hols P, Hancy F, Fontaine L, Grossiord B, Prozzi D, et al.: New insights in the molecular biology and physiology of Streptococcus thermophilus Tolmetin revealed by comparative genomics. FEMS Microbiol Rev 2005, 29:435–463.PubMed 14. Poyart C, Quesne G, Coulon S, Berche P, Trieu-Cuot P: Identification of streptococci to species level by sequencing the gene encoding the manganese-dependent superoxide dismutase. J Clin Microbiol 1998, 36:41–47.PubMed 15. Papanikou E, Karamanou S, Economou A: Bacterial protein secretion through the translocase nanomachine. Nat Rev Microbiol 2007, 5:839–851.CrossRefPubMed 16. Cox MM: Motoring along with the bacterial

RecA protein. Nat Rev Mol Cell Biol 2007, 8:127–138.CrossRefPubMed 17. Sapp J: Two faces of the prokaryote concept. Int Microbiol 2006, 9:163–172.PubMed 18. Selmer M, Dunham CM, Murphy FVt, Weixlbaumer A, Petry S, et al.: Structure of the 70S ribosome complexed with mRNA and tRNA. Science 2006, 313:1935–1942.CrossRefPubMed 19. Janda JM, Abbott SL: 16S rRNA gene sequencing for bacterial identification in the diagnostic laboratory: pluses, perils, and pitfalls. J Clin Microbiol 2007, 45:2761–2764.CrossRefPubMed 20. Gold VA, Duong F, Collinson I: Structure and function of the bacterial Sec translocon. Mol Membr Biol 2007, 24:387–394.CrossRefPubMed 21. Li X, Heyer WD: Homologous recombination in DNA repair and DNA damage tolerance. Cell Res 2008, 18:99–113.CrossRefPubMed 22. Rasmussen TB, Danielsen M, Valina O, Garrigues C, Johansen E, et al.:Streptococcus thermophilus core genome: comparative genome hybridization study of 47 strains.

Conclusion In DLBL patients, mortality was affected by the RDI of R-CHOP as the initial treatment and the retention of high RDI could be crucial, especially in elderly patients. Epigenetics inhibitor To optimize the RDI of conventional chemotherapy in order to achieve better outcomes for patients with DLBL, further investigation of RDI will be required. Acknowledgements We thanks for clinical

research nurse. Yukari Umemoto (Hematology, Graduate School of Medicine, Osaka City University, Osaka, Japan) for assistance in obtaining clinical data and follow-up information. References 1. Fisher RI, Gaynor ER, Dahlberg S, Oken MM, Grogan TM, Mize EM, Glick JH, Coltman CA Jr, Miller TP: Comparison of a standard regimen

(CHOP) with three intensive chemotherapy regimens for advanced non-Hodgkin’s lymphoma. N Engl J Med 1993, 328: 1002–6.CrossRefPubMed 2. International Non-Hodgkin’s Lymphoma Prognostic Factors Project: A predictive model for aggressive non-Hodgkin’s lymphoma. NSC23766 cost N Engl J Med 1993, 329: 987–94.CrossRef 3. Epelbaum R, Haim N, Ben-Shahar M, Ron Y, Cohen Y: Dose intensity analysis for CHOP chemotherapy in diffuse aggressive large cell lymphoma. Isr J Med Sci 1990, 24: 533–8. 4. Kwak LW, Halpern J, Olshen RA, Horning SJ: Prognostic the significance of actual dose intensity in diffuse large-cell lymphoma: Results of a tree-structured survival analysis. J Clin Oncol 1990, 8: 963–77.PubMed 5. Epelbaum R, Faraggi D, Ben-Arie Y, Ben-Shahar M, Haim N, Ron Y, Robinson E, Cohen Y: Survival of diffuse large cell lymphoma. A multivariate analysis including dose intensity variables. Cancer 1990, 66: 1124–9.CrossRefPubMed

6. Lepage E, Gisselbrecht C, Haioun C, Sebban C, Tilly H, Bosly A, Morel P, Herbrecht R, Reyes F, Coiffier B: Prognostic significance of received relative dose intensity in non-Hodgkin’s lymphoma patients: Application to LNH-87 protocol: The GELA (Groupe d’Etude des Lymphomes de l’Adulte). Ann Oncol 1993, 4: 651–6.PubMed 7. Bosly A, Bron D, Van Hoof A, De Bock R, Berneman Z, Ferrant A, Kaufman L, Dauwe M, Verhoef G: Achievement of optimal average relative dose intensity and correlation with survival in diffuse large B-cell lymphoma patients treated with CHOP. Ann Hematol 2008, 87: 277–83.CrossRefPubMed 8. Coiffier B, Lepage E, Briere J, Herbrecht R, Tilly H, Bouabdallah R, Morel P, Neste E, Salles G, Gaulard P, Reyes F, Lederlin P, Gisselbrecht C: CHOP chemotherapy plus rituximab compared with CHOP alone in elderly patients with diffuse large B-cell lymphoma. N Engl J Med 2002, 346: 235–42.CrossRefPubMed 9.

The Raman spectra were obtained using a Senterra R200-L Raman spectrometer (Bruker Optik GmbH, Ettlingen, Germany) with a 514-nm line of https://www.selleckchem.com/products/carfilzomib-pr-171.html laser source. Fourier transform infrared (FTIR) spectra were recorded using a Vertex 70 vacuum FTIR spectrometer (Bruker Optik GmbH) and scanned from 4,000 to 400 cm−1 with KBr as background. Thermogravimetric analysis (TGA; Pyris 1, PerkinElmer, Waltham, MA, USA) was performed under a highly pure nitrogen atmosphere with a heating rate of 1°C to 10°C/min from 30°C to 700°C. The films with 5-mm width and 4- to 5-cm length were measured by dynamic mechanical analysis (DMA; TA-Q800, TA Instruments, Newcastle, DE, USA) at the room temperature. A

four-probe detector (RTS-8,

4 PROBES TECH, Guangzhou, China) was used to measure the sheet resistance of the films. Results and discussion The modified Hummers method had been used to prepare graphene oxide. By sonicating the graphene oxide in water, graphene oxide sheet aqueous solution was obtained. From the tapping-mode AFM image as shown in Figure 3, it is observed that the thickness of the obtained graphene oxide sheet is approximately 1.05 nm, which indicates that the graphene oxide can be easily exfoliated into single layer by the oxidation and sonication Selleckchem SB431542 treatment [40]. The graphene oxide films with a large area were fabricated by casting method. The graphene oxide sheets can be easily assembled into graphene oxide films by volatizing water in the oven at 80°C. PTFE, a hydrophobic substrate, is used Cediranib (AZD2171) to make sure that the films are easily peeled off and the large-area free-standing films fabricated. As shown in Figure 1a, the yellow-brown paper-like films with a semitransparent characteristic are obtained. In order to obtain the graphene films, ascorbic acid, as an excellent reducing agent,

has been used here to reduce the graphene oxide films [39]. As a result of the reduction process, the opaque graphene films with black color (Figure 1b) are obtained. Excitingly, the morphology of the graphene films can be perfectly maintained after the reduction process (Figure 4a,b), which suggests that this facile and novel method is suitable for the large-scale production of graphene films. For the improvement of the conductivity of the films, Ag particles have been in situ introduced during the process of the reduction reaction. The morphology of the graphene-Ag composite films has been observed by SEM, as shown in Figure 4. It can be found that the films are decorated with Ag particles with an average particle size from approximately 20 nm to approximately 1 μm (Figure 4c,d,e,f,g). When the mass ratio of AgNO3/graphene oxide is 1:75, these Ag particles with a size of about 20 nm were distributed uniformly at the surface of the composite films (Figure 4c).

PubMed 2. Jackson MR, Olson DW, Beckett WC Jr: Abdominal vascular trauma: a review of 106 injuries. Am Surg 1992, 58:622–626.PubMed 3. Ombrellaro MP, Freeman MB, Stevens SL, et al.: Predictors of survival after inferior vena cava injuries. Am Surg 1997, 63:178–183.PubMed 4. Leppaniemi AK, Savolainen HO, Salo JA: Traumatic

inferior vena caval injuries. Scand J Thorac 1994, 28:103–108.CrossRef Repotrectinib cell line 5. Huerta S, Bui T, Nguyen T, Banimahd F, Porral D: Predictors of mortality and management of patients with traumatic inferior vena cava injuries. Am Surg 2006,72(4):290–296.PubMed 6. Burch JM, Feliciano DV, Mattox KL: The atriocaval shunt. Facts and fiction. Ann Surg 1988, 207:555–568.PubMedCrossRef 7. Klein SR, Baumgartner FJ, Bongard FS: Contemporary management strategy for major inferior vena caval injuries. J Trauma 1994, 37:35–41.PubMedCrossRef 8. Kudsk KA, Bongard F, Lim RX Jr: Determinants of survival after

vena caval injury. Analysis of a 14year experience. Arch Surg 1984, 119:1009–1012.PubMedCrossRef 9. Rosengart M, Smith D, Melton S, May A: Prognostic factors in patients with inferior vena cava injuries. Am Surg 1999,65(9):849–856.PubMed 10. Turpin I, State D, Schwartz A: Injuries to the inferior vena cava and their management. Am J Selleckchem SB525334 Surg 1977, 134:25–32.PubMedCrossRef 11. Wilson RF, Wiencek RG, Balog M: Factors affecting mortality rate with iliac vein injuries. J Trauma 1990, 30:320–323.PubMedCrossRef 12. Buckman RF, Pathak AS, Badellino MM, et al.: Injuries of the inferior vena cava. Surg Clin North Am 2001, 81:1431–1447.PubMedCrossRef 13. Blaisdell FW, Lim RC Jr: Liver resection. Major Probl

Clin Surg 1971, 3:131–145.PubMed 14. Bricker DL, Morton JR, Okies JE, et al.: Surgical management of injuries to the vena cava: changing patterns of injury and newer techniques of repair. J Trauma 1971, 11:722–735. 15. Brown RS, Boyd DR, Matsuda T, et al.: Temporary internal vascular shunt for retrohepatic G protein-coupled receptor kinase vena cava injury. J Trauma 1971, 11:736–737.PubMedCrossRef 16. Byrne DE, Pass HI, Crawford FA Jr: Traumatic vena caval injuries. Am J Surg 1980, 140:600–602.PubMedCrossRef 17. Graham JM, Mattox KL, Beall AC Jr, et al.: Traumatic injuries of the inferior vena cava. Arch Surg 1978, 113:413–418.PubMedCrossRef 18. Millikan JS, Moore EE, Cogbill TH, et al.: Inferior vena cava injuries: a continuing challenge. J Trauma 1983, 23:207–212.PubMedCrossRef Competing interests The author’s declare that they have no competing interests. Authors’ contributions All authors: 1) have made substantial contributions to conception and design, or acquisition of data, or analysis and interpretation of data; 2) have been involved in drafting the manuscript or revising it critically for important intellectual content; 3) have given final approval of the version to be published. MC: Study conception and design, acquisition of data, analysis and interpretation of data, drafting of manuscript.

The semi-quantitative evaluation of both the absolute values of the apposition bands and the width of daily bone apposition values increased for treated compared to untreated rats, but these effects were not significant. Table 2 Results of the intravital fluorochrome labeling   SHAM SHAM Vib. OVX OVX Vib. OVX vs. SHAM Vib vs. non vib Mean STD Mean STD Mean STD Mean STD p value p value Absolute apposition bandwidth (m -6 ) Calcein green (d0 − d18) 696 275 822 226 1093 182

1032 290 <0.0001 0.4829 Alizarin red (d18–d24) 823 271 804 229 889 181 944 274 0.0267 0.6943 Tetracycline (d24–d35) 659 333 641 226 669 219 709 242 0.4267 0.8278 Sum 2,178 2,267 2,651 2,685             Absolute apposition bandwidth per day (m –6 ) Calcein green (d0–d18) 38.6 15.3 45.7 Selleck GSK3326595 12.5 60.7 10.1 57.3 16.1 <0.0001 0.4877 Alizarin VX-809 nmr Red (d18–d24) 137.2 45.2 134.1 38.2 148.2 30.2 157.3 45.6 0.0269 0.7024 Tetracycline (d24–d35) 59.9 30.3 58.3 20.5 60.8 19.9 64.5 22.0 0.4275 0.8227 Sum 235.7 238.1 269.7 279.1             Relative apposition bandwidth per day (%) Calcein green (d0–d18) 16.8 4.0 19.4 3.4 22.9 3.9 20.7 2.7 <0.0001 0.7371 Alizarin red (d18–d24) 58.5

5.0 56.3 4.7 54.9 3.3 56.2 6.1 0.0436 0.6052 Tetracycline (d24–d35) 24.7 7.0 24.3 4.8 22.2 4.0 23.2 5.5 0.0831 0.8085 The p value of the difference between treated and untreated animals was calculated using a two-way ANOVA. p values <0.05 were considered significant Flat-panel volumetric computed tomography The SHAM group had

a significantly improved BMD, cancellous and cortical bone density compared to OVX animals (p < 0.0001 for all). Vibration led to an improvement of total BMD, cancellous and cortical BMD (Table 1). The cortical bone density after vibration was significantly improved (p = 0.0035), while the BMD (p = 0.0532) and cancellous bone density (p = 0.0634) showed improvement; however, the improvement failed 5-Fluoracil chemical structure to reach significant values. The main disadvantage of the fpVCT used in this study was the lower spatial resolution compared to the µCT. The former method does not allow a detailed description of the trabecular microstructure. Ashing The ash-BMD of SHAM rats was significantly improved compared to OVX rats (p < 0.0001). Vibration yielded a significant improvement of ash-BMD in all groups (p = 0.0011). There were no differences between groups before ashing. After ashing, the SHAM-operated animals had higher ash weights compared to OVX, but these changes were not significant. After calculating the ash-BMD, more differences between the groups were observed (Table 1). Discussion Osteoporosis primarily affects trabecular bone. In humans, the majority of osteoporotic fractures occur in the spine and metaphysis of long bones. In the rat osteopenia model, osteoporosis mainly affects the metaphyseal tibia and lumbar spine [19–23].

Colorectal Dis 2009,11(2):168–72.PubMed 177. Catena F, Ansaloni L, Lauro

A, Ercolani G, D’Alessandro L, Pinna A: Prospective controlled randomized trial on prevention of postoperative abdominal adhesions by Icodextrin 4% solution after laparotomic operation for small bowel obstruction caused by adherences [POPA study: Prevention of Postoperative Adhesions on behalf of the World Society of Emergency Surgery]. Trials 2008, 9:74.PubMed 178. Menzies D, Pascual MH, Walz MK, Duron JJ, Tonelli F, Crowe LY2835219 cost A, Knight A: ARIEL Registry. Use of icodextrin 4% solution in the prevention of adhesion formation following general surgery: from the multicentre ARIEL Registry. Ann R Coll Surg Engl 2006,88(4):375–82.PubMed 179. Johns DA, Ferland R, Dunn R: selleck screening library Initial feasibility study of a sprayable hydrogel adhesion barrier

system in patients undergoing laparoscopic ovarian surgery. J Am Assoc Gynecol Laparosc 2003, 10:334–338.PubMed 180. Tang CL, Jayne DG, Seow-Choen F, et al.: A randomized controlled trial of .5% ferric hyaluronate gel (Intergel) in the prevention of adhesions following abdominal surgery. Ann Surg 2006, 243:449–455.PubMed 181. Sparnon AL, Spitz L: Pharmacological manipulation of postoperative intestinal adhesions. Aust N Z J Surg 1989, 59:725–9.PubMed 182. Fang CC, Chou TH, Lin GS, Yen ZS, Lee CC, Chen SC: Peritoneal infusion with cold saline decreased postoperative intra-abdominal adhesion formation. World J Surg 2010,34(4):721–7.PubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions FC, SDS: conception and design of the study; organised the consensus conference; preparation of the draft; merged the committee preliminary statements with the observations and recommendations from the panel, summarised

the discussion on standards of diagnosis and treatment for ASBO SDS, FC manuscript writing, drafting and review. FC, SDS, MDK, JJ organised the consensus conference, merged the committee preliminary statements with the observations and recommendations from the panel, critically Thiamine-diphosphate kinase contributed to the consensus statements MDK, WLB, LA, VM, HVG, EEM, JJ contributed to critical discussion of the draft All authors read and approved the final manuscript”
“Introduction Babesiosis, most commonly caused by Babesia microti infection is becoming a more prevalent disease. In the United States, Martha’s Vineyard, Nantucket, Shelter Island, and Long Island are considered some of the endemic areas for this infection[1]. Disease manisfestations range from subclinical to severe critical illness. Spontaneous splenic rupture is a rare complication that has been previously documented leading to emergent splenectomy in all cases[2, 3].

The inoculated leaves did not show any yellowing (data not shown) as seen in the tomato leaves. Thus, rice plants NVP-BGJ398 chemical structure are non-hosts to the bacteria. As Arabidopsis thaliana has been used extensively as a plant host model for several pathogens, we tested B. thailandensis and B. pseudomallei infection in Arabidopsis plantlets via the roots. The average disease scores were

maintained at 1 and increased only slightly at days 6 and 7 and were identical for both B. thailandensis and B. pseudomallei infection (Fig 5B). Figure 5 B. pseudomallei and B. thailandensis infection of rice (A) and Arabidopsis (B) plantlets. Each graph represents an experiment of 6 plantlets infected either with B. pseudomallei or B. thailandensis as both types of infections Epigenetics inhibitor resulted in identical disease scores. Each experiment with B. pseudomallei or B. thailandensis infection had

been repeated twice. Discussion B. cepacia, the important opportunistic pathogen often associated with cystic fibrosis and chronic granulomatous disease patients [21], was originally described as a phytopathogen causing soft rot in onions [22]. Subsequently, many strains from various B. cepacia complex were shown to be able to cause disease in the alfalfa infection model as well as in the rat agar bead model [23]. In this study, we show that B. pseudomallei and B. thailandensis are also potential plant pathogens. They are capable of infecting susceptible plants such as tomato. Plant pathogenic bacteria have been shown to express a large number of T3SS effectors capable of interfering with plant basal defense triggered by bacterial pathogen-associated molecular patterns all (PAMPs) as well as Resistance (R) protein-mediated immunity typically characterized by the Hypersensitive Response (HR) [24–26]. The outcome of the interaction with susceptible hosts for these successful pathogens would be disease. We found that the virulence of B. pseudomallei in tomato is contributed

significantly by T3SS1 and T3SS2, but to a much lesser extent by T3SS3. T3SS1 and T3SS2 are likely non-redundant to each other in causing disease because each mutant demonstrates significant attenuation, possibly because both T3SS1 and T3SS2 are co-ordinately involved in pathogenesis. This is the first time that a role has been defined for T3SS1 and T3SS2 in B. pseudomallei, showing that they are functional and not simply vestiges of evolution. The role of T3SS3 could be due to its contribution of a structural component or chaperone to the other two T3SS or an effector which could also interfere with plant cell physiology albeit less efficiently than with mammalian cells. Nevertheless, our study shows the important role played by T3SS in B. pseudomallei pathogenesis in tomato plants. In contrast to tomato, we found that both B. pseudomallei and B. thailandensis are non-adapted for rice. This is not surprising as B.

Some of these findings have been supported by mechanistic studies in various muscle cell cultures, where IGF-1 [10], myogenesis [11] and protein synthesis [10, 12, 13] were increased, and also a more explorative approach using microarrays on muscle biopsies from creatine supplemented individuals revealed cytoskeleton remodelling, protein and glycogen synthesis regulation, as well as cell proliferation and differentiation [8]. Other techniques such as proteomics and metabonomics may reveal additional insight into some of the biochemical effects of creatine supplementation at the protein and metabolite level. XAV-939 solubility dmso High-resolution 1H nuclear magnetic resonance (NMR) spectroscopy is

www.selleckchem.com/products/YM155.html a well-established analytical technique for metabolic fingerprinting of biofluids and various tissues and has also been used for elucidating the metabolic effects of dietary factors in both humans [14–17], animals [18–20], and also in cell cultures [21]. These studies have demonstrated that NMR-based metabonomics is extremely efficient in detecting endogenous and exogeneous metabolic perturbations. However, while being capable of identifying biomarkers and

metabolic perturbations, the metabolic network responsible for the perturbations can only be hypothesised. Proteomics displays protein products as a result of gene expression and efficiency of translation, and has been used to separate and identify differentially regulated proteins much in response to various treatments of cultured cells [22, 23] and muscles [24]. Linking information obtained from metabolic fingerprinting with proteomics would pave the way for obtaining a better understanding of the primary pathways

involved in perturbations associated with CMH supplementation. In this study we have for the first time examined and integrated the NMR metabolite profile and the proteomic profile of myotubes in the presence and absence of creatine supplementation in a systems biology approach. Methods Muscle Cell Culture Myotube cultures were established from a mouse myoblast line (C2C12) originally derived from a thigh muscle [25] (American Type Culture Collection, Manassas, VA). A clone from this cell line, which effectively fused and formed myotubes, was isolated [26]. The clone was grown in 80 cm2 culture flask in 10 mL of medium consisting of Dulbecco’s modified Eagle’s medium (DMEM), 10% (vol/vol) fetal calf serum (FCS), and supplemented with 1% antibiotics giving 100 IU/mL penicillin, 100 μg/mL streptomycin sulfate, 3 μg/mL amphotericin B, and 20 μg/mL gentamycin (growth medium). Cells were maintained in an atmosphere of 95% air and 5% CO2 at 37°C. Prior to confluence, cells were harvested in 0.25% trypsin and sub-cultured into 80 cm2 culture flasks or 96 well plates.

This thicker layer decreases transparency and therefore also reduces efficiency. Weak adhesion of nanowires to the substrate is another important issue. Without

any special processing, scratches or shear stresses on the surface can easily wipe the nanowires from the surface [11]. Several papers in the literature have addressed the roughness and adhesion issues of nanowire electrodes. Solutions fall into three general categories. The first involves using a transparent conductive material to fill the spaces between the nanowires [14, 18, 20–22]. Gaynor et al. pressed silver nanowires into a layer of the transparent conductive polymer (PEDOT:PSS) to decrease the root-mean-square (RMS) surface roughness to 12 nm and maximum peak-to-valley

values to around 30 nm [21]. Choi et al. instead deposited the PEDOT:PSS layer on top of the nanowire film to achieve an RMS roughness of 52 nm Savolitinib [14]. Chung et al. alternatively Selleck VX-689 used ITO nanoparticles to fill the spaces between the wires and reduced the RMS roughness to 13 nm and the maximum peak-to-valley to below 30 nm. In the latter paper, polyvinyl alcohol (PVA) was also added to the ITO nanoparticle solution to increase the adhesion of the nanoparticle/nanowire film to the substrate [22]. The downside of all these approaches is that to significantly reduce surface roughness, the required thickness of the conductive material needs to be at least three times the diameter of the nanowires. At these thicknesses, there is a reduction in the electrode transparency and consequently the efficiency of the devices due to the limited transparency of the conductive materials [18]. The second category to reduce roughness is to deposit a transparent but nonconductive polymer on top of the nanowire

film [12, 23–25]. This allows a material that is more transparent than PEDOT:PSS or ITO to be used. Using an optical adhesive in this manner, Miller et al. reduced Niclosamide the RMS roughness of silver nanowire films to 8 nm and there was only a 2% change in sheet resistance after an adhesion test [25]. Zeng et al. buried silver nanowires in PVA to reduce the surface RMS to below 5 nm and increase adhesion of the nanowires to the substrate [24]. However, because the polymers used are not conductive, in all these studies the nanowire/polymer composite must be peeled off the original substrate to expose the conductive nanowire-mesh surface, which adds a complex manufacturing step. Although not reported in the literature (to our knowledge), the nanowire film could instead be pressed into a transparent nonconductive polymer, to avoid the peeling step. This technique however would still be less than ideal as an extra polymer layer would still add manufacturing complexity and some devices may not be compatible with the polymer used.

New York: IEEE; 2011:103–106. [Electron Devices Meeting (IEDM), 2011 IEEE International: December 5–7 2011] 4. Li Y, Cheng H-W, Chiu Y-Y, Yiu C-Y, Su H-W: A unified 3D device simulation of random dopant, interface trap and work function fluctuations on high-κ/metal gate device. Washington, DC. New York: IEEE; 2011:107–110. [Electron Devices Meeting (IEDM), IEEE International 2011;December 5–7 2011] 5. Yang B, Buddharaju

K, Teo S, Singh N, Lo G, Kwong D: Vertical silicon-nanowire formation and gate-all-around MOSFET. Electron Device Letters, IEEE 2008, 29:791–794.CrossRef 6. Numata T, Uno S, Kamakura Y, Mori N, Nakazato K: Fully analytic compact model of ballistic gate-all-around MOSFET with rectangular cross section. Osaka. New York: CBL-0137 sIEEE; 2011:39–42. [Simulation of Semiconductor Processes and Devices (SISPAD), 2011 International Conference; September 8–10 2011] 7. Singh P, Singh N, Miao J, Park W-T, Kwong D-L: Gate-all-around junctionless nanowire MOSFET with improved low-frequency noise behavior. Electron Device Letters, IEEE

2011, 32:1752–1754.CrossRef 8. Synopsys, Inc: Sentaurus Process User Guide, Version F-2011.09. Mountain selleck kinase inhibitor View; 2011. 9. Martin-Bragado I: Process atomistic simulation for microelectronics. University of Valladolid; 2004. [Doctoral thesis] 10. Help UVAS: University of Valladolid Atomistic Simulator. Spain: University of Valladolid; 2006. 11. Takeda H, Mori N: Three-dimensional quantum transport simulation of ultra-small FinFETs. J Comput Electron 2005, 4:31–34.CrossRef 12. Mil’nikov G, Mori N, Kamakura Y, Ezaki T: Dopant-induced intrinsic bistability in a biased nanowire. Phys Rev Lett 2009, 102:036801.1–4. 13. Asenov A, Jaraiz M, Roy S, Roy G, Adamu-Lema

F, Brown AR, Moroz V, Gafiteanu R: Integrated atomistic process and device simulation D-malate dehydrogenase of decananometre MOSFETs. Kobe, Japan. New York: IEEE; 2002:6.2.1–4. [Simulation of Semiconductor Processes and Devices (SISPAD), 2002 International Conference: September 4–6 2002] 14. Solmi S, Nobili D: High concentration diffusivity and clustering of arsenic and phosphorus in silicon. J Appl Phys 1998, 83:2484–2490.CrossRef 15. Uematsu M: Transient enhanced diffusion and deactivation of high-dose implanted arsenic in silicon. Jpn J Appl Phys (Part 1) 2000, 39:1006–1012.CrossRef 16. Kamakura Y, Mil’nikov G, Mori N, Taniguchi K: Impact of attractive ion in undoped channel on characteristics of nanoscale multigate field effect transistors: a three-dimensional nonequilibrium Green’s function study. Jpn J Appl Phys 2010, 49:04DC19.1–5.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions MU carried out the KMC calculations to obtain random discrete As distributions in the S/D extensions of NW transistors and drafted the manuscript. KMI supervised the KMC simulation. GM and HM participated in the NEGF simulation of NW transistors. NM carried out the NEGF calculations and analyzed the I-V characteristics of NW transistors.