In previous experiments, using cell lines (J774A.1 and MM6) instead of primary blood cells, we had made observations diverging from the results reported in Selleckchem GSK872 this study. In those cell lines the MDP1-down-regulated strain showed better growth than the control strain [27]. There are several possible

explanations for the different outcomes of infections of the cell lines versus blood monocytes. One plausible explanation is that primary monocytes on the one hand and cell lines on the other hand Protein Tyrosine Kinase inhibitor dispose of very different properties. It was shown that cell lines such as MM6, U-937 or THP-1 correspond to immature monocytes expressing biochemical markers characteristic of immature cells in monocyte development, which are not expressed by peripheral blood monocytes. Correspondingly, markers expressed at high levels in mature monocytes (e.g. lysozyme, CD14, MHC class II) were not expressed or expressed at low levels in these cell lines [35]. Deregulation of immune signalling may also occur in cell lines. The cell line J774A.1, for instance,

continuously synthesizes IL-1β (ATTC product description). Such properties may affect the mycobactericidal activity of cell lines compared to primary blood monocytes. Mdivi1 In contrast to the cell line cultures which consisted of only one cell type, namely the MM6 or J774A.1 cells, our blood monocyte preparations

which were purified by Ficoll/Percoll gradient centrifugation contained about 70% monocytes and about 30% CD14-negative cells (data not shown). The latter fraction contained cells such as CD4-positive IFN-γ-secreting lymphocytes able to activate monocytes. An activation of the primary monocytes by IFN-γ-producing cells may have intensified the bactericidal activity of blood-derived monocytes compared to the cell lines. Infection with M. bovis BCG (pAS-MDP1) caused a lesser activation of PBMC than infection with BCG (pMV261), as is evident from the cytokine expression of infected PBMC: 24 hours after infection the pro-inflammatory cytokine IL1-β was secreted at significantly lower amounts upon infection with the antisense-strain (Figure 3). IFN-γ as well as the anti-inflammatory cytokine IL-10 were also secreted at lower Thalidomide amounts, but due to donor variation no significance was obtained for the latter cytokines if the mean of all donors was calculated. The expression of these cytokines is mediated via binding of pathogen molecules to Toll-like receptors (TLR) located on the plasma and/or phagosome membranes. Among the TLR, TLR2, TLR9 and TLR4 are responsible for recognising M. tuberculosis. TLR4 is activated by heat shock proteins 60/65 [36, 37]. The heterodimers TLR2/TLR1 and TLR2/TLR6 can recognise mycobacterial lipoproteins.

Science 1989,245(4924):1374–1377.PubMedCrossRef 18. Huang HC, He SY, Bauer DW, Collmer A: The check details Pseudomonas syringae pv . syringae 61 hrpH product, an envelope protein required for elicitation of the hypersensitive response in plants. J Bacteriol 1992,174(21):6878–6885.PubMed 19. Lee J, Klusener B, Tsiamis G, Stevens C, Neyt C, Tampakaki AP, Panopoulos NJ, Noller J, Weiler EW, Cornelis GR, et al.: HrpZ(Psph) from the plant pathogen Pseudomonas syringae pv. phaseolicola binds to lipid bilayers and forms an ion-conducting pore in vitro. Proc Natl Acad Sci USA 2001,98(1):289–294.PubMedCrossRef 20. Preston GM, Bertrand N,

Rainey PB: Type III secretion in plant growth-promoting Pseudomonas fluorescens SBW25. Mol Microbiol 2001,41(5):999–1014.PubMedCrossRef 21. Ma Q, Zhai Y, Schneider JC, Ramseier TM, Saier MH Jr: Protein secretion Avapritinib systems of Pseudomonas aeruginosa selleck inhibitor and P fluorescens . Biochim Biophys

Acta 2003,1611(1–2):223–233.PubMedCrossRef 22. Rezzonico F, Binder C, Defago G, Moenne-Loccoz Y: The type III secretion system of biocontrol Pseudomonas fluorescens KD targets the phytopathogenic Chromista Pythium ultimum and promotes cucumber protection. Mol Plant Microbe Interact 2005,18(9):991–1001.PubMedCrossRef 23. Mazurier SLM, Siblot S, Mougel C, Lemanceau P: Distribution and diversity of type III secretion system-like genes in saprophytic and phytopathogenic fluorecent Pseudomonas . FEMS Microbiology Ecology 2004, 49:455–467.PubMedCrossRef 24. Toussaint B, Delic-Attree I, Vignais PM: Pseudomonas aeruginosa contains an IHF-like protein that binds to the algD promoter. Biochem Biophys Res Commun 1993,196(1):416–421.PubMedCrossRef 25. Dacheux D, Goure J, Chabert J, Usson Y, Attree I: Pore-forming activity of type III system-secreted proteins leads to oncosis of Pseudomonas aeruginosa -infected macrophages. Mol Microbiol 2001,40(1):76–85.PubMedCrossRef 26. Broek D, Chin AWTF, Bloemberg GV, Lugtenberg Dipeptidyl peptidase BJ: Molecular nature of spontaneous modifications

in gacS which cause colony phase variation in Pseudomonas sp . strain PCL1171. J Bacteriol 2005,187(2):593–600.PubMedCrossRef 27. Hakansson S, Schesser K, Persson C, Galyov EE, Rosqvist R, Homble F, Wolf-Watz H: The YopB protein of Yersinia pseudotuberculosis is essential for the translocation of Yop effector proteins across the target cell plasma membrane and displays a contact-dependent membrane disrupting activity. Embo J 1996,15(21):5812–5823.PubMed 28. Clerc P, Baudry B, Sansonetti PJ: Plasmid-mediated contact haemolytic activity in Shigella species: correlation with penetration into HeLa cells. Ann Inst Pasteur Microbiol 1986,137A(3):267–278.PubMedCrossRef 29. Shaw RK, Daniell S, Ebel F, Frankel G, Knutton S: EspA filament-mediated protein translocation into red blood cells. Cell Microbiol 2001,3(4):213–222.PubMedCrossRef 30.

If the mutation is indeed linked to the phenotype, then the mutant is further studied by additional transcriptomic, proteomic, physiological,

biochemical, and biophysical analyses. Preliminary studies in this case suggest that the cgl28 mutation is not linked to the photosynthetic phenotype Before we can be certain that the insertion in CGL28 is responsible for the mutant phenotype, it is critical that genetic crosses be done to demonstrate that the CGL28 gene is linked to the mutant phenotype (Zeocin or paromomycin resistance, depending on the marker gene used in the screen, always segregates with the photosynthetic phenotype) and ultimately that the phenotype can be rescued by introducing a wild-type copy of the CGL28 gene into the mutant strain (step 5); not

all phenotypes identified by reverse genetic screening are actually https://www.selleckchem.com/products/z-vad(oh)-fmk.html caused by the inserted DNA. In most cases, the linkage and complementation analyses would be performed either before or at the same time that check details the physiological and biophysical characterizations are being performed. Additional analyses of the mutant strains, such as detailed studies of light sensitivity, sensitivity to compounds that facilitate the generation of reactive oxygen compounds, and analyses of the polypeptides present in the individual complexes associated with photosynthetic ACP-196 chemical structure activities would add new perspectives to our view of photosynthesis and its regulation. Concluding remarks Numerous studies over the last half century have defined activities associated with photosynthetic function and identified proteins critical for the harvesting and utilization of excitation energy, electron transport reactions, ATP formation, and CO2 fixation. However, with more in-depth analyses of photosynthetic function, it is Leukotriene-A4 hydrolase becoming clear that photosynthetic activities are exquisitely sensitive

to environmental change (and developmental stage) and that various regulatory mechanisms interact to yield a final output from the system. Rapid responses of photosynthetic activities to fluctuations in the environment help to coordinate the products of photosynthesis with the metabolic demands of the cell and minimize damage associated with reactive oxygen species that may be formed as a consequence of excitation of pigment molecules and the generation of reactive intermediates. These short-term responses may reflect changes in protonation, phosphorylation, and the association of various pigment and protein components of the photosynthetic complexes. Longer-term responses may result in changes in subunit stoichiometries, pigment composition, and the insertion of novel proteins into individual complexes.

Her oxygen saturation was 90%. Physical examination revealed a tender abdomen. The gastrostomy tube drained coffee ground material. Laboratory Napabucasin research buy studies showed marked leukocytosis of 23000 and Creatinine level was 1.4 mg/dl. Urinalysis showed amylase level of 11,460 U/L. Plain abdominal and chest radiograph were normal. No free air was detected. An upper abdominal Ultrasound was preformed, demonstrating an enlarged gallbladder with no gallstones or sludge. There were no signs of cholecystitis but the common bile duct (CBD) was dilated to 16 mm. An

abdominal CT with IV contrast revealed a peripancreatic fat stranding and an edematous pancreatic head. These finding were consistent with acute pancreatitis. The Foley catheter balloon was seen

deep in the second part of the duodenum facing Vaters’ papilla (Figure  1). Figure 1 Abdominal CT scan showing Foley catheter balloon located in the second part of the duodenum and peripancreatic fat stranding with an edematous pancreatic head. The gastrostomy tube was pulled back to the stomach and secured to the abdominal wall with silk stich. The patient was treated with fluid and analgesics. The next day a follow-up sonographic evaluation was done indicating a reduction of the CBD diameter to 11 mm. During her stay in the hospital her respiratory symptoms were significantly relieved, she regained hemodynamic stability, was normothermic and her abdominal tenderness disappeared. Laboratory results normalized. Bilirubin and amylase levels returned to normal within three days of her admission. She was discharged after 6 days, having significantly improved and was sent back to her retirement home. I-BET-762 concentration Discussion Percutaneous Endoscopic Gastrostomy

Methocarbamol (PEG) tube was first described in 1980 by Gaunderer [2]. PEG is consider safe and effective method for providing long term enteral nutrition while offering advantages over nasogastric tube feeding [3, 4]. The incidence of short and long term complications related to PEG actual insertion is low [5]. However, tube related complications such as granulation tissue, broken or leaking tube, leakage around the tube site and stomal site infection exceed 60% [6]. Migration of feeding gastrostomy has been described in the past as the cause for gastric outlet obstruction [7], duodenal obstruction [8] and biliary obstruction [9]. Our case presents CFTRinh-172 cell line pancreatitis as a potential complication of a balloon gastrostomy tube. In our case it seems that the Foley catheter’s balloon obstructed the ampulla of Vater, therefore resulting in acute pancreatitis. Gastrostomy tube dislodgement pancreatitis is rare. Review of the English literature revealed 10 cases of pancreatitis as a result of migration of feeding gastrostomy [5, 10–17]. The first case was published in 1986 by Bui et al. [10]. He described a migration of a Foley catheter that was inadvertently left in place after establishing a permanent surgical Gastrostomy.

Moreover, back pain in Ruxolitinib solubility dmso patients who did not sustain a fracture during the follow-up period would reduce due to the natural course of the disease [2]. EFOS provided information on the use of different osteoporosis medications after the end of teriparatide treatment in normal clinical practice. The majority of patients selleck chemical (70.7%) received

antiresorptives (primarily bisphosphonates). Whether it was the long-term pharmacological effect of teriparatide on bone tissue, the contribution of this sequential medication, or both that affected the post-treatment risk of fracture is unclear, but the clinically relevant finding was that there was no evidence of deterioration in the odds of fracture or a rebound increase

in back pain after teriparatide was discontinued. Antiresorptives such as alendronate, calcitonin and raloxifene have been reported to reduce back pain in postmenopausal women with osteoporosis [29–35]. It is unclear why we did not observe a further decline in back pain after teriparatide discontinuation when most patients were receiving antiresorptives. One possible explanation is that the patients had already reached a low level of back pain (~30 mm). Our study has several limitations. First, the results are specific to postmenopausal RepSox datasheet women with severe osteoporosis and may not be applicable to other types of patients receiving teriparatide. Second, we did not determine morphometric 17-DMAG (Alvespimycin) HCl vertebral fractures as X-rays were only performed in symptomatic patients, so we may have underestimated the effectiveness in overall risk of vertebral fracture. Third, we did not gather data on the use of analgesics during the study. Fourth, the study was not designed to examine the maintenance of fracture efficacy after discontinuation of treatment, and the wide CIs show lack of power to determine

fracture efficacy after teriparatide treatment was discontinued. Finally, the lack of a randomised control group prevents determination of the cause of the observed findings, especially subjective symptoms, such as back pain. The strengths of the EFOS study include the prospective examination of clinical fractures in postmenopausal women with osteoporosis in real-life clinical practice both during teriparatide therapy and after teriparatide discontinuation. We also evaluated changes in pain over time using patient-completed instruments, thereby gaining the patients’ perspective. Our analyses adjusted for factors that may influence back pain, such as age, baseline level of pain, co-morbid rheumatoid arthritis, prior medication and fracture history.

2) were lower than that of the pure SA monolayer, indicating that the mixed monolayers

were less condensed and more compressible than the pure monolayer. This is consistent with the plateau region existing in the π-A isotherm of every mixed system (Figure  1). Figure 3 Compressional modulus of SA/BSA monolayers vs surface pressure for discrete X BSA on pure water subphase at 26°C. The isotherm of pure SA showed two Apoptosis inhibitor distinct regions: the first one corresponding to the monolayer in its liquid-condensed (LC) phase and the second one of a solid (S) film that was characterized AZD6244 by higher C s -1 values. The values of C s -1 obtained that were relatively high at X BSA = 0.1 are characteristic of a LC phase. The reason for this observation could be that at low concentrations of BSA, less lipid-protein interaction occurred in the mixed system. At surface pressure 30 and 35 mN m-1, C s -1 was observed to be below 50 mN m-1 for the entire range of BSA mole ratios, from X BSA ≥ 0.2 onwards, this being indicative of

the formation of the LE phase. This implied that the incorporation of BSA into the SA monolayers reduced their condensation. Molecular interactions can be expressed quantitatively in thermodynamic analysis. Total free energy of mixing ΔG mix is defined by the following equation: (4) where (5) and the excess free energy of mixing ΔG ex can be calculated from CB-839 in vivo π-A isotherms by [11, 17] (6) where A 12, A 1 and A 2 represent the area of the mixed system and

respective areas of components as 1 and 2, respectively, and π is the surface pressure of the monolayer. If the monolayer is ideally mixed, ΔG ex should be zero. Negative values of ΔG ex in the entire range of the monolayer composition indicated very strong attractions between molecules in the mixed system (Figure  4). The results showed that the binary SA/BSA mixed monolayers were thermodynamically stable. The most stable intermolecular interaction was observed at X BSA = 0.8, at discrete surface pressures, suggesting that SA interacted strongly with BSA molecules and were miscible in the system. This observation was supported by the A 12 and C s -1 measurements as discussed above. Figure 4 Free excess energy Δ G ex of SA/BSA monolayers vs X BSA on pure water subphase at 26°C. For discrete surface pressure of Cyclin-dependent kinase 3 5 mN m -1 (diamond), 10 mN m -1 (circle), 15 mN m -1 (triangle), 20 mN m -1 (square) and 25 mN m -1 (right-pointing triangle). ΔG ex gradually decreased as the concentration of BSA rose. There was a slight recovery of ΔG ex at X BSA = 0.9. When the monolayer contained BSA only, ΔG ex was almost similar to X BSA = 0.9. This might be due to intermolecular repulsion occurring in the mixed monolayer system when the concentration of BSA was saturated in the system. The most compatible mixture of SA/BSA in a mixed monolayer was when X BSA = 0.8.

Clin Pharmacol Ther 34:234–239PubMedCrossRef 19. Laing YY, Zeger SL (1986) Longitudinal find more data analysis using generalised linear models. Biometrika 73:13–22CrossRef 20. Hosmer DW Jr, Lemershow S (2000) Applied logistic regression, 2nd edn. Wiley, New YorkCrossRef 21. Adami S, San Martin J, Muñoz-Torres M, Econs MJ, Xie L, Dalsky GP, McClung M, Felsenberg D, Brown JP,

Brandi ML, Sipos A (2008) Effect of raloxifene after recombinant teriparatide [hPTH(1-34)] treatment in postmenopausal women with osteoporosis. Osteoporos Int 19:87–94PubMedCrossRef 22. Eastell R, Nickelsen T, Marin F, Barker C, Hadji P, Farrerons J, Audran M, Boonen S, Brixen K, Melo Gomes J, Obermayer-Pietsch B, Avramidis A, Sigurdsson G, Gluer CC (2009) Sequential treatment of severe postmenopausal osteoporosis after teriparatide: final results of the randomized, controlled European Study https://www.selleckchem.com/products/mm-102.html of Forsteo (EUROFORS). J Bone Miner Res 24:726–736PubMedCrossRef 23. Lindsay R, Scheele WH, Neer R, Pohl G, Adami S, Mautalen C, Reginster J-Y, Stepan JJ, Myers

SL, Mitlak BH (2004) Sustained vertebral fracture risk reduction after withdrawal of teriparatide in postmenopausal women with osteoporosis. Arch Intern Med 164:2024–2030PubMedCrossRef 24. Prince R, Sipos A, Hossain A, Syversen U, Ish-Shalom S, Marcinowska E, Halse J, Lindsay R, Dalsky GP, Mitlak BH (2005) Sustained nonvertebral fragility fracture risk reduction those after discontinuation of teriparatide treatment. J Bone Miner Res 20:1507–1513PubMedCrossRef 25. Nevitt MC, Chen P, Dore RK, Reginster JY, Kiel DP, Zanchetta JR, Glass EV, Krege JH (2006) Reduced risk of back pain following teriparatide treatment: a meta-analysis. Osteoporos Int 17:273–280PubMedCrossRef 26. Nevitt MC, Chen P, Kiel DP, Reginster JY, Dore RK, Zanchetta JR, Glass EV, Krege JH (2006) Reduction in the risk of developing back pain persists at least 30 months after discontinuation of teriparatide treatment: a meta-analysis. Osteoporos Int 17:1630–1637PubMedCrossRef 27. Buchbinder R, Osborne RH, Ebeling PR, Wark JD, Mitchell P, Wriedt C, Graves S, Staples MP,

Murphy B (2009) A randomized trial of vertebroplasty for painful osteoporotic vertebral fractures. N Engl J Med 361:557–568PubMedCrossRef 28. Kallmes DF, Comstock BA, Heagerty PJ, Turner JA, Wilson DJ, Diamond TH, selleck compound Edwards R, Gray LA, Stout L, Owen S, Hollingworth W, Ghdoke B, Annesley-Williams DJ, Ralston SH, Jarvik JG (2009) A randomized trial of vertebroplasty for osteoporotic spinal fractures. N Engl J Med 361:569–579PubMedCrossRef 29. Nevitt MC, Thompson DE, Black DM, Rubin SR, Ensrud K, Yates AJ, Cummings SR, for the Fracture Intervention Trial Research Group (2000) Effect of alendronate on limited-activity days and bed-disability days caused by back pain in postmenopausal women with existing vertebral fractures. Arch Intern Med 160:77–85PubMedCrossRef 30.

The volume and surface area of the nanoparticles

were calculated during the compression process using a tool available with the Materials Studio (Accelrys, Inc., San Diego, CA, USA) modeling package. Figure 5a,b shows the volume and surface area of the nanoparticles as a function of applied compression strain, respectively. Overall, both volume and surface area decrease NU7441 order with increasing levels of strain for the three chain architectures. This indicates that densification occurs during the whole compression process, independent of the chain architecture. However, the chain architecture influences the initial and deformed volumes and surface areas of the deformed nanoparticles. In the undeformed state, the networked

molecules have a more compact structure compared to the other two and demonstrate a larger compressibility during deformation. This behavior originates from the relatively low mobility of the cross-linked network chains. Several local changes of volume and surface area in the curves indicate a complex deformation process that includes stepwise chain slipping and large configurational changes to relax the strain energy. At very large deformations, a steep decrease of volume and surface area appears, which corresponds to the fourth click here regime of the selleck chemicals compressive stress–strain curves in Figure 4b. The lateral extension strain of the compressed nanoparticles versus the applied compressive strain for each of the three chain architectures is shown in Figure 5c. The negligible lateral extension strain below an applied compressive strain of 0.06 corresponds to the first deformation regime, thus confirming the compression of the low-density surface region. From Figure 5c, it is clear that the chain architecture plays an insignificant role on the lateral deformation of the nanoparticles for the entire range of applied compressive strains.

Figure 5 Volume (a), surface area (b), and lateral strain (c) of PE nanoparticles. As a function of compression strain. Visualization of the PE new chains in the nanoparticles during the compression loading process helps to reveal the molecular deformation mechanisms. Figure 6 shows representative three-dimensional (3D) molecular configurations extracted from the simulation of nanoparticle systems at different compressive strains. The selected molecules exhibit kinking and physical entanglement. Figure 6a, b presents side and top views, respectively, of distinct changes in the network chain conformation during the compression process. Specifically, as shown in Figure 6a, the network chain undergoes significant realignment due to the contraction in z direction and expansion in x direction. However, from Figure 6b, the network expands in the x-y plane when compressed in the z direction.

4), 10% (v/v) FBS, and 10 mM PBS, respectively. The suspensions were constantly mixed on a shaker at room temperature for 9 days. One hundred fifty microliter samples were diluted in 2 mL

ISRIB order ultrapure water at different time points, and the particle size was measured by Malvern Nano-ZS zetasizer. The measurements were performed in triplicate at room temperature. Determination of KLH content in NPs KLH in NPs was quantified using a modified method [14]. Briefly, 10 mg of NPs was dissolved in 1 mL of 0.1 M NaOH solution and incubated at 2°C for 12 h. The solution pH was adjusted BAY 1895344 cost to 7.0 using 1 M HCl. Two hundred microliters of DOC (0.15, w/v) was added and the final volume was adjust to 2 mL using ultrapure water. After sitting at room temperature for 15 min, the mixture was added with 200 μL of TCA (80%, w/v) and incubated for 5 min. Samples were vortexed for 2 min and centrifuged at 5,000 g for 20 min at room temperature. Pellets were dissolved in 500 μL of SDS (5%, w/v) containing 0.01 M NaOH. Following the protocol from the supplier, KLH concentration was determined using Micro BCA Protein Assay Kit (Thermo Fisher Scientific Inc., Waltham, MA, USA). In vitrorelease of KLH from NPs in human plasma Five milligrams

of NPs see more containing rhodamine B-labeled KLH was suspended in 1 mL of 10% (v/v) human serum (pH 7.4) and incubated in darkness (covered by foil) at 37°C. Samples were centrifuged at 10,000 g for 15 min at determined time points. The supernatant (200 μL) was added into a blank 96-well plate (Thermo Fisher Scientific Inc., Waltham, MA, USA) and measured find more using Synergy HT Multi-Mode

Microplate Reader (BioTek Instruments, Inc., Winooski, VT, USA) with excitation at 530 nm and emission at 590 nm. The pellets were resuspended in 1 mL of 10% (v/v) human serum. Release of KLH at certain time points was calculated by using the following equation: KLH release% = Absorbance at certain time point/Total absorbance × 100. Flow cytometry measurement of endocytosis of NPs by DCs JAWSII (ATCC® CRL-11904™) immature DCs from ATCC were cultured with alpha MEM (80%v) including ribonucleosides, deoxyribonucleosides, 4 mM l-glutamine, 1 mM sodium pyruvate and 5 ng/mL murine GM-CSF, and FBS (20%v) at 37°C, 5% CO2 in 24-well plates (CORNING, Tewksbury, MA, USA). NPs were assembled according to the above-mentioned method, except that KLH was labeled with rhodamine B and 0.5 mg of NBD PE was added to existing lipids. One milligram of NPs suspended in 2 mL complete medium with a final concentration of 0.5 mg/mL was added into each well containing 106 cells and incubated for 1, 2, and 3 h, respectively. After incubation, the medium was immediately removed and cells were washed with ultrapure water for five times. Cells were detached from culture plate using trypsin/EDTA solution and centrifuged at 200 g for 10 min, and cell pellets were resuspended in 10 mM PBS (pH 7.4).

Electronic supplementary material Additional file 1: Supporting information on the scalable and number-controlled synthesis of carbon nanotubes by nanostencil lithography. Includes a detailed fabrication process of the nanostencil mask, images of the various nanostencil apertures, and images 17DMAG of the synthesized CNTs. (PDF 440 KB) References 1. Baughman RH, Zakhidov AA, de Heer WA: Carbon nanotubes – the route toward applications. Science 2002, 297:787–792.Selumetinib cell line CrossRef 2. Tans SJ, Verschueren ARM, Dekker C: Room-temperature transistor based on a single carbon nanotube. Nature 1998, 393:49–52.CrossRef

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nanotube transistor arrays for multistage complementary logic and ring oscillators. Nano Lett 2002, 2:929–932.CrossRef 4. de Heer WA, Bacsa WS, Chatelain A, Gerfin T, Humphrey-Baker R, Forro L, Ugarte D: Aligned carbon nanotube films: production and optical and electronic properties. Science 1995, 268:845–847.CrossRef 5. Kim P, Lieber CM: Nanotube nanotweezers. Science 1999, 286:2148–2150.CrossRef 6. Baughman RH, Cui C, Zakhidov AA, Iqbal Z, Barisci JN, Spinks GM, Wallace GG, Mazzoldi A, De Rossi Selleckchem Entospletinib D, Rinzler AG, Jaschinski O, Roth S, Kertesz M: Carbon nanotube actuators. Science 1999, 284:1340–1344.CrossRef 7. Sazonova V, Yaish Y, Ustunel

H, Roundy D, Arias TA, McEuen PL: A tunable carbon nanotube electromechanical oscillator. Nature 2004, 431:284–287.CrossRef 8. Rueckes T, Kim K, Joselevich E, Tseng GY, Cheung C-L, Lieber CM: Carbon nanotube-based nonvolatile random access memory for molecular computing. Science 2000, 289:94–97.CrossRef 9. Choi J, Lee J-I, Eun Y, Kim M-O, Kim J: Aligned carbon nanotube arrays for degradation-resistant, intimate contact in micromechanical devices. Adv Mater 2011, 23:2231–2236.CrossRef 10. Stampfer C, Helbling T, Obergfell Nintedanib (BIBF 1120) D, Schoberle B, Tripp MK, Jungen A, Roth S, Bright VM, Hierold C: Fabrication of single-walled carbon-nanotube-based pressure sensors. Nano Lett 2006, 6:233–237.CrossRef 11. Kong J, Franklin NR, Zhou C, Chapline MG, Peng S, Cho K, Dai H: Nanotube molecular wires as chemical sensors. Science 2000, 287:622–625.CrossRef 12. Star A, Gabriel J-CP, Bradley K, Gruner G: Electronic detection of specific protein binding using nanotube FET devices. Nano Lett 2003, 3:459–463.CrossRef 13. Choi J, Kim J: Batch-processed carbon nanotube wall as pressure and flow sensor. Nanotechnology 2010, 21:105502.CrossRef 14. Chung J, Lee K-H, Lee J, Ruoff RS: Toward large-scale integration of carbon nanotubes. Langmuir 2004, 20:3011–3017.CrossRef 15.