Hippo D, Nakamine Y, Urakawa K, Tsuchiya Y, Mizuta H, Koshida N,

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10.1063/1.2756522CrossRef 10. Zighem F, Maurer T, Ott F, Chaboussant G: Dipolar interactions in arrays of ferromagnetic nanowires: a micromagnetic study. J Appl Phys 2011, 109:013910. 10.1063/1.3518498CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions KR and PG fabricated the samples by conventional etching and performed all the electrodeposition and also carried out the magnetization measurements. NK provided the magnetic field-assisted porous silicon samples.

PP performed the SEM Phosphatidylinositol diacylglycerol-lyase investigations. All authors discussed the data and prepared the manuscript. All authors read and approved the final manuscript.”
“Background Nanoporous anodic alumina (NAA) is one of the smartest materials in which scientists have centered their research with considerable interest in recent years [1, 2] due to their physicochemical properties like thermal stability, environmental toughness, and biocompatibility. Alumina has been studied for decades [3]. The fabrication technology permits to obtain highly ordered and customized porous nanostructures that makes NAA very attractive for different applications such as nanomaterial synthesis [4, 5], photonics [6], or sensors [7–9]. In particular, NAA has demonstrated its sensing capabilities: a great wealth of work has been carried out with this material in biotechnology areas [10], and it presents reliable possibilities of working as portable chemical and biochemical sensors [11], as well as label-free biosensors [12]. Furthermore, if the optical waveguide properties of NAA are exploited, much higher sensitivities than conventional surface plasmon resonance (SPR) sensors [2, 13, 14] can be achieved. Sensors based on alumina improve their sensitivity by the measurement of the oscillations in the reflectance spectrum produced by the Fabry-Pérot (F-P) interferences in a NAA thin film [15, 16].

BMC Microbiol 2008,8(1):132 PubMedCrossRef 27 Ly KT, Casanova JE

BMC Microbiol 2008,8(1):132.PubMedCrossRef 27. Ly KT, Casanova JE: Mechanisms of Salmonella entry into host cells. Cell Microbiol 2007,9(9):2103–2111.PubMedCrossRef 28. Monack DM, Bouley DM, Falkow S: Salmonella typhimurium persists within mTOR inhibitor macrophages in the mesenteric lymph nodes of chronically infected Nramp1+/+ mice and can be reactivated

by IFNgamma neutralization. J Exp Med 2004,199(2):231–241.PubMedCrossRef 29. Spiehs MJ, Shurson GC, Johnston LJ: Effects of two direct-fed microbials on the ability of pigs to resist an infection with Salmonella enterica serovar Typhimurium. Journal of Swine Health and Production 2008,16(1):27–36. 30. Wells JE, Yen JT, Miller DN: Impact of dried skim milk in production diets on Lactobacillus and pathogenic bacterial shedding in growing-finishing swine1. J Appl Microbiol 2005,99(2):400–407.PubMedCrossRef 31. Ten Bruggencate SJ, Bovee-Oudenhoven IM, Lettink-Wissink ML, Katan MB, Van Der Meer R: Dietary fructo-oligosaccharides and inulin decrease resistance of rats to salmonella: protective role of calcium. Gut 2004,53(4):530–535.PubMedCrossRef 32. Kirby AC, Yrlid U, Wick MJ: The innate immune response differs in primary and secondary

Salmonella SRT1720 price infection. J Immunol 2002,169(8):4450–4459.PubMed 33. Lalmanach AC, Lantier F: Host cytokine response and resistance to Salmonella infection. Microbes and infection/Institut Pasteur 1999,1(9):719–726.PubMedCrossRef 34. Barman M, Unold D, Shifley K, Amir E, Hung K, Bos N, Salzman N: Enteric Salmonellosis disrupts the microbial ecology of the murine gastrointestinal tract. Infect Immun 2008,76(3):907–915.PubMedCrossRef 35. Tanaka T, Imai Y, Kumagae N, Sato S: The effect of feeding lactic acid to Salmonella typhimurium experimentally infected swine. The Journal of veterinary medical science/the

PFKL Japanese Society of Veterinary Science 2010,72(7):827–831.PubMedCrossRef 36. de Moreno de LeBlanc A, Castillo NA, Perdigon G: Anti-infective mechanisms induced by a probiotic Lactobacillus strain against Salmonella enterica serovar Typhimurium infection. Int J Food Microbiol 2010,138(3):223–231.CrossRef 37. Ibrahim SA, Yang H, Seo CW: Antimicrobial activity of lactic acid and copper on growth of Salmonella and Escherichia coli O157:H7 in laboratory medium and carrot juice. Food Chem 2008,109(1):137–143.CrossRef 38. Eloff JN: Which extractant should be used for the screening and isolation of antimicrobial components from plants? J Ethnopharmacol 1998,60(1):1–8.PubMedCrossRef 39. Santos RL, Raffatellu M, Bevins CL, Adams LG, Tükel Ç, Tsolis RM, Bäumler AJ: Life in the inflamed intestine, Salmonella style. Trends Microbiol 2009,17(11):498–506.PubMedCrossRef 40. Winter SE, Keestra AM, Tsolis RM, Bäumler AJ: The blessings and curses of intestinal inflammation. Cell Host Microbe 2010,8(1):36–43.PubMedCrossRef 41.

A total of 39 type III effectors have been identified in E coli

A total of 39 type III effectors have been identified in E. coli 0157:H7 strain Sakai through a combination of bioinformatics, “”secretome”" analysis, and translocation assays with Cya fusions [5]. However, the absence of a convenient model host system for E. coli O157:H7 has impeded in vivo characterization of host interaction phenotypes on the level conducted in P. syringae, with the result Metabolism inhibitor that annotation of E. coli O157:H7 effectors has relied more extensively on inferences made from sequence similarity. Among the O157:H7 effectors studied in greater depth is the Translocated Intimin Receptor protein (Tir), which plays a key role in bacterial

attachment to host cells [12–15]. Given that attachment has proven a tractable process for studying in cell culture models, it is possible to assign GO annotations to Tir with a specificity comparable to that of AvrPtoB. Tir is secreted into host cells via the LEE (locus of enterocyte effacement) T3SS and then trafficked to the host cell plasma membrane (GO:0020002), where it binds the (also LEE-encoded) intimin protein on the bacterial cell surface.

This binding activity is captured by the combination of Molecular Function ontology terms “”GO:0051635 bacterial cell surface binding”" and “”GO:0005515 protein binding”" using the IPI evidence code and “”with”" qualifier to specify the interacting partner as intimin. The role of Tir in bacterial attachment is reflected by the Biological Process term Cell Cycle inhibitor “”GO:0044406 adhesion to host”", with subsequent effects of Tir on the cascade of host signaling, described by “”GO:0052027 modulation by symbiont of defense-related host MAP kinase-mediated signal transduction pathway”" and major host cytoskeletal remodeling captured by “”GO:0052039 modification

by symbiont of host cytoskeleton”" easily accommodated by child terms of “”GO:0051701 interaction with host”". The term “”GO:0052057 modification by symbiont of host morphology or physiology via protein secreted by type III secretion system”" links Tir to other T3SS effectors, while “”GO:0009405 crotamiton pathogenesis”" indicates its role in disease. The Tir effector also highlights some of the challenges inherent to cross-genome term assignments. Given that transitive annotation based on sequence and structural similarity forms the basis of most annotations in the GO database, discussion of the limitations of such annotations is warranted. Specifically, similar gene products involved in the interaction between organisms can have very different properties depending on both their source organism and the host with which they are interacting. For example, Tir has been shown to have different molecular functions depending on whether it is produced by enterohemorrhagic (EHEC) O157:H7 or enteropathogenic (EPEC) strains of E. coli.

Table 1 Effect on vertebral fracture rates (from randomized contr

Table 1 Effect on vertebral fracture rates (from randomized controlled trials)   Osteopenia Osteoporosis (without prevalent vertebral fractures) Established osteoporosis (with prevalent vertebral fractures) Raloxifene ● ■ ■ Alendronate NA ■ ■ Risedronate NA ● ■ Ibandronate NA ■ ■ Zoledronate NA ■ ■ Teriparatide NA NA ■ Strontium ranelate ● ■ ■ Denosumab NA ■ ■ NA No evidence available ■ Denotes a preplanned analysis in the entire study population ● Denotes

a post hoc analysis Table 2 Effect on nonvertebral/hip fracture rates (from randomized controlled trials) mTOR inhibitor   Nonvertebral Hip Osteoporosis (without prevalent vertebral fractures) Established osteoporosis (with prevalent vertebral fractures) Osteoporosis (without prevalent vertebral fractures) Established osteoporosis (with prevalent vertebral fractures) Raloxifene NA ● NA NA Alendronate ■ ■ NA ■ Risedronate NA ■ NA ■ Ibandronate NA ● NA NA Zoledronate ■ NA ■ NA Teriparatide NA ■ NA NA Strontium Ranelate ● ■ ● ▲ Denosumab ■ NA ■ click here NA NA no evidence available ■ Denotes a preplanned analysis in the entire study population ▲ Denotes a preplanned analysis on a subset

of the study population ● Denotes a post hoc analysis Calcium and vitamin D supplementation should be a first-line strategy for the management of osteoporosis. Based on the very low mean dietary intake of calcium in the Belgian population, a systematic pharmacological supplementation (1,000–1,200 mg of calcium ion daily) in postmenopausal women appears to be an appropriate strategy (unless an individual dietary assessment reveals a satisfactory intake). The high prevalence of vitamin D deficiency in elderly Belgian subjects, combined

with the low marginal cost of a calcium–vitamin D supplementation compared with calcium alone, suggest that, after the age of 65, calcium and (800–1,000 IU) vitamin D should be systematically offered to all postmenopausal women, either alone or, if needed, in combination with another therapeutic regimen. HRT can no longer be considered as a first-line treatment for osteoporosis. It should only be considered in women experiencing PFKL climacteric symptoms, for the shortest possible duration and with the lowest effective doses. Selective-estrogen receptor modulators are a first-line option for women with low BMD, with or without fractures. Their effect on vertebral fracture is unequivocal, across different degrees of skeletal fragility, ranging from osteopenia to severe osteoporosis. Evidence of antifracture efficacy against nonvertebral fractures is limited to a post hoc analysis performed in a high-risk subset of the population. Breast benefits have been documented and should be taken into account when assessing the overall risk/benefit ratio of SERMs. Bisphosphonates reduce vertebral, nonvertebral, and hip fractures in women with established osteoporosis (low BMD and prevalent fractures).

It is likely that blood serum and tissue concentration levels of

It is likely that blood serum and tissue concentration levels of carnitine and propionate increase over time to some point of saturation. It is recommended that future investigations examine the time by dosage dynamics involved in GPLC supplementation. The mechanisms involved in acute enhancement of power output and reduced lactate accumulation are possibly (in higher intake levels) also responsible for the reduced mean Selleck BAY 80-6946 values of power seen with long-term intake. These authors suggest that it is unlikely that greater levels

of propionate or carnitine in the blood stream or muscle tissue would reduce the production of power during the repeated sprints. However, it appears quite probable that the vasodilatory effects of GPLC surpassed a beneficial magnitude in the 3.0 and 4.5 g/d groups. A post-hoc

examination of participant statements regarding their condition following the final testing session revealed that 13 of the 38 individuals completing the study complained that discomfort associated with leg pump limited their sprinting performance. These 13 included five of the 12 individuals in the 3.0 g/d group, and seven of the 14 participants in the 4.5 g/d group but only one individual in the 1.5 g/d group reported leg pump as a limiting factor. While not statistically significant, the 3.0 and 4.5 g/d groups displayed greater mean increases in thigh Nintedanib (BIBF 1120) girth with sprinting compared with baseline

while BIBF 1120 research buy the 1.5 g/d group exhibited the same relative leg pump. Thus, while the results of this study cannot definitively explain the lack of power output enhancement with long-term intake of GPLC, the limited information available suggests that excessive localized muscle pumping is involved. With increasing intensity of exercise, there is proportional increase in local blood flow of the exercising musculature. Vasodilation provides up to 25 -50 times resting levels of local blood flow by means of relaxation of the smooth arterial musculature and of the sphincter allowing flow into the capillary bed [9]. The process of vasodilation is closely associated with NO as this short-lived, reactive nitrogen molecule is responsible for regulation of vascular muscle tone [10]. Since it was determined that NO has a vital role in the control of blood flow, scientists have speculated on the effects increased levels would have on cardiovascular functioning in particular and exercise performances in general. However, this question has remained a matter of supposition as no nutritional supplementation has proven capable of influencing NO synthesis, until recently. The only food supplement shown to directly affect the production of NO is GPLC. It has been shown that 28 d GPLC at 4.5 g/d produces significantly elevated levels of nitrites and nitrates [6, 7]. Acute supplementation at 4.

The mechanisms underlying the anti-tumor effects of adiponectin a

The mechanisms underlying the anti-tumor effects of adiponectin and the functional properties of AdipoR have not Compound C cell line been fully elucidated. Although further research in this field is necessary, the presence of AdipoR1 could be a novel anticancer therapeutic

target in gastric cancer. References 1. Scherer PE, Williams S, Fogliano M, Baldini G, Lodish HF: A novel serum protein similar to C1q, produced exclusively in adipocytes. J Biol Chem 1995, 270:26746–26749.PubMedCrossRef 2. Hu E, Liang P, Spiegelman BM: AdipoQ is a novel adipose-specific gene dysregulated in obesity. J Biol Chem 1996, 271:10697–10703.PubMedCrossRef 3. Chandran M, Phillips SA, Ciaraldi T, Henry RR: Adiponectin: more than just another fat cell hormone? Diab Care 2003, 26:2442–2450.CrossRef

4. Maeda K, Okubo K, Shimomura I, Funahashi T, Matsuzawa Y, Matsubara K: cDNA cloning and expression of a novel adipose specific collagen-like factor, apM1 (AdiPose Most abundant Gene transcript 1). Biochem Biophys Res Commun buy Small molecule library 1996, 221:286–289.PubMedCrossRef 5. Nakano Y, Tobe T, Choi-Miura NH, Mazda T, Tomita M: Isolation and characterization of GBP28, a novel gelatin-binding protein purified from human plasma. J Biochem 1996, 120:803–812.PubMed 6. Yamauchi T, Kamon J, Waki H, Terauchi Y, Kubota N, Hara K, Mori Y, Ide T, Murakami K, Tsuboyama-Kasaoka N, Ezaki O, Akanuma Y, Gavrilova O, Vinson C, Reitman ML, Kagechika H, Shudo K, Yoda M, Nakano Y, Tobe K, Nagai R, Kimura S, Tomita M, Froguel P, Kadowaki T: The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity. Montelukast Sodium Nat Med 2001, 7:941–946.PubMedCrossRef 7. Berg AH, Combs TP, Du X, Brownlee M, Scherer PE: The adipocyte secreted protein Acrp30 enhances hepatic insulin action. Nat Med 2001, 7:947–953.PubMedCrossRef 8. Arita Y, Kihara S, Ouchi N, Takahashi M, Maeda K, Miyagawa J,

Hotta K, Shimomura I, Nakamura T, Miyaoka K, Kuriyama H, Nishida M, Yamashita S, Okubo K, Matsubara K, Muraguchi M, Ohmoto Y, Funahashi T, Matsuzawa Y: Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity. Biochem Biophys Res Commun 1999, 257:79–83.PubMedCrossRef 9. Hara K, Horikoshi M, Yamauchi T, Yago H, Miyazaki O, Ebinuma H, Imai Y, Nagai R, Kadowaki T: Measurement of the high-molecular weight form of adiponectin in plasma is useful for the prediction of insulin resistance and metabolic syndrome. Diabetes Care 2006, 29:1357–1362.PubMedCrossRef 10. Ryo M, Nakamura T, Kihara S, Kumada M, Shibazaki S, Takahashi M, Nagai M, Matsuzawa Y, Funahashi T: Adiponectin as a biomarker of the metabolic syndrome. Circ J 2004, 68:975–981.PubMedCrossRef 11. Daimon M, Oizumi T, Saitoh T, Kameda W, Hirata A, Yamaguchi H, Ohnuma H, Igarashi M, Tominaga M, Kato T: Decreased serum levels of adiponectin are a risk factor for the progression to type 2 diabetes in the Japanese population: the Funagata study.

FGF-2-initiated signaling results in upregulation of p21WAF1/Cip1

FGF-2-initiated signaling results in upregulation of p21WAF1/Cip1 [14] and p27KIP1 [56] and re-expression of integrins lost with de-differentiation [3], which collectively contribute to the dormant phenotype observed. Acknowledgements Supported by DAMD17-03-1-0524 (RW) and the

Ruth Estrin Goldberg Memorial for Cancer Research (RW) Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. References 1. Braun S, Pantel K, Muller P et al (2000) Cytokeratin-positive cells in the bone marrow and survival Akt inhibitor of patients with stage I, II, or III breast cancer. N Engl J Med 342:525–533CrossRefPubMed

2. Braun S, Kentenich C, Janni W et al (2000) Lack of an effect of adjuvant chemotherapy on the elimination of single dormant tumor cells in bone marrow of high risk breast cancer patients. J Clin Onc 18:80–86 3. Korah R, Boots M, Wieder R (2004) Integrin α5β1 promotes survival of breast cancer cells: an in vitro paradigm for breast cancer cell dormancy in the bone marrow. Can Res 64:4514–4522CrossRef 4. Nguyen PL, Taghian AG, Katz MS et al (2008) Breast cancer subtype approximated by estrogen receptor, progesterone this website receptor, and HER-2 is associated with local and distant recurrence after breast-conserving therapy. J Clin Oncol 26:2373–2378CrossRefPubMed 5.

Haffty BG, Yang Q, Reiss M et al (2006) Locoregional relapse and distant metastasis in conservatively managed triple negative early-stage breast cancer. J Clin Oncol 24:5652–5657CrossRefPubMed 6. Dent R, Trudeau M, Pritchard KI et al (2007) Triple-negative breast cancer: clinical features and patterns of recurrence. Clin Cancer Res 13(15 Pt 1):4429–4434CrossRefPubMed 7. Cazzaniga M, Pronzato P, Leto di Priolo SL et al (2004) Patterns of relapse either and modalities of treatment of breast cancer: the ‘IRIS’ Project, a multicenter observational study. Oncology 66:260–268CrossRefPubMed 8. Nicolini A, Giardino R, Carpi A et al (2006) Metastatic breast cancer: an updating. Biomedicine & Pharmacotherapy 60:548–556CrossRef 9. Nilsson SK, Debatis ME, Dooner MS et al (1998) Immunofluorescence characterization of key extracellular matrix proteins in murine bone marrow in situ. J Histochem & Cytochem 46:371–377 10. Van der Velde-Zimmermann D, Verdaasdonk MA, Rademakers LH et al (1997) Fibronectin distribution in human bone marrow stroma: matrix assembly and tumor cell adhesion via α5β1 integrin. Exp Cell Res 230:111–120CrossRefPubMed 11. Balduino A, Hurtado SP, Frazao P et al (2005) Bone marrow subendosteal microenvironment harbours functionally distinct haemosupportive stromal cell populations. Cell & Tissue Research 319:255–266CrossRef 12. Psaila B, Kaplan RN, Port ER et al (2006) Priming the ‘soil’ for breast cancer metastasis: the pre-metastatic niche.

We next assessed the ability of RBE to inhibit the intracellular

We next assessed the ability of RBE to inhibit the intracellular replication of Salmonella in MSIE cells (Figure 3B). After infection and incubation, extracellular bacteria were removed by washing and antibiotic treatment, and kept for 24 h with RBE. The 2 mg/ml dose of RBE reduced intracellular Salmonella replication by 30% (p < 0.05) in comparison to control. No direct effect of RBE on Salmonella

extracellular growth and replication was detected (data not shown). These results suggest that the rice bran extract contains bioactive compounds that block Salmonella entry into MSIE cells as well as inhibit intracellular Salmonella replication in in vitro model. Rice bran diet components and weight of selleck screening library animals Dietary rice bran intake did not significantly change the body weight of animals in the experimental and control groups throughout

the various studies (data not shown). The total lipid content of the Neptune rice variety is 13.8%; therefore we adjusted the amount of corn oil in the diets to equalize the total fat content in the control, 10% and 20% rice bran diets (Table 1). Also, various dietary components may act as substrates for the gut microflora, and for that reason the total amounts of starch and cellulose were adjusted to balance the macronutrient content across groups. Table 1 Composition of control (AIN93-M) and Rice Bran supplemented mice diets Constituents (g/kg) Control 10% RB 20% RB Casein 140 140 140 L-Cystine 1.8 1.8 1.8 Corn Starch 465.7 422.7 377.7 Maltodextrin 155 155 155 Sucrose 100 100 100 Corn Oil 40 19 0 Cellulose 50 29 8 Mineral Mix Selleckchem ATM Kinase Inhibitor Pomalidomide nmr 35 35 35 Vitamin Mix 10 10 10 Choline Bitartrate 2.5 2.5 2.5 TBHQ* 0.008 0.008 0.008 Rice Bran (RB) 0 100 200 *TBHQ- Tertiary butyl-hydroquinone Discussion In this study, we examined the ability of dietary rice bran to protect mice

against an oral challenge with Salmonella. Decreased Salmonella fecal shedding is a reliable marker for reduced susceptibility to infection [28–30] and was used herein to determine whether dietary rice bran supplementation reduced susceptibility to Salmonella infection. Fecal shedding of Salmonella from orally challenged mice fed 10 and 20% rice bran diets was significantly reduced as compared to control diet (Figure 1). Consistent with previous research, the highest number of fecal Salmonella in the control diet fed mice was observed on day 7, followed by a reduction in Salmonella numbers on days 8–13 (Figure 1) [28]. Salmonella fecal shedding in rice bran fed mice was consistently lower than control diet fed mice until day 9-post infection. We chose this mouse model of Salmonella infection over other models because the 129 S6/SvEvTac mice do not die from disseminated Salmonella infection due to presence of both functional copies of the nramp1 gene whereas other strains would die within 7–14 days of inoculation [28].

045 According to the saturation region of the presented conductan

045 According to the saturation region of the presented conductance model and given that gm,min

belongs to the graphene-based biosensor, the control parameter with respect to the iteration method is suggested as: (9) where l 1 = 0.4157 and l 2 = -0.543. In addition, α for the neutrally, negatively, Selleck Salubrinal and positively charged membrane is assumed to be 0, 1, and -1, respectively. Consequently, the justified model for the interaction of charged impurity and the consequence of charged lipid membranes in a biomimetic membrane-coated graphene biosensor is proposed as (10) The proposed model, coupled with the experimental data, is shown in this work to confirm that the conductivity of the graphene-based biosensor is changed by the electric charge and membrane thickness of the lipid bilayer. In a nutshell, electrolyte-gated graphene field-effect transistor structure was used after chemical vapor deposition (CVD) as the electrical transduction stage because of its high electrical conductivity, optical

transparency, and large area, given the likelihood of manufacturing a dual-mode optical and electrical detection system for detecting the changes of membrane properties. Based on what has been discussed, one could firmly claim that, in response to changes of the charged lipid membranes and charges of biomimetic membranes of different thicknesses, a significant shift in V g,min of the ambipolar FET occurs due to the electronic devices on both the n-doping PRN1371 and p-doping materials. Conclusion The emerging potential of nanostructured graphene-based biosensors in the highly sensitive and effective detection of single-base polymorphism or mutation, which is thought to be the key to diagnosis of genetic diseases and the realization of personalized medicine, has been demonstrated. In a

lipid bilayer-based biosensor, the graphene carrier concentration as a function of the lipid bilayer can be modeled. In this research, the total conductance of graphene as a function of the electric charge (Q LP) and thickness of the adsorbed lipid bilayer (L LP) is presented. A dramatic decrease in the minimum conductance related to the gate voltage (V g,min) by both changing the electrical charge from negative to positive and decreasing the lipid thickness has been reported. In the presented model, the V g, Neratinib min variation based on the adopted experimental data as an electrical detection platform is considered and the sensor control parameters are defined. The presented model confirms the reported experimental data and in addition facilitates the employment of alpha and beta as biosensor control parameters to predict the behavior of graphene in graphene-based biosensors. Acknowledgment The authors would like to acknowledge the financial support from the Fundamental Research Grant Scheme for research grant ‘Novel hybrid nanocomposite large sensor array for future nose on a chip’ of the Ministry of Higher Education (MOHE), Malaysia.

For example, the electrical conductivity rose from 21 to 54 S/cm

For example, the electrical conductivity rose from 21 to 54 S/cm with a density increase from 0.25 to 0.65 g/cm3. Significantly, we observed that the taller the forest used in the buckypaper fabrication,

the higher the electrical conductivity. Comparing buckypapers with almost the same density, the buckypaper obtained from forests with heights of 1,500 μm exhibited approximately twice the electrical conductivity of buckypaper made from 350-μm forests, (i.e., 45 vs. 19 S/cm at 0.50 g/cm3, and 27 vs. 16 S/cm around 0.35 g/cm3). Figure 2 Electrical conductivity of buckypapers MK-4827 (a) and sheet resistance of SWCNT forest (b). (a) The electrical conductivity of buckypapers as a function of the mass density of buckypapers. Red, black, and blue dots indicate the buckypaper fabricated from SWCNT forest with the heights of 1,500, 700, and 350 μm, respectively. (b) Sheet resistance

of SWCNT forest with different heights measured by a micro 4-probe. Red, black, and blue dots indicate the SWCNT forest with the heights of 1,500, 700, and 350 μm, respectively. Inset shows the photograph of the gold electrode Selleckchem MK-1775 on Si substrate used as a micro 4-probe. In order to verify that this apparent height-dependent variation in buckypaper conductivity was not due to differences in CNT quality, which has been shown to be essential for the various properties of buckypaper in previous works [34], Raman spectroscopy and electrical resistivity measurements of the as-grown SWCNT forests were carried out. The intensity ratios of the G-band (1,600/cm) and the D-band (1,350/cm) in the Raman spectra (see additional file 1: Figure S2), an indicator of CNT quality, were very similar (approximately 7). Peak positions and intensities in the radial breathing modes (RBM; 100 to 300/cm) were also nearly identical for all SWCNT forest heights. As the RBM peak position w (cm-1) is reported to be inversely proportional to the SWCNT diameter (nm), i.e., w = 248/d[35], these findings indicate that the effect of forest

height on SWCNT diameter distribution was small. Furthermore, electrical conductivity of raw material forest was evaluated by applying a micro 4-probe onto the sides of SWCNT forests. Since the distances between the probes (50 μm) in a micro 4-probe was sufficiently short compared Bacterial neuraminidase with the forest height, CNT length had almost no influence on the resistance values observed with this measurement. The measured resistance was nearly identical (206 to 220 Ω/sq) regardless of forest height (Figure 2b), indicating that quality of the SWCNTs did not degrade when growing forests of height to 1,500 μm, in accordance with the results of Raman spectroscopy. As shown in the previous paragraph, taking into consideration the fact that forest height did not influence CNT quality, we conclude that the increase in buckypaper conductivity accompanying forest height was a result of the increased length of individual SWCNTs.