Tumors are able to grow independently of vascularization until they reach a size of approximately 2 mm. At this size the tumor is unable to grow further due to the lack of nutrients and gas exchange, resulting in tumor

dormancy [1]. Continued TGF-beta inhibitor growth requires tumor vascularization. Cancer cells are able to induce angiogenesis by secreting angiogenic factors including vascular endothelial growth factor (VEGF) in order to activate certain actions by endothelial cells [2]. Normally, endothelial cells divide infrequently, being held in check by angiogenesis inhibitors. Once BI 2536 manufacturer activated the endothelial cells secrete matrix-metalloproteases which begin to digest the extracellular matrix surrounding the blood vessels. The endothelial cells can then remodel the tissue. These migrating cells also divide and increase in number, eventually organizing into discrete tubules. Eventually these tubules connect via anastomosis to form the neovasculature of the tumor. The up-regulated VEGF promotes the activation of matrix-metalloproteases CB-839 datasheet [3–5]. We hypothesize that an anti-VEGF agent is able to maintain tumor dormancy, and we aim to prove this hypothesis using in vitro cell growth assay, angiogenesis assay and invasion assay. For solid tumors, such as prostate cancer, breast cancer and lung cancer, there is the chance that the cancer will become

advanced and spread to the bone. DNA ligase In fact, for prostate cancer the bone is the most common

site of recurrence: approximately 80% of prostate cancer recurrences are in the bone [6]. In this study, we will report how anti-VEGF therapy affects the growth and invasion of the bone metastatic prostate cancer cell. Materials and methods Cell culture and reagents Human bone metastatic prostate cancer C4-2B cell line is a derivative of the LNCaP prostate cancer cell line with androgen-independent characteristics. C4-2B cells were obtained from ViroMed Laboratories, and LNCaP cells were purchased from American Type Culture Collection (Manassas, VA). Both C4-2B and LNCaP cells were maintained as monolayer cultures in RPMI 1640 medium supplemented with 2 mM L-glutamine, 10% fetal bovine serum and penicillin-streptomycin in a humidified atmosphere of 5% CO2 at 37°C. Human microvessel cells (VEC Technologies company, Rensselaer, New York) were cultured in endothelial cell growth medium (PromoCell, Heidelberg, Germany) in a humidified atmosphere of 5% CO2 at 37°C. Bevacizumab (Genentech, San Francisco, CA) is a recombinant humanized monoclonal IgG1 antibody that contains human framework regions and the complementarity-determining regions of a murine antibody that binds to and inactivates all isoforms of VEGF. VEGF, bFGF and IL-8 ELISA assays The secretion of VEGF, basic fibroblast growth factor (bFGF) and interleukin 8 (IL-8) by C4-2B cells to culture medium was quantified by an enzyme-linked immunosorbent assay (ELISA).

RhoA inhibits p21Cip1, p27Kip and p16Ink4 activities, permitting cell cycle progression [20–24]. Furthermore, RhoA has been shown involved in the regulation

of apoptosis, migration, proliferation, differentiation [18, 19]: for example, in vitro, constitutively active RhoA can stimulate transformation. In normal AR-13324 molecular weight epithelia, RhoA contributes to the generation of epithelial polarity and junction assembly and function but also affects epithelial disruption during tumor progression [25]. Recently, clinical studies have revealed the correlation of increased expression of RhoA and invasion, metastasis and progression of several solid tumors including liver, bladder, esophageal, head and neck, ovary, gastric, testicular, lung and breast carcinomas [18]. As an upstream regulator, the loss of function GSK2118436 chemical structure BI-D1870 nmr of GRAF might prevent the physiologic down-regulation of RhoA and lead to the repression of p21. Then, the GRAF-defective cell will be driven into the S phase [9]. Several mechanisms, including translocations, allelic loss, insertions and promoter methylation observed in AML and MDS, can lead to the inactivation of GRAF [9, 10]. The mechanisms responsible for the disease progression of CML remained poorly understood. Recent studies have suggested that several alterations promote this progress, including differentiation arrest caused by the suppression of translation of the transcription factor CEBPα induced by the BCR-ABL oncoprotein

in CML cell, increasing genomic instability in CML cell resulting from the reduced capability of genome surveillance system, telomere shortening and loss of tumor

suppressor gene (TSG) such as TP53, retinoblastoma 1, CDKN2A, DAPK1 and others [16, 26, 27]. Interestingly, we found that GRAF transcript was further down-regulated during CML progression. p210 Bcr-Abl, containing a centrally located Rho-specific guanine nucleotide exchange factors (RhoGEF) domain, affects the actin cytoskeleton assembly and thereby http://www.selleck.co.jp/products/Paclitaxel(Taxol).html the cellular adhesion and migration by RhoA signaling pathway [28]. Further studies are required to elucidate the function of GRAF and RhoA in the pathogenesis and progression of CML. Our preliminary results showed that MDS with 5q deletion might have lower expression of GRAF than those without 5q deletion. Deleted 5q is a one of common chromosomal abnormalities in AML and MDS. Although GRAF maps telomeric to the previously delineated commonly deleted 5(q31) region, Borkhardt et al found that one allele of GRAF was consistently lost in all studied 10 patients with 5q deletion and with either MDS or AML [9]. Besides GRAF deletion, abnormal methylation of GRAF promoter was also observed in AML and MDS [10]. These results suggested that haploinsufficiency (i.e., decreased GRAF mRNA expression) caused by deletion of GRAF allele or promoter methylation might be instrumental in the development and progression of hematopoietic malignancies.

Sessoli R, Tsai H-L, Schake AR, Wang S, Vincent OSI906 JB, Folting K, Gatteschi D, Christou G, Hendrickson DN: High-spin molecules: [Mn 12 O 12 (O 2 CR) 16 (H 2 O) 4 ]. J Am Chem Soc 1993, 115:1804–1816.CrossRef 3. Sessoli R, Gatteschi D, Caneschi A, Novak MA: Magnetic bistability in a metal-ion cluster. Nature 1993, 365:141–143.CrossRef 4. Aubin SMJ, Sun Z, Pardi L, Krzystek J, Folting K, Brunel L-C, Rheingold AL, Christou G, Hendrickson DN: Reduced anionic Mn 12 molecules with half-integer ground states as single-molecule magnets. Inorg Chem 1999, 38:5329–5340.CrossRef 5. Leuenberger MN, Loss D: Quantum computing in click here molecular magnets.

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EKA: Ferromagnetic mixed-valent Mn supertetrahedron: towards low-temperature magnetic refrigeration with molecular clusters. Angew Chem Int Ed Engl 2007, 46:4456–4460.CrossRef 7. Evangelisti M, Brechin EK: Recipes for enhanced molecular cooling. Dalton Trans 2010, 39:4672–4676.CrossRef 8. Christou G, Gatteschi D, Hendrickson DN, Sessoli R: Single-molecule magnets. MRS Bulletin 2000, 25:66–71.CrossRef 9. Mannini M, Bonacchi D, Zobbi L, Piras FM, Speets EA, Caneschi A, Cornia A, Magnani A, Ravoo BJ, Reinhoudt DN, Sessoli R, Gatteschi buy E7080 D: Advances in single-molecule magnet surface patterning through microcontact printing. Nano Lett 2005,5(7):1435–1438.CrossRef 10. Barraza-Lopez S, Avery MC, Park K: First-principles study of a single-molecule magnet Mn 12 monolayer on the Au(111) surface. Phy Rev B Am Phys Soc 2007, 76:224–413. 11. Glaser T, Heidemeier M, Weyhermüller T, Hoffmann R-D, Rupp H, Müller P: Property-oriented rational design of single-molecule magnets: a C 3 -symmetric Mn 6 Cr complex based on three molecular building blocks with a spin ground state of S t = 21/2. Angewandte Chemie International Edition 2006, 45:6033–6037.CrossRef 12. Glaser T: Rational design of single-molecule magnets: a supramolecular approach. Chem Commun 2011, 47:116–130.CrossRef 13. Glaser T, Heidemeier M, Lügger T: The novel triplesalen

ligand bridges three Ni II -salen subunits ID-8 in a meta-phenylene linkage. Dalton Trans 2003, 12:2381–2383.CrossRef 14. Glaser T, Heidemeier M, Grimme S, Bill E: Targeted ferromagnetic coupling in a trinuclear copper(II) complex: analysis of the S t = 3/2 spin ground state. Inorg Chem 2004,43(17):5192–5194.CrossRef 15. Hoeke V, Heidemeier M, Krickemeyer E, Stammler A, Bögge H, Schnack J, Postnikov A, Glaser T: Environmental influence on the single-molecule magnet behavior of [Mn III 6Cr III ]3+: molecular symmetry versus solid-state effects. Inorg Chem 2012, 51:10929–10954.CrossRef 16. Helmstedt A, Müller N, Gryzia A, Dohmeier N, Brechling A, Sacher MD, Heinzmann U, Hoeke V, Krickemeyer E, Glaser T, Bouvron S, Fonin M, Neumann M: Spin resolved photoelectron spectroscopy of [Mn 6III Cr III ] 3+ single-molecule magnets and of manganese compounds as reference layers.

Polym Int 2007, 56:1272–1280.CrossRef 30. Mei L, Zhang Y, Zheng Y, Tian G, Song C, Yang D, Chen H, Sun

H, Tian Y, Liu K, AZD2171 Li Z, Huang L: A novel paclitaxel-loaded poly (ε-caprolactone)/pluronic F68 nanoparticle overcoming multidrug resistance for breast cancer treatment. Nanoscale Res Lett 2009, 4:1530–1539.CrossRef 31. Mei L, Sun H, Jin X, Zhu D, Sun R, Zhang M, Song C: Modified paclitaxel-loaded nanoparticles for inhibition of hyperplasia in a rabbit arterial learn more balloon injury model. Pharm Res 2007,24(5):955–962.CrossRef 32. Ma Y, Huang LQ, Song CX, Zeng XW, Liu G, Mei L: Nanoparticle formulation of poly(ε-caprolactone-co-lactide)-d-α-tocopheryl polyethylene glycol 1000 succinate random copolymer for cervical cancer treatment. Polymer 2010, 51:5952–5959.CrossRef 33. Barr WH, Riegelman S: Intestinal drug absorption and metabolism. I. Comparison of methods and VS-4718 ic50 models to study physiological factors of in vitro and in vivo intestinal absorption. J Pharm Sci 1970,59(2):154–163.CrossRef

34. Hosseinzadeh H, Atyabi F, Dinarvand R, Ostad SN: Chitosan–pluronic nanoparticles as oral delivery of anticancer gemcitabine: preparation and in vitro study. Int J Nanomedicine 2012, 7:1851–1863.CrossRef 35. Florence AT: Nanoparticle uptake by the oral route: fulfilling its potential? Drug Discov Today 2005, 2:75–81.CrossRef 36. Norris DA, Puri N, Sinko PJ: The effect of physical barriers and properties Teicoplanin on the oral absorption of particulates. Adv Drug Deliv Rev 1998,34(2–3):135–154.CrossRef 37. Hariharan S, Bhardwaj V, Bala I, Sitterberg J, Bakowsky U, Ravi Kumar MN: Design

of estradiol loaded PLGA nanoparticulate formulations: a potential oral delivery system for hormone therapy. Pharm Res 2006, 23:184–196.CrossRef 38. Artursson P, Palm K, Luthman K: Caco-2 monolayers in experimental and theoretical predictions of drug transport. Adv Drug Deliv Rev 2001, 46:27–43.CrossRef 39. Nabholtz JM, Tonkin K, Smylie M, Au HJ, Lindsay MA, Mackey J: Chemotherapy of lung cancer: are the taxanes going to change the natural history of lung cancer? Expert Opin Pharmacother 2000,1(2):187–206.CrossRef 40. Yan F, Zhang C, Zheng Y, Mei L, Tang L, Song C, Sun H, Huang L: The effect of poloxamer 188 on nanoparticle morphology, size, cancer cell uptake, and cytotoxicity. Nanomedicine 2010,6(1):170–178.CrossRef 41. Leroueil PR, Hong S, Mecke A, Baker JR Jr, Orr BG, Banaszak Holl MM: Nanoparticle interaction with biological membranes: does nanotechnology present a Janus face? Acc Chem Res 2007, 40:335–342.CrossRef 42. Song C, Labhasetwar V, Cui X, Underwood T, Levy RJ: Arterial uptake of biodegradable nanoparticles for intravascular local drug delivery: results with an acute dog model. J Control Release 1998,54(2):201–211.CrossRef 43.

Spa-typing

with the standard AZD8931 mw primer sets (1095 F/1517R) demonstrated that AE only ever carried one strain, which was type t230 at most time points, the spa-type t008 on one occasion and one non-typeable strain. Re-typing the same DNA extractions with our alternative novel primers (spaT3-F/1517R) showed that all samples had mixed sequence traces, apart from the formerly non-typeable strain that had deletion E associated with spa-type t012. Therefore, 12 single colonies GW3965 mouse were isolated for each sample and re-typed with alternative primers. This identified five spa-types carried by AE at various time points, and mixed strain colonization by two-three spa-types on four occasions, including two strains with deletion E. We were unable to resolve all samples by typing 12 individual colonies, even though they showed presence of mixed sequence traces (time points 4, 10, 12 and 14), which could buy Barasertib be explained by a low frequency of one of the colonizing strains. Table 3 Spa -typing of S. aureus strains from a single individual AE with two sets of primers: standard primers 1095 F/1517R and novel primers spaT3-F/1517R Time points, months DNA prep (mixed boilate) 12 single colony picks2   1095 F/1517R spaT3-F/1517R spaT3-F/1517R AE-0 t230 MST1 t230/t012 AE-1 non-typable t012 t012 AE-2 t230 MST t230/t012 AE-4 t230 MST t230 AE-6 t230 MST t230/t528 AE-8 t008 MST t008/t012/t571 AE-10 t230 MST t230 AE-12 t230 MST t230 AE-14 t230 MST t230

1mixed sequence traces; 2 spa-types in bold have delE and could not be typed with standard primers; spa-repeats: t230: 08-16-02-16-34. t571: 08-16-02-25-02-25-34-25. t008: 11-19-12-21-17-34-24-34-22-25. t012: 15-12-16-02-16-02-25-17-24-24. t528: 04. The limitations of the conventional spa-typing protocol make it impossible to identify and type S. aureus strains with rearrangements in the spa-gene in individuals with multiple strain colonization.

The staged spa-typing protocol allows us to resolve cases of mixed strain colonization with deletions in one or more strains. Even 12 single colony picks could not always identify the presence of low-frequency strains with deletions, Morin Hydrate illustrating the even greater challenge of estimating the proportion of non-typeable strains within mixed colonization. Thus diversity in colonizing and infecting strains is inevitably underestimated. Inpatients’ strains can acquire deletions in the spa-gene We also found that S. aureus strains can acquire deletions in the spa-gene during inpatients’ hospital admission. Such acquisition of deletions was never observed for longitudinal carriage strains from individuals in the community, with those deletions observed being present from the first time the strain carrying the deletion was identified (Additional file 1: Table S1). Among six hospital patients with deletions that affect spa-typing, three individuals (BA, BB and BF) already carried the strain with the deletion when they were admitted.

[13]. Although these studies have provided some insight into the benefits of using cycling as an alternate exercise selleck screening library modality, it remains unclear whether such differences may improve iron status

over an extended training period. Currently, limited studies have attempted to examine how exercise might affect post-exercise hepcidin production over an extended period, and what EVP4593 manufacturer the implications may be for iron status. Recently, Auersperger et al. [14] reported that serum hepcidin and ferritin decreased in athletes adopting an eight week interval running program. In addition, McClung et al. [15] showed that nine weeks of basic combat training (BCT) compromised numerous iron parameters in female soldiers. On the contrary, McClung et al. [16] reported that seven days of training (military specific exercise and ski marching) elevated hepcidin levels without affecting iron status in male soldiers. Of importance, the iron status of an athlete may also dictate both the pre-exercise selleck chemicals llc levels of hepcidin, and the magnitude of hepcidin response to an acute exercise stimulus (e.g. serum ferritin <30 μg.L−1, hepcidin suppressed) [17]. Considering that the aforementioned

investigations used mainly weight-bearing activity (that may have increased the degree of exercise-induced hemolysis), it remains to be investigated how accumulated bouts of weight-bearing (running) vs. Silibinin non-weight-bearing (cycling) exercise may impact iron status over time. Additionally, previous investigations [14–16] have only measured basal hepcidin levels; however, the acute post-exercise hepcidin response over consecutive exercise bouts currently remains unknown. As such, this study set out to compare the effects of a seven day period of running vs. cycling exercise on hepcidin production and iron status in active individuals. Methods Ten active males participated in this study [age = 24 ± 1 y, body mass = 70.5 ± 3.2 kg, stature = 175.9 ± 2.6 cm, running peak oxygen

uptake (VO2peak) = 58.0 ± 2.0 ml.kg−1.min−1, cycling VO2peak = 49.7 ± 1.8 ml.kg−1.min−1]. At the time of recruitment, participants were performing a minimum of three exercise training sessions per week. The sample size was determined via customised computer software (GPOWER Version 2, Department of Psychology, Bonn University, Bonn, Germany) using effect sizes (ES) attained from similar research [3–7, 18]. A sample size of 10 was recommended to yield a power of 0.90 at a significance level of p ≤ 0.05. When recruited, all participants had a healthy iron status (serum ferritin = 79.3 ± 15.0 μg.L−1, transferrin saturation = 33 ± 3%), and were not taking any iron supplements. Prior to participation, written consent was obtained with approval granted by the Human Ethics Committee of The University of Western Australia (RA/4/1/5636).

Based on present literature, we hypothesized to find a loss in body mass as has previously reported for ultra-cycling [21, 24, 36] and non-stop ultra-endurance races [15, 22, 24, 26]. We hypothesized

that this type of MTB races would lead to an increase in foot volume due to peripheral oedema. Methods Participants The present work combines data from two 24-hour races held in the Czech Republic in 2012. Subjects were recruited via pre-race emails and during race registration. A total of 28 (22 men and 6 women) recreational 24-hour ultra-MTBers in the solo category from the ‘Czech Championship 24-hour MTB 2012’ in Jihlava city in the Czech Republic and 24 (18 men and 6 women) Lazertinib nmr ultra-MTBers from the ‛Bike Race Marathon MTB Rohozec 24 hours’ in Liberec city in the Czech Republic in the solo category consented to participate in the study. Of those, 37 men and 12 women finished the race successfully. One cyclist had to give up due to technical problems and two athletes because of medical complications. Athletes were Chk inhibitor informed that participation was voluntary and that the project had received approval in accordance with the law (No. 96/2001 Coll. M. S. on

Human Rights and Biomedicine and Act No. 101/2000 Coll. Privacy). The pre-race anthropometry and training data of the participants are presented in Table  1. Table S3I-201 concentration 1 The pre-race experience and training parameters (n = 49)   Male ultra-MTBers Female ultra-MTBers (n = 37) (n = 12) M ± SD M ± SD Years as active biker (yr) 9.2 ± 5.8 8.8 ± 5.9 Number of finished ultra-marathons (n) 8.0 ± 6.5 6.7 ± 5.3 Personal best km in 24 hour (km) 315.5 ± 89.7 279.6 ± 106.7 Total hours weekly (h) 10.5 ± 5.3 10.2 ± 5.5 Weekly cycling kilometers (km) 225.8 ± 149.5 191.8 ± 134.5 Weekly cycling hours (h) 9.9 ± 5.1 9.2 ± 5.2 Mean cycling intensity (beat/min) 133.8** ± 7.6 134.5** ± 22.8 Mean cycling speed (km/h) 23.0** ± 3.6 21.1** ± 5.3 Longest trail (km) 176.8** ± 84.7 141.7** ± 75.5

Amount of km in 2011 (km) 7,107.5 ± 5,782.4 5,696.9 ± 5,037.9 Results are presented as mean ± SD; * = P < 0.05, ** = P < 0.001. Races details The first measurement was performed at the 3rd edition of the ‘Czech Championship 24-hour MTB 2012’ in Jihlava. The ultra-MTBers began the race at Bay 11-7085 12:00 on 19th May 2012 and finished at 12:00 on 20th May 2012. The course comprised a 9.5 km single-track with an elevation of 220 m. A single aid station, located at the start/finish area was provided by the organizer where a variety of food and beverages such as hypotonic sports drinks, tea, soup, caffeinated drinks, water, fruit, vegetables, energy bars, bread, soup, sausages, cheese, bread, chocolate and biscuits were available. The ultra-MTBers could also use their own supplies in their pit stops. Temperature was +16˚C at the start, rose to a maximum of +20˚C, dropped to +6˚C during the night and rose to +23˚C from the morning of the next day till the end of the race.

baumannii might also be easily isolated from nature. Recently, 10 phages were obtained from wastewater using 125 clinical isolates of A. baumannii as indicator hosts [20, 23]. These phages were designated AB1 to AB9 and AB11. Examination by transmission electron microscopy suggested that phages AB1-7 and AB9 belonged to the

Podoviridae family, and phages AB8 and AB11 belonged to the Myoviridae family. Two of the 10 phages, AB1 and AB2, were further characterized at 35°C and 37°C, respectively. Based on morphology and genomic analysis, the two phages IWP-2 were classified as new members of the ϕKMV-like phages [20, 23]. In this study, the phage ZZ1, which is specific to A. baumannii, was isolated from fishpond water, which further confirmed that phages specific to A. baumannii are waiting to be exploited as an abundant natural resource. The ability of phage ZZ1 to form clear plaques on lawns of AB09V is indicative of lytic phage, and a large burst size with a short latent period is further suggestive of the lytic nature of phage ZZ1. Morphologically, ZZ1 exhibits features similar to the Myoviridae family (order Caudovirales), which, broadly, are tailed phages with icosahedral head symmetry and contractile tail structures. Genome analysis of ZZ1 showed that it is fairly similar to four other Acinetobacter phages (Acj9, Acj61, Ac42, and 133).

In a recent review by Petrov et al. [18], the four Acinetobacter Go6983 research buy phages were initially assigned to the “T4-like Viruses” genus. Each of these Acinetobacter phages has a unique set of ORFs that occupy ~35% of the genome. That is, each represents a different type of T4-related phage genome [18]. The genome size of the phage ZZ1 (166,682 bp) is also close to the genome size of T4-like phages. These genomes vary between ~160,000 and

~250,000 bp [18]. Therefore, the above features confirmed that the phage Baf-A1 molecular weight ZZ1 is most likely a new member of the T4-like virus family of Acinetobacter phages. click here However, according to the 2011 Virus Taxonomy List (current) from the International Committee for the Taxonomy of Viruses (http://​www.​ncbi.​nlm.​nih.​gov/​ICTVdb/​index.​htm.), only the Acinetobacter phage 133 can be searched and classified in the unassigned genus of the Myoviridae family, most likely because the phage is inadequately characterized. At the very least, the current sequence database for the Myoviridae phages should prove to be a rich source of genetic markers for bioprospecting and a mine of reagents for basic research and biotechnology. Our future research will focus on further detailed analysis of the whole ZZ1 genome to understand the genetic characteristics of this phage. The main aim of this study was the isolation and characterization of a lytic bacteriophage with potential for prophylactic/therapeutic use. Therefore, the antibacterial activity of the phage against its different host cells was the focus of our research.

As the temperature is reduced from 340 to 5 K, the increase of the four-layer graphene resistance is much larger, which is around 40%, compared to the trilayer 4SC-202 in vitro graphene, which is found to be 20%. Figure 5 Normalized electrical resistance per square measurements as function of temperature of tri- and four-layer graphene interconnects. The results show that when the temperature increases from 5 to 340 K, the resistance of the tri- and four-layer graphene interconnects drops significantly, indicating a semiconductor property of the graphene. The symbols are the measured data, and the lines are fits. At low temperature, the main scattering mechanisms in graphene are largely

due to the Coulomb impurity and the short-range defect scatterings [24]. Based on Matthiessen’s rule, the overall mobility can be written as [22]: (1) Based on a model proposed by Hwang et al. [24], we can assume that the scattering centres of charge are at the SiO2-graphene interface, and the short-range scattering is constant. Then this website the energy average scattering time is deduced as [21, 22]: (2) where E k is the wave vector energy and τ(E k ) is the transport scattering rate. For the low temperature limit, the scattering time averaged over energy can be written as 〈τ〉 ≈ τ(E F ) [21]. The density of states

D(E F ) in tri- and four-layer graphene is assumed to be a constant . Here, the Fermi energy is , and based on the Boltzmann equation of mobility as function of the scattering time: , we can obtain the mobility of graphene as . As such, at low temperatures, the Coulomb scattering is proportional to the carrier density in the tri- and four-layer graphene structures [21–23]. In the high temperature regime, the Coulomb scattering is a strong

function of temperature while the short-range scattering is independent of temperature. This is attributed to the density of states, the matrix element of graphene and the screening function being energy independent in FLG [21–23]. Hence, the mobility increases proportionally with the temperature (μ3-4 4-Aminobutyrate aminotransferase layers ∝ k B T) [21]. For tri- and four-layer graphene, the resistance can be expressed as: (3) where we have defined , R sr−3–4 layers = C, and A, B and C are the fitting parameters. In our measurements, we have observed a linear approximation for the temperature-dependent normalized resistance of tri- and four-layer graphene: (4) (5) These considerations Selleckchem GS 1101 explain qualitatively why the resistance of tri- and four-layer graphene decreases with the increasing temperature. We note that due to the complexity of the FLG band structure, these anomalous electrical properties are believed to originate in the unusual band structures near the Fermi level of graphene [26–29]. More rigorous theoretical explanation of FLG intrinsic semiconductor behaviours would be interesting and requires further experimental investigations.

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