Strain 870 had caused fatal septicaemia in a 34 year-old man and

Strain 870 had caused fatal septicaemia in a 34 year-old man and strain 901, meningitis in a 1 year-old infant. The RIFS 1958 invasive strain was responsible for septicaemia in an infant aged 2, and since the absence of mutations in the Selleckchem JIB04 rpoB gene, was chosen as control strain. Bacterial protein extraction was performed according to the protocol previously described [13], with some modifications. In particular, the confluent bacterial growth was scraped from the plates and washed twice with PBS, suspended in 5 ml of lysis buffer (500 mM NaCl, 10 mM EDTA, 50 mM Tris pH 8.0) containing 0.3 mg/ml protease inhibitor

(CompleteMini, Roche Diagnostic, Mannheim, Germany) and 150U DNase I (Roche Diagnostic). The sample analysed by 2-DE approach corresponds to the cytosolic fraction, in which most of the proteins involved in the metabolic pathway and in essential biological processes have been described in bacteria. Two-dimensional gel electrophoresis Before electrophoresis an aliquot of protein extract corresponding to 350 μg of each sample was precipitated by adding nine volumes of cold-ethanol

click here and keeping at -20°C overnight. Samples were centrifuged at 14. 000 g for 15 min at 4°C and pellets were dried and then dissolved in 185 μl of a rehydration buffer containing 7 M urea, 2 M thiourea, 2% w/v CHAPS, 50 mM DTT, 0.2% v/v Bio-Lytes™pH range 3-10. Each sample was loaded on an 11-cm precast Immobiline strip with a linear pH 4-7 gradient and three replica maps were performed. First- and second-dimension electrophoresis, and image analysis were carried out as already described by Mignogna et al. [13]. Protein identification Spots selected according to the procedure previously described [13], were manually excised from gels and digested with trypsin. Digestion was performed at 37°C overnight.

Briefly, after several destaining steps using 50 mM ammonium bicarbonate (15 min), 50% acetonitrile in 50 mM ammonium bicarbonate (10 min) and 100% acetonitrile (15 min), subsequently, Tau-protein kinase about 100 ng of trypsin (Trypsin Gold, Mass Spectrometry Grade, Promega, Madison, WI, USA), solubilised in 10 μl of a 25 mM ammonium bicarbonate digestion buffer, were added to vacuum-dried gel. An aliquot (1 μl) of each mixture peptide was mixed with the same volume of α-cyano-4-hydroxy-trans-cinnamic acid matrix solution (5 mg/ml) in 70% acetonitrile containing 0.1% TFA (v/v) for MRT67307 purchase MALDI-ToF analysis, performed in a Voyager-DE STR instrument (Applied Biosystems, Framingham, MA) equipped with a 337 nm nitrogen laser and operating in reflector mode. Mass data were obtained by accumulating several spectra from laser shots with an accelerating voltage of 20 kV. Two tryptic autolytic peptides were used for the internal calibration (m/z 842.5100 and 2807.3145). Identification by peptide mass fingerprint (PMF), was performed using the Mascot search engine version 2.2 [14] against NCBlnr database (10386837 sequences).

pylori at a multiplicity of infection (MOI) of 20 The infected c

pylori at a multiplicity of infection (MOI) of 20. The infected cells were cultured for additional 16 h after which the media was collected and stored for ELISA and BioPlex analyses and the RNA extracted for microarray and real-time PCR studies. RNA extraction and microarray To extract the RNA from the AGS cells, coculture supernatants were removed by aspiration and 1 ml of TRIZOL (Invitrogen, Carlsbad, CA) was added immediately to each well. RNA was extracted as recommended by the manufacturer and was stored at −80°C until further

use. RNA was dissolved in DNase/RNase-free water, quantified by NanoDrop (Fisher Scientific) and set at a concentration of find more ~1.0 μg/μl. The quality of the RNA was confirmed AZD5582 cell line by Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). Each experiment was repeated four times. Two hundred ng of RNA were used to make biotinylated cRNA using the Illumina TotalPrep RNA Amplification Kit (Ambion, high throughput screening Austin, TX), and hybridized to the Illumina chips for 14 hours at 58°C. After washing and staining, the arrays were scanned with the BeadArray Reader (Illumina Inc.) and analyzed with the GenomeStudio software (Illumina). Microarray data analysis After subtracting the background, the samples were normalized assuming a similar distribution of transcript abundance in all the samples [37]. The net expression level was obtained

by subtracting the intensity obtained on each treatment (including non-treated cells) from the intensity at 0 h (prior to seeding the cells into the plate). Then, the gene levels on the infected BCKDHB cells were compared against the levels on the non-infected

cells setting the p value for the difference at <0.05. Scatter plots comparing the non-infected cells against each one of the other treatments (AGS + WT, AGS + rocF-, AGS + rocF +) were used to select only those genes with > 3 fold difference (up or down-regulated) as compared with the non-infected cells, and p values less than 0.05 (p < 0.05). In addition, the Log10 of the ratio between the normalized intensity in the infected cells and the normalized intensity in the non-infected cells was determined and used to generate heat maps. Quantitative real-time PCR For real-time PCR (qPCR), total RNA extracts were DNase treated and reverse-transcribed with SuperScriptase III (Invitrogen) with random hexamers. TaqMan pre-designed arrays were used to check the levels of mRNA expression of IL-8, using cyclophilin A as housekeeping gene, and following the vendor’s recommendations (Applied Biosystems, Foster City, CA). The 5 μl reaction was subjected to two minutes at 50°C, 10 minutes at 95°C and finally 40 cycles at 95°C for 15 seconds and 60°C for one minute in a 7900HT real-time PCR machine (Applied Biosystems). The delta Ct’s (ΔCt and ΔΔCt) and fold induction of IL-8 were determined using an internal control as calibrator.

From the study of Den Hartog et al (1998b), we conclude that the

From the study of Den Hartog et al. (1998b), we conclude that the Selleck BAY 11-7082 combination of HB and FLN experiments prove to be very powerful in unravelling spectral distributions of ‘traps’ for energy transfer in large photosynthetic complexes at liquid-helium temperatures, such as in CP47–RC, CP47 and the RC of PSII of green plants. Lowest k = 0 exciton states in the B850 band of light-harvesting

2 complexes of purple bacteria We know, from X-ray crystallography, that the B850 ring of the LH2 complex of Rps. acidophila consists of 18 close-lying BChl a molecules that are at GW3965 in vitro distances of less than 1 nm from each other (McDermott et al. 1995; Papiz et al. 2003). Similar distances have been found within the B850 ring of Rs. molischianum (Koepke et al. 1996) and have been implied for Rb. sphaeroides from cryoelectron microscopy (Walz et al. 1998). Such short distances lead to strong electronic interactions of a few 100 cm−1 and thus to delocalization of the excitation energy

and the formation of coherent exciton states (Alden et al. 1997; Dahlbom et al. 2001; Freiberg et al. 1999; Hu et al. 1997, 2002; Krueger et al. 1998; Linnanto et al. 1999; Novoderezhkin et al. 1999, 2003; Sauer et al. 1996; Scholes selleck chemicals llc and Fleming 2000; Scholes et al. 1999; Sundström et al. 1999; Wu et al. 1997b; Zazubovich et al. 2002b). The intensity of the B850 absorption band originates principally from two degenerate components of the excitation manifold, the k = ±1 (‘allowed’) states, labelled according to the assumed change in (pseudo) angular momentum. For a perfectly circular B850 ring, the excitation energy is delocalized over all 18 BChl a molecules and

the lowest k = 0 exciton state is forbidden. Any deviation from this ideal situation, such as disorder, will localize the excitation energy over fewer BChl a molecules, allowing k = 0 to become (somewhat) radiative (Cheng and Silbey 2006; Freiberg et al. 1999, 2003; Hofmann et al. 2004; Jang and Silbey 2003; Jang et al. 2001; Novoderezhkin et al. 1999, 2003; Van Oijen et al. 1999; Wu et al. 1997a, b, c). The 2-hydroxyphytanoyl-CoA lyase relative intensity of k = 0 with respect to that of k = ±1 is thus a measure of the extent of disorder in the B850 ring. The degree of excitation-energy delocalization, which is limited by static and dynamic disorder, however, remains a subject of debate. Although the majority of the calculations are based on disordered Frenkel-exciton models (for reviews, see Cogdell et al. 2006; Hu et al. 2002; Jang et al. 2001; Scholes and Fleming 2000; Van Grondelle and Novoderezhkin 2006), an alternative polaron description leading to self-trapped excitons has been put forward by Freiberg and co-workers (Freiberg and Trinkunas 2009; Freiberg et al. 2009).

Am J Reprod Immunol 2011, 66:534–543 PubMedCrossRef

Am J Reprod Immunol 2011, 66:534–543.PubMedCrossRef Apoptosis inhibitor 59. Darville T, Hiltke TJ: Pathogenesis of genital tract disease due to Chlamydia trachomatis. J Infect Dis 2010, 201(2):S114–S125.PubMedCentralPubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contribution BD performed the experiments, acquired, analyzed and interpreted the data, and drafted the manuscript. FN and ADW: made substantial contributions to the conception and design of experiments,

interpretation of results, and drafted and critically revised the manuscript. JT and HH made substantial contributions to the conception and design of experiments. All authors read and approved the final manuscript.”

Approximately 20% of healthy adults are persistent nasal carriers of S. aureus and 60% harbour it intermittently. Such carriers have been shown to participate in the epidemiology and pathogenesis of S. aureus infections and are a potential source of outbreaks especially in hospital settings [1,2]. Nasal carriers are at an increased risk of acquiring surgical site infections, foreign body infections and bacteremias [3,4]. Although nasal colonisation with MRSA is low but such carriers are a major threat factor for themselves (through auto-infection/endogenous source) as well as can disseminate these highly resistant strains that pose serious difficulty in compound screening assay treatment thereafter. The current treatment strategies for nasal decolonisation rely on the use of topical antibiotics such as bacitracin, fusidic acid, ciprofloxacin, 4EGI-1 cost rifampicin [5]. However, emergence of resistant strains has led to treatment failures. Mupirocin is another potent anti-MRSA agent which has been found to be effective in decolonising the nares. Long term studies

have however, shown that there is an initial clearance of bacteria from nares following mupirocin treatment but re-colonization takes place after 3 months [6,7]. The rapid emergence of resistance to mupirocin therefore calls for search for alternative options. Phage therapy has been shown to be a potential alternative treatment for treating various S. aureus infections [8-13]. Hence, an alternative Selleck Gemcitabine or supplement to antibiotic therapy, is the use of bacterial viruses (phage/bacteriophage) to target MRSA colonisation in the anterior nares of the affected population. However, there is comparatively limited work published on the use of phages as nasal decolonising agents as compared to their proven therapeutic potential in other infections. Moreover, the combined application of phage and antibiotic in eliminating the nasal load of S. aureus has not been looked into earlier studies. Combination therapy (use of two different agents) represents an attractive option for nasal decolonisation due to its ability to check emergence of resistant mutants [13,14].

TW reconstruction is a real challenge for thoracic surgeons as we

TW reconstruction is a real challenge for thoracic surgeons as well. The reconstructive options are reduced under circumstances of potential of demonstrated wound infection. Biologic materials are specially indicated in potentially contaminated or contaminated surgical fields [18]. Their resistance to the proteases activity either bacterial either human is demonstrated. Moreover they have the unique characteristic to promote the early revascularization of the regenerate tissue. This allows to antibiotics to early reach the infected zone and by click here reducing the bacterial possibilities

to create biologic niches as in synthetic prosthesis it favors the infection healing. A mild inflammatory response to these materials encourages active tissue EGFR inhibitor deposition and natural cytokine production with a consequent healing process and tissue repair. As organized tissue deposition Selleckchem AZD5363 occurs,

bio-scaffold is gradually remodeled by host, yielding a repaired tissue structure that is entirely host derived [14, 19, 20]. The challenge in TW reconstruction is the complex mechanisms involved in respiration. It implies muscular and elastic forces whom combined work results in the respiratory equilibrium. It briefly consists in a mild intra-thoracic negative pressure. A prosthetic material have to maintain this equilibrium constant to allow the patient to breath. It also has to avoid at the same time the air passage through the prosthesis preventing the subsequent pneumo-thorax. The alteration of the respiratory equilibrium results in either obstructive or restrictive impairment. Thoracic reconstructive materials must have either enough rigidity to allow the thorax to move

symmetrically Ponatinib cell line either elasticity to be able to adapt to the thorax movement. When a big portion of TW have to be removed and consequently many ribs lack, the reconstruction process risks to create an additional respiratory death space. Some reconstructive methods insert metal devices to guarantee the necessary rigidity. However if infection is suspected or demonstrated the insertion of a foreign body becomes a risky procedure. In infected fields two are the possibilities: anatomic reconstruction with flap transposition or the use of biologics. The use of synthetic materials have been widely described with very good results, but in our opinion is very risky in potentially contaminated or infected fields. Reported side effects of synthetic materials include secondary wound infection in up to 6% of cases, seroma formation, insufficient tensile strength with respiratory failure, long-term onset of restrictive lung disease, graft dehiscence, chronic pain, hemorrhage and wall deformities in pediatric patients [3, 21–23]. As counterpart, the experience in TW reconstruction with biologics is limited. Their use is progressively increasing and giving good results [24].

J Nat Prod 75:311–335PubMed Nguyen T, Ishida K, Jenke-Kodama H, D

J Nat Prod 75:311–335PubMed Nguyen T, Ishida K, Jenke-Kodama H, Dittmann E, Gurgui C, Hochmuth T, Taudien S, Platzer M, Hertweck C, Piel J (2008) Exploiting the mosaic structure of trans-acyltransferase polyketide synthases for natural product discovery and pathway dissection.

Nat Biotechnol 26:225–233PubMed Ni ZW, Li GH, Zhao PJ, Shen YM (2008) Antimicrobial components of the endophytic fungal strain Chaetomium globosum Ly50′ from Maytenus hookeri. Nat Prod Res Dev 20:33–36 Nützmann HW, Reyes-Dominguez Belnacasan research buy Y, Scherlach K, Schroeckh V, Horn F, Gacek A, Schümann J, Hertweck C, Strauss J, Brakhage AA (2011) Bacteria-induced natural product formation in the fungus Aspergillus nidulans requires Saga/Ada-mediated histone acetylation. Proc Natl Acad Sci USA 108:14282–14287PubMed Oelmüller R, Sherameti I, Tripathi S, Varma A (2009) Piriformospora

indica, a cultivable root endophyte with multiple biotechnological applications. Symbiosis buy Ipatasertib 49:1–17 Oh DC, Kauffman CA, Jensen PR, Fenical W (2007) Induced production of emericellamides A and B from the marine-derived fungus Emericella sp. in competing co-culture. J Nat Prod 70:515–520PubMed Okamura N, Haraguchi H, Hashimoto K, Yagi A (1993) Altersolanol-related antimicrobial compounds from a strain of Alternaria solani. Phytochemistry 34:1005–1009 Okuno T, Natsume I, Sawai K, Sawamura K, Furusaki

A, Matsumoto T (1983) Structure of antifungal and phytotoxic pigments produced by Alternaria sps. Tetrahedron Lett 24:5653–5656 Olson JB, Kellogg CA (2010) Microbial ecology of selleck products corals, sponges, and algae in mesophotic coral environments. FEMS Microbiol Ecol 73:17–30PubMed Paranagama PA, Wijeratne EM, Gunatilaka AA (2007) Uncovering biosynthetic potential of plant-associated fungi: effect of culture conditions on metabolite production by Paraphaeosphaeria quadriseptata and Chaetomium chiversii. J Nat Prod 70:1939–1945PubMed Peškan-Berghöfer T, Shahollaria B, Giong PH, Hehl S, Markerta C, Blanke V, Kost G, Varma A, Oelmüller R (2004) Association of Piriformospora indica with Arabidopsis thaliana roots represents a novel system to study beneficial Cyclic nucleotide phosphodiesterase plant-microbe interactions and involves early plant protein modifications in the endoplasmatic reticulum and at the plasma membrane. Physiol Plant 122:465–477 Pieterse CMJ, Dicke M (2007) Plant interactions with microbes and insects: from molecular mechanisms to ecology. Trends Plant Sci 12:564–569PubMed Qin S, Krohn K, Hussain H, Schulz B, Draeger S (2011) Pestalotheols E–H: antimicrobial metabolites from an endophytic fungus isolated from the tree Arbutus unedo. Eur J Org Chem 5163–5166. Rateb ME, Ebel R (2011) Secondary metabolites of fungi from marine habitats.

However, this factor should be insignificant as it was found that

However, this factor should be insignificant as it was found that for smaller holes, the PDMS formed only very shallow bumps, so it did not fill the hole and thus the trapped air was not compressed. Moreover, the vacuum level (between 0.01 MPa and 10 Pa) was found unimportant for PDMS filling, though

it affected the mechanical properties of the filled PDMS since the PDMS cured at poor vacuum was less dense due to trapped air and solvent molecule [16]. That is, the air at the dead end would dissolve in PDMS rather than get compressed since PDMS is air PFT�� permeable.   3) Composition of the Sylgard 184 and buy Talazoparib its curing agent, which contains many additives. One important additive is silica nanoparticle filler for reinforcing purpose [17, 18], which may block the hole when its size is not negligible compared to the hole diameter.   4) Size effect. The above derivation for capillary filling speed applies to large channels. For nanoscale holes, the filling mechanism is much more complicated. For example, the surface energy can differ significantly from macro-scale surface when the liquid pillar diameter is no longer orders larger than the range of van de Waals force, and the meniscus may be ‘pinned’ due to the abrupt change of surface topography or charges. In addition, at nanoscale, highly viscous fluid usually behaves like non-Newtonian fluid with much higher effective viscosity. Molecular

dynamic simulation can be employed to better understand the PDMS filling mechanism.   Our GDC0449 current study only serves to suggest Y-27632 2HCl alternative roles of solvent in PDMS filling, and it cannot identify which factors play the most critical role in filling nanoscale

holes. Systematic further study is needed to unambiguously elucidate the role of solvent for the hole filling by diluted PDMS, and why sub-100-nm holes are so difficult to fill. For instance, in order to focus on the effect of viscosity, pure PDMS with different molecular weights, thus very different viscosities, must be used to fill open-ended holes and examined in its liquid state (without curing). This will be studied and published elsewhere. From the point of view of practical application, PDMS filling into nanoscale holes can be improved by solvent dilution, surface treatment by solvent or surfactant other than FOTS such that the surface energy is just low enough for clean demolding, vacuum to drive off solvent and assure PDMS’s mechanical property, and applied pressure that is the most effective approach [4]. Conclusions We, here, studied the effect of solvent treatment of the master mold surface (that was already coated with a silane anti-adhesion monolayer) on PDMS filling into nanoscale holes on the master mold. We achieved improved filling into holes with diameter down to sub-200 nm versus approximately 300 nm for master mold without this additional solvent surface treatment using toluene or hexane.

We need a list with the criteria not a list of genetic conditions

We need a list with the criteria not a list of genetic conditions. Guidelines for all laboratories describing what results should be returned, in what age, the severity of condition, what would happen with late-onset, with minors …things like that (Participant 06). Finally, many suggested that we do not need to “re-invent the wheel” but we could instead look to what was available in other countries and adapt it to the Greek context. I would like to have some short of soft-law,

i.e. guidelines from a professional association that would describe what is happening in other countries, what is the state of the art abroad. And from this website that they could bring something and adapt it according to our need here. We don’t need to start from the beginning when there could be Smad inhibitor something available

abroad (Participant 09). Discussion Our goal was to investigate Greek experts’ attitudes toward clinical sequencing and return of IFs. Their extensive experience and expertise was used to help us acquire a better understanding of the existing situation in Greece regarding clinical sequencing and the return of IFs. From the interviews, a consensus could be observed among experts from different backgrounds that IFs that are clinically valid and actionable should be returned, always according to patients’ wishes. In the same way, they all acknowledged the importance of pre- and post-test counselling and the fact that when it comes to NGS testing, interpretation of results is the area requiring the most attention. Most experts agreed that IFs discovered in minors should be returned in most of the cases

but with extra caution. Finally, they all insisted on the need to have guidelines as soon as possible but preferred a list with criteria and detailed counselling advice rather than simply a list of genetic conditions they would be required to search for and if found, about which they would need to inform their patients. On the other hand, no consensus could be found regarding what actions should be taken regarding clinically valid (-)-p-Bromotetramisole Oxalate but non-actionable results and the best time to return IFs. Several differences were observed between clinicians and geneticists. Clinicians preferred more targeted genetic testing while geneticists were more willing to use NGS. R428 in vitro Additionally, clinicians were less in favour of returning non-actionable results and informing a patient’s family of them. Greek experts seemed to consider that genetic testing, and the genetic information derived from it, differs in some important ways from other medical information, as this data concerns family members apart from the patient and scientific knowledge and understanding change very quickly in this context. Additionally, the meaning of actionability was also raised by many and understood in more than one way. Patient autonomy was referred to as an ideal, but problems with managing this in practice were highlighted.

Cell Signal 2007,19(6):1348–1357 PubMedCrossRef 48 Thastrup O, C

Cell Signal 2007,19(6):1348–1357.PubMedCrossRef 48. Thastrup O, Cullen PJ, Drobak BK, Hanley MR, Dawson AP: Thapsigargin, a tumor promoter, buy GANT61 discharges intracellular Ca2+ stores by specific inhibition of the endoplasmic reticulum Ca2(+)-ATPase. Proc Natl Acad Sci U S A 1990,87(7):2466–2470.PubMedCrossRef 49. Ohtsu H, Dempsey PJ, Eguchi S: ADAMs as mediators of EGF receptor transactivation by G protein-coupled receptors. Am J Physiol Cell Physiol 2006,291(1):C1-C10.PubMedCrossRef 50. Santiskulvong C, Rozengurt E: Galardin (GM 6001), a broad-spectrum matrix metalloproteinase inhibitor, blocks bombesin- and LPA-induced EGF

receptor transactivation and DNA synthesis in rat-1 cells. Exp Cell Res 2003,290(2):437–446.PubMedCrossRef 51. Odegard J, Aasrum M, Tveteraas IH, Bharath SP, Sandnes D, Christoffersen T: Role of ErbB2 in the prostaglandin E(2)-induced enhancement of the mitogenic response to epidermal growth buy Bucladesine factor in cultured hepatocytes. Biochem Biophys Res Commun 2012,421(2):255–260.PubMedCrossRef 52. Meisdalen K, Dajani OF, Christoffersen T, Sandnes D: Prostaglandins enhance

epidermal growth factor-induced DNA synthesis in hepatocytes by stimulation of E prostanoid 3 and F prostanoid receptors. J Pharmacol Exp Ther 2007,322(3):1044–1050.PubMedCrossRef 53. Bronstad GO, Gladhaug IP, Haffner F, Rugstad HE, Christoffersen T: The regulation of cyclic AMP levels in cultured MH1C1 rat hepatoma cells and in solid tumours derived from MH1C1 cell inoculates. Anticancer Res 1987,7(2):155–160.PubMed GM6001 mw 54. Hashimoto N, Watanabe T, Ikeda Y, Yamada H, Taniguchi S, Mitsui H, Adenosine triphosphate Kurokawa K: Prostaglandins induce proliferation of rat hepatocytes through a prostaglandin E2 receptor EP3 subtype. Am J Physiol 1997,272(3 Pt 1):G597-G604.PubMed 55. Shoji Y, Takahashi M, Kitamura T, Watanabe K, Kawamori T, Maruyama T, Sugimoto Y, Negishi M, Narumiya S, Sugimura T, et al.: Downregulation of prostaglandin E receptor subtype EP3 during colon cancer

development. Gut 2004,53(8):1151–1158.PubMedCrossRef 56. Andreev J, Galisteo ML, Kranenburg O, Logan SK, Chiu ES, Okigaki M, Cary LA, Moolenaar WH, Schlessinger J: Src and Pyk2 mediate G-protein-coupled receptor activation of epidermal growth factor receptor (EGFR) but are not required for coupling to the mitogen-activated protein (MAP) kinase signaling cascade. J Biol Chem 2001,276(23):20130–20135.PubMedCrossRef 57. Han C, Michalopoulos GK, Wu T: Prostaglandin E2 receptor EP1 transactivates EGFR/MET receptor tyrosine kinases and enhances invasiveness in human hepatocellular carcinoma cells. J Cell Physiol 2006,207(1):261–270.PubMedCrossRef 58. Itabashi H, Maesawa C, Oikawa H, Kotani K, Sakurai E, Kato K, Komatsu H, Nitta H, Kawamura H, Wakabayashi G, et al.

5 × 10−9 and 7 × 10−9

5 × 10−9 and 7 × 10−9 BYL719 mouse F as the best-fit parameters, respectively. Knowing the interface capacitance C, the thickness of the Al oxide interfacial layer, d = ε 0 εS / C, can be estimated, where ε 0, ε, and S are the vacuum permittivity, the dielectric constant of aluminum oxide, and the electrode area, respectively [33]. With ε 0 = 8.85 × 10−14 F/cm, ε = 10, and S = 2 × 10−3 cm2, d is obtained to be 7 and 2.5 nm in the high and low MM-102 clinical trial resistance states, respectively. The thickness of the Al oxide interfacial layer obtained by impedance spectroscopy in this work was in good agreement with that estimated by HRTEM

and XPS [18–20]. The oxidation of the Al electrode plays a dominant role MK-0457 price in the bipolar resistance switching in the PCMO-based

devices. On the contrary, the resistance change at the interface might not give a dominant contribution to the overall resistance change of Ni/PCMO/Pt and Ag/PCMO/Pt devices because with Ni and Ag, it is difficult to form the oxide interface layer as compared with Al. As a result, the resistance change ratio of Ni/PCMO/Pt and Ag/PCMO/Pt devices is smaller than that of the Al/PCMO/Pt device. It is rather difficult to categorize Ni and Ag into the group of top electrode materials that cause the ReRAM effect. Conclusions The electric-pulse-induced resistance switching in manganite film-based devices with various metal electrodes of Al, Ni, Ag, and Au was studied by dc current–voltage measurements and ac impedance spectroscopy. The hysteretic I-V characteristics and resistance switching were observed in the PCMO-based devices with top electrode of Al, Ni, and Ag. The Al/PCMO/Pt device showed larger resistance switching than other PCMO-based learn more devices with top electrode of Ni and Ag. The electrode material dependence of the

resistance switching in polycrystalline manganite films was investigated in more detail by impedance spectroscopy. Two semicircular arcs were observed in the impedance spectra of the Al/PCMO/Pt device, while the Cole-Cole plots in the devices with Ni, Ag, and Au showed only one semicircular arc. These two distinctive features of the Al/PCMO/Pt device could be assigned to the PCMO bulk and to the interface between the PCMO film and the Al electrode, respectively. By comparing the impedance spectra between the high and low resistance states in the Al/PCMO/Pt device, we suggested that the resistance switching in the PCMO-based devices was mainly due to the resistance change in the interface between the film and the electrode. According to the theoretical simulation of impedance spectra, the interface component observed by impedance spectroscopy in the Al/PCMO/Pt device might be due to Al oxide layer formed by oxidation of Al top electrode. The interfacial transition layer of Al oxides is possibly responsible for the large resistance change in the Al/PCMO/Pt device.