The extracted proteins were subjected to immunoblotting analysis

The extracted proteins were subjected to immunoblotting check details analysis with anti-phospho-JNK, -phospho-p38 and -phospho-ERK1/2 antibodies. The stripped membranes were re-probed with anti-total-JNK, -p38, -ERK1/2 antibody to detect the total level of each MAPK protein present in the samples and to control for loading quantities. JNK and p38 were phosphorylated in cells co-incubated with the WT bacteria, in comparison to samples

obtained from untreated Caco-2 cells which showed no MAPK activation (Figure 1). Strong activation of JNK and p38 was observed at the 2 h time point, but not at earlier time points. In contrast, little or no phosphorylation of JNK and p38 was detected in cells incubated for 2 h with the heat-killed WT bacteria, indicating that the induction of activation of these two MAPK is an active selleck inhibitor process of V. parahaemolyticus requiring viable bacteria. The patterns of ERK activation in response to V. parahaemolyticus were similar with lower phosphorylation signals detected. These studies indicate that V. parahaemolyticus induces activation of the

JNK, p38 and ERK MAPK signalling pathways via a mechanism requiring metabolically active bacteria. Figure 1 V. parahaemolyticus induces JNK, p38 and ERK phosphorylation in intestinal epithelial cells. Caco-2 cells were co-incubated with viable V. parahaemolyticus WT RIMD2210633 for 15, 60 or 120 min, with 50 μg/ml anisomycin for 30 min or with heat-killed SC79 cost WT V. parahaemolyticus for 2 h. Cell lysates were prepared and proteins

separated by SDS-PAGE. Following transfer of proteins to nitrocellulose membranes, the membranes were probed with anti-phospho-JNK, -phospho-p38 and -phospho-ERK1/2 antibodies. The stripped membranes were re-probed with the corresponding anti-total-MAPK antibodies to control for equivalent protein loading. A. Representative image of MAPK immunoblot. Results are representative of at least three independent experiments. B. Quantification of MAPK activation. Results are expressed as the ratio of phospho-MAPK to total MAPK and as relative to levels in Caco-2 cells alone. Results indicate mean ± standard error of the mean (SEM) of three independent experiments. **P < 0.01; ***P < 0.001 vs medium. TTSS1 Fludarabine ic50 of V. parahaemolyticus is responsible for activation of JNK, p38 and ERK in epithelial cells TTSS effectors of several pathogenic bacteria have been shown to modify MAPK activation levels in eukaryotic cells [24, 34–36]. As V. parahaemolyticus was able to induce phosphorylation of p38, JNK and ERK MAPK by an active process, we next investigated the involvement of the TTSS of V. parahaemolyticus in the activation of these MAPK. Bacteria lacking a functional TTSS1 or a functional TTSS2 were constructed by deleting the corresponding vscN gene for each secretion system.

However, we have previously shown that several B burgdorferi str

However, we have previously shown that several B. burgdorferi strains, including Selleckchem SB-715992 N40D10/E9, barely recognize chondroitin sulfate A and chondroitin sulfate C [49, 61, 62]. Therefore, we conclude that the adherence of both B.

burgdorferi strains to glial cells was mediated primarily by dermatan sulfate. Figure 2 Binding of B. burgdorferi strains B31 and N40D10/E9 to C6 glioma and T/C-28a2 chondrocyte cell monolayers was significantly reduced on pretreating these cells Entinostat molecular weight with chondroitinase ABC but remain unaffected on their pretreatment with heparinase I. The experiments were repeated at least three times using four replicates for each treatment. Each value represents the mean ± SD of quadruplicate samples. Asterisks indicate significant reduction (p < 0.05) in binding percentage

relative to mock-treated cells as determined by t-test for pairwise comparison of samples with unequal variance. Similarly, binding of B31 to T/C-28a2 chondrocyte cells was reduced, by the treatment of chondroitinase ABC, from 28% to 13% (Figure 2C). N40D10/E9 binding was reduced from 26% to 15% (Figure 2D). Since heparinase I had no significant effect on the binding of both strains to T/C-28a2 cells (Figures 2C and 2D), adherence of B31 and N40D10/E9 to chondrocyte cells PFT�� research buy appeared to be mediated primarily by dermatan sulfate and receptor(s) other than GAGs. Majority of the known virulence factors encoding genes of the B31 strain are also present in the N40D10/E9 strain Since the first demonstration of the essential role of OspC in mammalian infection using the genetic approach in 2004 [13], several molecules have been shown to be important for causing infection and disease in the mouse model [44, 82–100]. The N40D10/E9 strain is not yet sequenced and its plasmid profile is different from the B31 strain [29]. Therefore, limited genomic and proteomic analyses were conducted to compare these two strains. To determine

if these two B. burgdorferi strains show differences in the presence of genes encoding known adhesins, other virulence factors and their regulatory proteins, we amplified these genes by PCR Carbohydrate to investigate and differentiate these two strains. Interestingly, all previously established virulence factors encoding genes were present both in B31 [101] and N40D10/E9 strains except the bbk32 gene (Figure 3A). Two different size PCR products were observed in B31 when internal VlsE1 primers were used for gene amplification. This agrees with the presence of two homologs shown in the genome website, bbf0041 and bbj51 but only bbf0041 (VlsE1) is functional since bbj51 has a stop codon after 57 amino acids. However, only one vlsE1 gene was detected in N40D10/E9 probably because lp38, which contains bbj51, is missing in this strain [29]. Figure 3 The gene homologous to the bbk32 was not detected in N40D10/E9 strain by PCR and Southern hybridization. (A).

The RFLP-PCR analysis of 16S–23S rRNA intergenic

The RFLP-PCR analysis of 16S–23S rRNA intergenic region confirmed that the isolated strain belonged to Cp. pecorum specie. These data and those reported previously regarding Cp. pecorum involvement in abortion in Tunisia and in Morocco (unpublished data) indicated that Cp. pecorum may cause abortion in small ruminants in North Africa countries. Cp. pecorum

pathogeniCity may be associated with nutritional deficiency or parasitic infestations as are often encountered in theses countries. It could be also considered that no pathogenic Cp. pecorum strains might be spread from the intestine through the blood circulation because of some unknown physiopathologic events and reach the placenta where they induce abortion. The recent finding that mixed infection with Cp. abortus

and Cp. pecorum was associated with abortion Fosbretabulin cell line in water buffalo cows in the southern of Italy [37] suggests that Cp. pecorum could also be involved in abortion in large ruminants. Nevertheless, it is still unknown whether or not Cp. pecorum-related abortion might be either a consequence of Cp. pecorum alone or an enhancement of its pathogenesis mediated by the co-infection with Cp. abortus. Conclusion The m-PCR assay developed in this study provides a new tool for Chlamydiosis and Q fever diagnosis. The usefulness of this assay to detect the animals that actively shed the bacteria may prevent animal, human, and environment contamination. In addition, since Cp. pecorum infection is still not well understood, this m-PCR may yield new insights into the pathogenesis of Chlamydiosis disease. Acknowledgements We sincerely thank the staff of the Institute and Veterinary

Carbachol Research of Tunisia, the involved French county veterinary laboratories (Tourraine and Alpes-de-Hautes-Provence), as well as the experimental unit staff of INRA Research Centre of Tours-Nouzilly (France) for their help to provide animal samples. References 1. Rodolakis A, Salinas J, Papp J: Recent advances on ovine chlamydial abortion. Vet Res 1998, 29:275–288.PubMed 2. Maurin M, Raoult D: Q fever. Clin Microbiol Rev 1999, 12:518–553.PubMed 3. Woese CR: Bacterial evolution. Microbiol Rev 1987, 51:221–527.PubMed 4. Lukacova M: Are Coxiella burnetii and Chlamydia related? Antigenic properties of Coxiella burnetii and Chlamydiae. Alpe Adria Microbiol J 1996, 5:3–13. 5. Everett KD:Chlamydiae and Chlamydiales : more than meets the eye. Vet Microbiol 2000, 75:109–126.Pevonedistat concentration CrossRefPubMed 6. Longbottom D, Coulter LJ: Animal Chlamydiosis and zoonotic implications. J Comp Path 2003, 128:217–44.CrossRefPubMed 7. Fukushi H, Hirai K: Proposal of Chlamydia pecorum sp. nov. for Chlamydia strains derived from ruminants. Int J Syst Bacteriol 1992, 42:306–308.CrossRefPubMed 8. Biesenkamp-Uhe C, Li Y, Hehnen HR, Sachse K, Kaltenboek B: Therapeutique Chlamydophila abortus and Cp. pecorum vaccination transiently reduces bovine mastitis associated with chlamydophila infection.

Cancer 1974, 33:1183–1189 CrossRef 14 Hughes R: Cases illustrati

Cancer 1974, 33:1183–1189.CrossRef 14. Hughes R: Cases illustrative of the influence of belladonna. BMJ 1860, 8:706.CrossRef check details 15. Cham C, Chan D, Copplestone J, Prentice A, Lyons C, Jones P, Watkins R: Necrosis of the female breast: a complication of oral anticoagulation in patients with protein S deficiency The Breast. 1994,3(2):116–118.

16. Archer C, Rosenberg W, Scott W, MacDonald D: Progressive bacterial synergistic gangrene in patient with diabetes mellitus. J R Soc Med 1984, 4:77. Supplement Competing interests The authors declare that they have no competing interests. Authors’ contributions designed the study, contributed in literature search, data analysis, manuscript writing. IB, FP, AM and RW helped in study design, data analysis, manuscript writing and editing. MS, IH, AM SW and WS participated in study design, supervised the write up of the manuscript and edited the manuscript before submission. All the authors read and approved the final manuscript”
“Background Gas gangrene or Clostridial myonecrosis is a necrotic infection of skin and soft tissue and it is characterized by the presence of gas under the skin which is produced by Clostridium. It is a potentially lethal disease which spreads quickly in soft tissues of the body. Tissue necrosis is due to production of exotoxins by spore forming gas producing bacteria

in an environment pentoxifylline of low oxygen. Gas gangrene is subclassified in two categories. Traumatic or postoperative is the most common form accounting for 70% of the cases followed by spontaneous or non traumatic gangrene. C. perfringens is isolated in approximately

80% of patients presenting with traumatic gas gangrene followed by C.septicum, C.novyi, C.histolyticum, C.bifermentans, C.tertium and C.fallax [1–3]. Herein we report a case of gas gangrene which was treated early with surgical debridement and enabled salvage of the limb with significant preservation of its function. Additionally, a review of the literature regarding cases of limb salvage after gas gangrene is presented. Case Presentation A 35-year-old Caucasian man with a history of chronic intravenous drug use presented to the emergency department with right upper limb pain and swelling lasting 24 hours. His initial vital signs were notable for temperature of 39°C, Protein Tyrosine Kinase inhibitor respiratory rate of 25 breaths per minute, heart rate of 120 beat per minute and blood pressure of 141/76 mmHg. He was distressed and on clinical examination severe edema of the upper limb, erythema, blistering of the arm and crepitus over the shoulder and arm was noted [Figure 1a]. At this time, motor and sensory function of the limb was not impaired and pulses of the radial and ulna artery could be palpated. His past medical history consisted of a diagnosis of hepatitis C. Intramuscular injections with normal saline in the shoulder were also reported.

Each point represents an organ from an individual bird at the ind

Each point represents an organ from an individual bird at the indicated day following the infection. The table summarizes the number of animals sampled (n), the geometric mean of the competitive indexes (mean CI), and the P value from a two-tailed T-test. Interestingly, the Δspi2 strain also significantly out-competed by KU-57788 solubility dmso the Δspi1 strain in the spleen at days three and fourteen post-AZD9291 price infection (Figure 5B). This result suggests that SPI1 contributes more than SPI2 to splenic colonization. Since SPI2 has been shown

in several animal models, including the mouse, to be a major factor for the survival of Salmonella in the systemic compartment of the host we decided to verify the accuracy of the results we obtained with the Δspi2 strain in chicken spleen by performing mixed infection experiments in mice. As expected the Δspi2 strain was out-competed by the wild type (Figure 7A) and the Δspi1 strains (Figure 7B) in both the liver and spleen after either intra-peritoneal (Day 3) or oral (Day 5) infections. Collectively, these results show that in contrast to the mouse, SPI2 contributes less than SPI1 to splenic colonization of the chicken. Figure 7 SPI2 is essential to the colonization of mouse spleen by Typhimurium. Competitive indexes are from mixed

infections in mice with the wild type and the Δspi2 (deletion of SPI2 structural genes), or the Δspi1 (deletion of SPI1) MLN2238 purchase and the Δspi2 strains. Data from day 3 and day 5 post-infection correspond to intra-peritoneal and oral infections respectively. Each point represents an organ from an individual mouse. Discussion SPI1 and SPI2 are important virulence determinants of S. enterica serovars that have been extensively studied in several animal models. Few studies have investigated the role of SPI1 and SPI2 in the colonization of the chicken by Typhimurium. These

studies have analyzed the colonization of different organs in chickens infected PLEK2 with a wild type strain or with mutants of SPI1 or SPI2 in which a single T3SS structural gene was inactivated. To gain better insight in the roles played by SPI1 and SPI2 in the chicken we used an approach that combined mixed infections, large deletions in SPI1 and SPI2, and the tracking of infections for fourteen days. We found that SPI1 contributes to colonization of both the cecum and the spleen in chickens. In contrast, SPI2 plays a role in the colonization of the spleen, but not of the cecum. Furthermore, we show for the first time to our knowledge, that SPI1 plays a more important role than SPI2 in colonization of the chicken spleen by Typhimurium.

There have been various investigations into the relationship betw

There have been various investigations into the relationship between obesity and renal impairment [17, 18]. Kambham et al. [19] defined a new entity, ORG, in which GH with FGS lesions or only GH developed in obese patients with a BMI of 30 kg/m2 or more, and proposed ORG as a renal disease that has been increasing in prevalence in recent years. These previous studies examined the renal histological features of obese patients with a BMI of 30 kg/m2 or more.

In contrast, the present see more study examined the characteristics of proteinuric patients without known primary or secondary glomerular diseases, especially focusing on the glomerular volume in the kidney biopsy specimens. We found that higher BMI levels, even if they were <30 kg/m2, had a significant correlation with the enlargement of the GV. Therefore, the present study was unique in terms of the methodology, which was based on the glomerular volume, not the BMI. We recently reported that a low GD associated with GH may be a characteristic histological finding of patients with ORG [12]. In that study, the analysis of autopsy cases without CKD, which were characterized by having an eGFR ≥60 ml/min/1.73 m2 and no persistent urinary abnormalities, showed that the GD in overweight or obese persons was similar to that in non-obese individuals, although the GV was Lazertinib purchase larger in the overweight

and obese groups as compared to the non-obese group, among the autopsy cases. In contrast to those results, we found in the present study that the GD levels in our proteinuric patients were significantly lower in the obese group as compared to the non-obese group. In addition, the GD had a significant inverse correlation with the GV in Benzatropine our 34 patients (Table 3), indicating the functional adaptation of remaining glomeruli in patients with a small number of functioning nephrons. Based on these findings,

it is Salubrinal plausible to speculate that, in the patients with a low GD and large GV, obesity-related hemodynamic changes such as an increase of plasma flow or blood pressure within the glomerulus can alter glomerular permselectivity. Thus, a low GD may play a crucial role in the development of proteinuria in association with GH in overweight or obese persons. Concerning the pathological findings of our 34 proteinuric patients, the population of patients with increased mesangial matrix was comparable between those with and without GH (Table 2), indicating that GH was caused by the enlargement of glomerular capillaries. Sasatomi et al. [20] previously demonstrated, using glomerular morphometry, that the GH observed in obese patients presenting with urine abnormalities was due to the enlargement of glomerular capillaries. This finding was consistent with our results showing that there was no significant mesangial matrix increase in the hypertrophied glomeruli.

Water Altern 3:14–42 Rowland EL, Davison JE, Graumlich LJ (2011)

Water Altern 3:14–42 Rowland EL, Davison JE, Graumlich LJ (2011) Approaches to evaluating climate change impacts

on species: a guide to initiating the adaptation planning process. Environ Manage 47:322–337PubMedCrossRef Saxon E (2008) Noah’s Parks: a partial antidote to the Anthropocene extinction event. Biodiversity 9:5–10CrossRef Saxon E, Baker B, Hargrove W, Hofman F, Zganjar C (2005) Mapping environments at risk under different global climate change scenarios. Ecol Lett 8:53–60CrossRef Schick RS, Lindley ST (2007) Directed connectivity among fish populations in a riverine network. J Appl Ecol 44:1116–1126. doi:10.​1111/​j.​1365-2664.​2007.​01383.​x learn more CrossRef Sinervo B, Mendez-de-la-Cruz F, Miles DB, Heulin B, Bastiaans E, Cruz MVS, Lara-Resendiz R, Martinez-Mendez N, Calderon-Espinosa ML, Meza-Lazaro RN, Gadsden H, Avila LJ, Morando M, De la Riva IJ, Sepulveda PV, Rocha CFD, Ibarguengoytia N, Puntriano CA, Massot M, Lepetz V, Oksanen TA, Chapple DG, Bauer AM, Branch WR, Clobert J, Sites JW (2010) Erosion of lizard diversity by climate change and altered thermal niches. Science 328:894–899. doi:10.​1126/​science.​1184695 PubMedCrossRef Tallis H, Kareiva P, Marvier check details M, Chang A (2008) An ecosystem services framework to support both practical conservation and economic development. Proc Natl Acad Sci USA 105:9457–9464PubMedCrossRef

USAID (2009) Adapting to coastal climate change—a guidebook for development planners. United States Agency for International Development,

Washington Venter O, Meijaard E, Possingham HP, Dennis R, Sheil D, Wich S, Hovani L, Wilson KA (2009) Carbon payments as a safeguard SPTLC1 for threatened tropical mammals. Conserv Lett 2:123–129CrossRef Vos CC, Berry P, Opdam P, Baveco H, Nijhof B, O’Hanley J, Bell C, Kuipers H (2008) Adapting landscapes to climate change: examples of climate-proof ecosystem networks and priority adaptation zones. J Appl Ecol 45:1722–1731. doi:10.​1111/​j.​1365-2664.​2008.​01569.​x CrossRef West JM, Salm RV (2003) Resistance and resilience to coral bleaching: implications for coral reef conservation and management. Conserv Biol 17:956–967CrossRef Wiens JA, Bachelet D (2010) Matching the multiple scales of conservation with the multiple scales of climate change. Conserv Biol 24:51–62. doi:10.​1111/​j.​Tariquidar purchase 1523-1739.​2009.​01409.​x PubMedCrossRef Wiens JA, Fargione J, Hill J (2011) Biofuels and biodiversity. Ecol Appl 21:1085–1095PubMedCrossRef Williams P, Hannah L, Andelman SJ, Midgley G, Araujo M, Hughes G, Manne L, Martinez-Meyer E, Pearson R (2005) Planning for climate change: identifying minimum-dispersal corridors for the Cape Proteaceae. Conserv Biol 19:1063–1074CrossRef Willis KJ, Bhagwat SA (2009) Biodiversity and climate change.

(a) Typical I-V characteristics of Cu/GeO x /W and (b) Al/GeO x /

(a) Typical I-V characteristics of Cu/GeO x /W and (b) Al/GeO x /W cross-point memories. Figure 5 Current–voltage characteristics. I-V measurements of pristine (a) Cu/GeO x /W (S1) and (b) Al/GeO x /W (S2) devices. A high formation voltage is needed for Al TE. More than eight devices were measured randomly. Further, the RESET current is independent of CCs from 1 nA to 1 mA for the Al/GeO x /W cross-point memory device, as shown in Figure  6. This suggests that the RESET current scalability as well as device scaling is difficult for the Al TE devices, which form larger filament diameter (or many conducting filaments) even at a small CC of 1 nA. This is due to a strong current overshoot

effect in the Al/GeO x /W cross-point memory devices. It is noted that the

diameters of the conducting filaments are the same at all CCs from 1 nA to 2 mA, which is due to the defective AlO x layer High Content Screening at the Al/GeO x interface or unstable interface. HDAC inhibition A high RESET current of >20 mA was also reported by Kato et al. using Al TE [44]. Lin et al. [12] also reported a high RESET current for Al2O3-based resistive switching memory using a Ti/Al2O3/Pt structure. According to several reported results, using Al electrode or Al2O3-based resistive memory devices requires higher operation voltages as well as high RESET currents [12, 44, 45]; however, a few results were reported on Akt inhibitor ic50 low-current operation [6–8, 14]. As we can see, the formation voltage of the Al/GeO x /W device is higher

than that of the Cu/GeO x /W device. It seems that the parasitic capacitance [46] of the Al/GeO x /W device as well as the current overshoot effect is higher. Even if the SET voltage is lower, the RESET current is still very high or the same with the RESET current of formation. This suggests that the current overshoot effect is not due to the higher operation voltage but to the AlO x formation at the Al/GeO x interface or unstable interface. This is a very important difference between these Al and Cu TEs. An excellent scaling of the RESET current is observed for the Cu/GeO x /W cross-point memory devices with CCs from 1 nA to 50 μA. Furthermore, the RESET current is lower than the SET current, which proves no current overshoot effect those even in the 1R configuration or no parasitic effect [46]. The formation and dissolution of Cu nanofilament under SET and RESET are responsible for the switching mechanism of the Cu/GeO x /W cross-point memory devices. The Cu ions will migrate through the defects into the GeO x film and start to grow first at the GeO x /W BE under SET operation by reduction process (Cu z+ + ze- → Cuo). The Cu nanofilament will start to dissolve at the Cu/GeO x interface under RESET operation by oxidation process (Cuo → Cu z+ + ze-). In the case of the Al/GeO x /W cross-point memory, oxygen vacancy filament formation and oxidation are responsible for the switching mechanism.

Diagn microbial Infect Dis 2004, 49:269–271 CrossRef 13 van Asbe

Diagn microbial Infect Dis 2004, 49:269–271.CrossRef 13. van Asbeck EC, Huang Y-C, Markham AN, Clemons KV, Stevens DA: Candida parapsilosis fungemia in neonates: genotyping results suggest healthcare workers hands as source, and review of published studies. Mycophatologia 2007, 164:287–293.CrossRef 14. Hube B, Stehr F, Bossenz M, Mazur A, Kretschmar M, Schäfer W: NU7026 in vivo Secreted lipases of Candida albicans : cloning, characterisation and expression analysis of a new gene family with at least ten members. Arch Microbiol 2000, 174:362–374.PubMedCrossRef 15. Khun DM, Mikherjee PK, Clark TA, Pujol C, Chandra J, Hajjeh RA, Warnock DW, Soil DR, Ghannoum MA: Candida parapsilosis characterization in an outbreak setting.

Emerg Infect Dis 2004, 10:1074–1081. 16. Bramono K, amazaki M, Tsuboi R, Ogawa H: Comparison of proteinase, lipase and alpha-glucosidase activities from the clinical isolates of Candida species . Jpn J Infec Dis 2006, 59:73–76. 17. Owaki T, Meneshian A, Maemura K, JQ-EZ-05 Takao S, Wang D, Fuh KC, Bulkley GB, Klein AS: Endothelial cells potentiate phagocytic killing by macrophages via platelet-activating factor release. Am J Physiol Heart Circ Physiol 2000, 278:H269-H276.PubMed 18. Gácser A, Trofa D, Schäfer W, Nosanchuk JD: Targeted gene

deletion in Candida parapsilosis demonstrates the role of secreted lipase in virulence. J Clin Invest 2007, 117:3049–3058.PubMedCrossRef 19. Gácser A, Schafer W, Nosanchuk JS, Salomon S, Nosanchuk JD: Virulence of Candida parapsilosis, Candida orthopsilosis , and Candida metapsilosis in reconstituted human tissue models. Fungal Genet Biol 2007, 44:1336–1341.PubMedCrossRef 20. Maródi L, Schreiber S, Anderson DC, MacDermott RP, Korchak HM, Johnston RB Jr: Enhancement of macrophage candidacidal activity by interferon-y – increased phagocytosis, killing, and calcium signal mediated oxyclozanide by a decreased number of mannose receptors. J Clin Invest 1993, 91:2596–2601.PubMedCrossRef 21. Camargo

MR, Venturini J, Vilani-Moreno FR, Arruda MSP: Modulation of macrophage cytokine profiles during solid tumor progression: susceptibility to Candida albicans infection. BMC Infectious Diseases 2009, 9:98–106.PubMedCrossRef 22. Lorenz MC, Fink GR: Life and death in a macrophage: role of the glyoxylate cycle in virulence. Eukaryot Cell 2002, 1:657–662.PubMedCrossRef 23. Orsi CF, Colombari B, Blasi E: Candida metapsilosis as the least virulent member of the C. parapsilosis complex. Med Mycol 2010, 48:1024–1033.PubMedCrossRef 24. Shin YK, Kim KY, Paik YK: Alterations of protein expression in macrophages in response to Candida albicans infection. Mol Cells 2005, 20:271–279.PubMed 25. Tavanti A, Campa D, Bertozzi A, Pardini G, Naglik JR, Barale R, Senesi S: Candida albicans isolates with different genomic backgrounds display a differential response to macrophage infection. Microbes Infect 2006, 8:791–800.PubMedCrossRef 26.

The dissociation of Er-OH bonds under dc stressing is proposed to

The dissociation of Er-OH bonds under dc stressing is proposed to be associated by the electrons in the oxide surface as follows: (2) Figure 5 Threshold voltage and drive current degradation and structural model. (a) Threshold voltage shift and current drive degradation as a function of

stress time for high-κ Er2O3 and Er2TiO5 a-IGZO TFT devices. Structural model of the (b) Er2O3 surface and (c) Er2TiO5 surface. The physical model to be presented is based on the structure of the Er2O3 and Er2TiO5 surfaces, as schematically depicted in Figure  5b,c, respectively. Briefly speaking, selleckchem during dc stress, hydroxyl ions (OH–) are released from the erbium hydroxide (Er-OH) by breaking the Er-OH bonds. The electrons in the oxide have gained enough energy from the applied gate and drain voltages. They collide selleck products with strained

Er-O-Er or Er-O-Ti bonds to generate trapped charges in bulk oxide, causing a threshold voltage shift. On the other hand, a-IGZO TFT with the Er2O3 dielectric has a larger drive current BMN 673 solubility dmso degradation than that with the Er2TiO5 one. The hygroscopic nature of RE oxide films forming hydroxide produces oxygen vacancies in the gate dielectric, leading to a larger flat-band voltage shift and higher leakage current [11]. The incorporation of Ti into the Er2O3 dielectric film can effectively reduce the oxygen vacancies in the film. Conclusions In conclusion, we have fabricated a-IGZO TFT devices using the Er2O3 and Er2TiO5 Interleukin-2 receptor films as a gate dielectric. The a-IGZO TFT incorporating a high-κ Er2TiO5 dielectric exhibited a lower V TH of 0.39 V, a larger μ FE of 8.8 cm2/Vs, a higher I on/I off ratio of 4.23 × 107, and a smaller subthreshold swing of 143 mV/dec than that of Er2O3 dielectric. These

results are attributed to the addition of Ti into the Er2O3 film passivating the oxygen vacancies in the film and forming a smooth surface. Furthermore, the use of Er2TiO5 dielectric film could improve the stressing reliability. The Er2TiO5 thin film is a promising gate dielectric material for the fabrication of a-IGZO TFTs. Acknowledgment This work was supported by the National Science Council (NSC) of Taiwan under contract no. NSC-101–2221-E-182–059. References 1. Su LY, Lin HY, Lin HK, Wang SL, Peng LH, Huang JJ: Characterizations of amorphous IGZO thin-film transistors with low subthreshold swing. IEEE Electron Device Lett 2011, 32:1245–1247.CrossRef 2. Nomura K, Ohta H, Takagi A, Kamiya T, Hirano M, Hosono H: Room-temperature fabrication of transparent flexible thin-film transistors using amorphous oxide semiconductors. Nature 2004, 432:488–492.CrossRef 3. Lee JS, Chang S, Koo SM, Lee SY: High-performance a-IGZO TFT with ZrO 2 gate dielectric fabricated at room temperature. IEEE Electron Device Lett 2010, 31:225–227.CrossRef 4.