001 peptidyl-Asp metallopetidases is underlined; (4) the three co

001 peptidyl-Asp metallopetidases is underlined; (4) the three conserved histidines (aa 167, 171, and 177), residues for zinc binding, and glutamate (aa 168), the catalytic residue, are in green; (5) two carbohydrate binding modules of the CBM_4_9 family, aa 302 to aa 432 and aa 461 to aa 586, in blue. (B) The P. aeruginosa predicted PA2783 is homologous to metalloendopeptidases from other bacteria. Interrogation of the non-redundant databases at NCBI (http://​www.​ncbi.​nlm.​nih.​gov/​; GSK872 accessed 10/18/2013) was done using BLASTP and the Peptidase Database MEROPS (http://​merops.​sanger.​ac.​uk/​index.​shtml; accessed 10/18/2013) was done

using BLAST. Identical aa are shown in red, similar aa in blue, and non-similar buy LY2874455 aa in black. PA2783 is homologous to the Pseudomonas mendocina ymp (Pmendo) carbohydrate-binding CenC domain-containing protein and the Ni,Fe-hydrogenase I small subunit of Hahella chejuensis KCTC 2396 (Hcheju) across the entire endopeptidase domain. Other proteins contain the GDC-0941 mouse HEXXHXXGXXH motif only (highlighted by a yellow box). Amacle, Alteromonas macleodii; Ahydro,

Aeromonas hydrophila; Vchole, Vibrio cholerae; Vmimic, V. mimicus; Vvulni, V. vulnificus; Xfraga, Xanthomonas fragariae; Xcampe, X. campestris; Xvesic, X. vesicatoria. Percentages of aa identity and similarity may be found in Additional file 2. PA2782 encodes a putative 22.7-kDa protein of 219 aa that contains no specific motifs, except for the presence of an alanine-rich region Inositol oxygenase within

its amino terminus (23 of the first 60 aa), and that has no functional homology with other known proteins (data not shown). Characterization of PA2783, a putative metalloendopeptidase The predicted protein PA2783 contains all the features of a potential endopeptidase including the putative glutamic acid catalytic residue and the three zinc-binding histidine residues within its amino terminus (Figure 5A) [39]. We tried to assess the proteolytic activity produced by PA2783 using dialyzed brain heart infusion skim milk agar. However, this approach proved unfeasible due to the production by P. aeruginosa of several proteases with strong proteolytic activities. Both PAO1/pUCP19 and PAO1/pAB2 produced identical clearing zones of protease activity (data not shown). We faced the same problem when we utilized strain PAO-R1 (Table 1), which produces a considerably reduced level of proteolytic activity due to the mutation of lasR[33]. Despite the reduction in the extracellular proteolytic activity of this strain, PAO-R1/pUCP19 and PAO-R1/pAB2 produced identical clearing zones on skim milk agar (data not shown). As an alternative, we assessed the potential proteolytic activity of PA2783 using the E. coli strain DH5α (Table 1).

The controlled

and well-aligned CNFs are used to investig

The controlled

and well-aligned CNFs are used to investigate cell spreading phenomena and related issues of cellular biocompatibility. The fundamental issues of cell spreading and extension guiding in a preferential direction are experimentally performed on parallel-aligned and grid patterns for the purpose of better realization of the ability to manipulate cellular architecture. Methods Materials Chitosan from crab shells with 85% deacetylation (Mw = 50 to 190 kDa) was purchased from Sigma Chemical Co (St. Louis, MO, USA). PEO (Mw = 900 kDa; Triton X-100™) was provided by Acros Co. (Geel, Belgium), and dimethylsulfoxide (DMSO) was obtained from Tedia Co. (Fairfield, OH, USA). All reagents were used as received from the manufacturer without further purification. Preparation of stock solutions for electrospinning Chitosan solution (5%) and 1% PEO solution were first selleck prepared separately by dissolving chitosan in 0.5 M acetic acid, then vacuumed in an oven at 0.8 Torr to remove air bubbles [17]. Solutions containing 0.5 wt.% of

Triton X-100™ and 5 to 10 wt.% of DMSO were mixed with the chitosan/PEO solutions, and the mixtures were again stirred for 16 h and vacuumed to remove air bubbles before use. Polypyrrole substrates Soluble PPy was synthesized chemically using ammonium persulfate (APS) as an oxidant and a dopant. Pyrrole of 0.3 mol and 1:50 ratio see more of APS and pyrrole solution were mixed with 500 ml of distilled water. The solution was spin-cast on a polystyrene Petri

dish to obtain a PPy film [25], and the electrical conductivity was measured to be 7.25 kΩ/square using the four-point probe method. NFES setup The stock solution for electrospinning was fed into a 1-ml disposable syringe fitted with a 0.4-mm-wide needle tip, the applied electrostatic voltage was in the range of 800 to 1,000 V (AU-1592, Matsusada Precision Inc., Kusatsu, Japan), and the distance between the syringe tip and the grounded collector was 500 μm. The substrate was mounted onto a programmable XY stage (Yokogawa Inc., Tokyo, Japan), controlled by a personal computer, which allows movement of the sample during nanofiber deposition. The experiment was carried out at room temperature and atmospheric Phosphatidylinositol diacylglycerol-lyase pressure. Cell culture, adhesion, and spreading Human embryonic kidney cells (HEK 293T) were cultured in 25-cm2 flasks in Dulbecco’s modified Eagle medium containing 10% fetal bovine serum. The cell suspension was added to each nanofiber pattern in a PPy-modified polystyrene Petri dish and cultured in an incubator at 37°C with 5% CO2. In order to seed HEK 293T cells onto the CNF, a confluent monolayer of cells was trypsinized and centrifuged at 1,000 rpm for 4 min. After supernatant Smoothened Agonist supplier removal and re-suspension in fresh culture medium, cells were transferred to a PPy-modified polystyrene Petri dish.

To validate the microarray results, quantitative RT-PCR (qRT-PCR)

To validate the microarray results, quantitative RT-PCR (qRT-PCR) of selected genes was performed. Five of the genes were selected from the up-regulated group and the other five from the down-regulated group in the polyP-treated P. gingivalis cells. We used 16S rRNA as a reference gene for normalization of the qRT-PCR data. There was a high correlation

between the expression ratios determined by the microarray and the qRT-PCR (r = 0.926) (Figure 2). Figure 1 Differential gene expression in P. gingivalis W83 by polyP75 treatment. Differentially expressed genes with 1.5 fold change and P-value < 0.05 were plotted. X-axis presents fold difference between log2 expression of polyP75 treatment and no treatment, and y-axis shows the –log10 P -value. Up-regulated genes (over-expressed in polyP75 treatment) were represented as red color and down-regulated genes were colored in blue. Figure 2 Comparison SIS3 order of transcription measurements by microarray and qRT-PCR. The relative transcription levels for 10 genes are listed in Table 6. The qRT-PCR log2 values were plotted against the microarray data log2 values.

The Navitoclax concentration correlation coefficient (r) for comparison of the two datasets is 0. 92. To broadly characterize the differentially expressed gene (DEG, up- and down-regulated genes) set, GO category enrichment analysis was performed. This analysis identified distinct biological themes selleck chemicals associated with each group of the up-regulated and the down-regulated genes. The down-regulated genes were associated with GO terms

related to metabolic process (GO:0008152, P = 0.0004), pyridine nucleotide biosynthetic Thiamine-diphosphate kinase process (GO:0019363, P = 0.0012), regulation of cell shape (GO:0008360, P = 0.002), and polysaccharide biosynthetic process (GO:0000271, P = 0.0015). The up-regulated genes were associated with GO terms related to cellular iron ion homeostasis (GO:0006879, P < 0.0001), ribosome (GO:0005840, P = 0.0032), transposase activity (GO:0004803, P < 0.0001), and DNA binding (GO:0003677, P < 0.0001). Using 202 DEGs belonging to the above biological themes, we generated the protein-protein interaction network based on a database of known and predicted protein interactions. The network analysis identified 162 DEGs that have direct interaction with one another (Figure 3), and 5 biological meaningful clusters related to 1) iron/hemin acquisition, 2) energy metabolism and electron carriers, 3) cell envelope and cell division, 4) ribosome, and 5) transposon functions. Figure 3 Protein-protein interaction network of differentially expressed functional genes. The network was constructed based on the STRING database. Nodes (symbolized as circles and square) and edges (linking lines) represent DEGs and interactions among DEGs, respectively. Up-regulated genes were represented as a circular shape and down-regulated genes were presented as a square shape. Node color represents the functional annotation of each gene.

J Chin Med Assoc 2007, 70:324–330 PubMedCrossRef 6 Alijani A, Ha

J Chin Med Assoc 2007, 70:324–330.PubMedCrossRef 6. Alijani A, Hanna GB, Cuschieri A: Abdominal wall lift versus positive-pressure selleckchem capnoperitoneum for laparoscopic cholecystectomy: randomized controlled trial. Ann Surg 2004, 239:388–394.PubMedCrossRef 7. Tai YP, Wei CK, Lai YY: Intraoperative pneumothorax during laparoscopic cholecystectomy. Acta

Anaesthesiol Taiwan 2006, 44:231–234.PubMed 8. Hasson HM, Galanopoulos C, Langerman A: Ischemic necrosis of small bowel following laparoscopic surgery. JSLS 2004, 8:159–163.PubMedCentralPubMed 9. Smith HJ: Carbon dioxide embolism during pneumoperitoneum for laparoscopic surgery: a case report. AANA J 2011, 79:371–373.PubMed 10. Korndorffer JR Jr, Fellinger E, Reed W: SAGES guideline for laparoscopic appendectomy. Surg Endosc 2010, 24:757–761.PubMedCrossRef 11. Smith RS, Fry WR, Tsoi EK, Henderson VJ, Hirvela ER, Koehler RH, Brams DM, Morabito DJ, Peskin GW: Gasless laparoscopy and conventional instruments. The next phase of minimally invasive surgery. Arch Surg 1993, 128:1102–1107.PubMedCrossRef 12. Chen D, Shi H, Dong H, Liu K, Ding K: Gasless single-incision laparoscopic appendectomy. Surg Endosc 2011, 25:1472–1476.PubMedCrossRef 13. McKinlay R, Mastrangelo MJ Jr: Current status of laparoscopic appendectomy. Curr Surg 2003, 60:506–512.PubMedCrossRef 14. Tiwari MM, Reynoso JF,

Tsang AW, Oleynikov D: Comparison of outcomes of laparoscopic and open appendectomy in management of uncomplicated find more and complicated appendicitis. Ann Surg 2011, 254:927–932.PubMedCrossRef 15. Kheirabadi BS, Tuthill D, Pearson R, Bayer V, Beall D, Drohan W, MacPhee tuclazepam MJ, Holcomb JB: Metabolic and hemodynamic effects of CO2 pneumoperitoneum in a controlled hemorrhage model. J Trauma 2001, 50:1031–1043.PubMedCrossRef 16. Holzman M, Sharp K, Richards W: Hypercarbia during carbon dioxide gas insufflation for therapeutic laparoscopy: a note of SIS 3 caution. Surg Laparosc Endosc 1992, 2:11–14.PubMed 17. Davidson BS, Cromeens DM, Feig BW: Alternative methods of exposure minimize cardiopulmonary risk in experimental animals during minimally

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Respiratory Med 2010, 104:840–848 CrossRef 3 Woodford N, Turton

Respiratory Med 2010, 104:840–848.CrossRef 3. Woodford N, Turton JF, Livermore DM: Multiresistant Gram-negative bacteria: the role of high-risk clones in the dissemination of antibiotic resistance. FEMS Microbiol Rev 2011, 35:736–755.PubMedCrossRef 4. Picazo JJ, Betriu C, Rodríguez-Avial I, Culebras E, Gómez M, López F, Grupo VIRA: Vigilancia de resistencias a los antimicrobianos: estudio VIRA 2006. Enferm Infecc Microbiol Clin 2006, 24:617–628.PubMedCrossRef 5. Denamur E, Picard B, Goullet P, Bingen E, Lambert N, Elion J: Complexity of Pseudomonas aeruginosa infection

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4-Hydroxytamoxifen cell line 7. Johnson JK, Arduino SM, Stine OC, Johnson JA, Harris AD: Multilocus sequence typing compared to pulsed-field gel electrophoresis for molecular typing of Pseudomonas aeruginosa . J Clin Microbiol 2007, 45:3707–3712.PubMedCrossRef 8. Curran B, Jonas D, EPZ5676 in vivo Crundmann H, Pitt T, Dowson C: Development of a multilocus sequence typing scheme for the opportunistic pathogen Pseudomonas aeruginosa . J Clin Microbiol 2004, 42:5644–5649.PubMedCrossRef 9. Clinical and Laboratory Standards Institute: Performance standards for antimicrobial susceptibility testing. Wayne, PA: Clinical and Laboratory Standard Institute; 2010. [20th informational supplement, document M100-S20] 10. Societé Française de Microbiologie: Comité de l’antibiograme de la societe française de microbiologie. Recommandations; 2010. 11. Magiorakos AP, Srinivasan A, Carey RB, et al.: Multidrug-resistant, extensively drug-resistant and pandrug-resistant bacteria: an international

expert proposal for interim standard definitions for acquired resistance. Clin Microbiol Infect 2012, 18:268–281.PubMedCrossRef 12. Gomila M, Ramírez www.selleck.co.jp/products/cobimetinib-gdc-0973-rg7420.html A, Lalucat J: Diversity of environmental Mycobacterium isolates from hemodialysis water as shown by a multigene sequencing approach. Appl Environm Microbiol 2007, 73:3787–3797.CrossRef 13. Librado P, Rozas J: DnaSP v5: a software for comprehensive analysis of DNA polymorphism data. Bioinformatics 2009, 25:1451–1452.PubMedCrossRef 14. Hammer Ø, Harper DAT, Ryan PD: PAST: Paleontological statistics software package for education and data analysis. Paleontol Electr 2001, 4:9. 15. Roy PH, Tetu SG, Larouche A, et al.: Complete genome sequence of the multiresistant taxonomic outlier Pseudomonas aeruginosa PA7. PLoS One 2010, 5:e8842.PubMedCrossRef 16. GarcíaYM155 mouse -Castillo M, Del Campo R, Morosini MI, et al.: Wide dispersion of ST175 clone despite high genetic diversity of carbapenem-nonsusceptible Pseudomonas aeruginosa clinical strains in 16 Spanish hospitals. J Clin Microbiol 2011, 49:2905–2910.PubMedCrossRef 17.

No temporal relationship was observed between the occurrence of t

No temporal relationship was observed between the occurrence of these opportunistic infections and administration of the Crenolanib investigational product (Fig. 1a). Nonserious adverse events of opportunistic infections were not specifically https://www.selleckchem.com/products/PF-2341066.html identified and categorized as such, but individual terms included tuberculosis, which was reported

as a nonserious adverse event in four subjects receiving placebo and no subjects receiving denosumab. Fig. 1 a Serious adverse events of opportunistic infections and relationship to timing of administration of investigational product. b Serious adverse events of cellulitis and erysipelas and relationship to timing of administration of investigational product. Denosumab subject 5 experienced a fatal adverse event associated with cellulitis. c Events of endocarditis and relationship to timing of administration of investigational product. Denosumab subjects 1 and 2 experienced serious adverse events of endocarditis;

denosumab subject 3 experienced a nonserious adverse event of endocarditis. Circles indicate denosumab injections; plus signs indicate placebo injections; rectangles indicate onset and duration of the adverse event Skin infections Serious adverse events of infections involving the skin occurred in 3 (<0.1%) placebo subjects and 15 (0.4%) denosumab subjects (P < 0.05; Table 3). These were not injection-site reactions. In the denosumab group, most of these skin BAY 73-4506 cell line infections were cellulitis or clinically diagnosed erysipelas involving the lower extremities that resolved with administration of common antibiotics.

The overall incidence of adverse events of cellulitis and erysipelas (i.e., FAD both serious and nonserious adverse events) was not significantly different between treatment groups (0.9% placebo, 1.2% denosumab) [8]. There was no temporal association between the onset of serious adverse events of cellulitis and erysipelas and duration of treatment or time since last dose of investigational product (Fig. 1b). Table 3 Incidence of serious adverse events of skin infection   Placebo (N = 3,876)a, n (%) Denosumab (N = 3,886)a, n (%) Serious adverse events of infection involving the skin 3 (<0.1) 15 (0.4)* Cellulitis and erysipelas 1 (<0.1) 12 (0.3)b Skin bacterial infection 0 (0) 2 (<0.1) Staphylococcal infection 1 (<0.1) 1 (<0.1) Infected skin ulcer 0 (0) 1 (<0.1)b Subcutaneous abscess 1 (<0.1) 0 (0) *P < 0.05 vs placebo aNumber of subjects who received ≥1 dose of investigational product bOne subject in the denosumab group experienced events of cellulitis and erysipelas and infected skin ulcer Cellulitis and erysipelas are usually caused by Streptococcus pyogenes, Staphylococcus aureus, and other gram-positive bacterial infections. In this study, serious adverse events of cellulitis and erysipelas were diagnosed clinically and not usually confirmed by culture. A positive S.

The metabolic activity of L-form bacteria has not been widely stu

The metabolic activity of L-form bacteria has not been widely studied, but previous work has shown that metabolic

activity for the L-form is often much lower than vegetative cells [23, 24]. Generally L-forms can be recognized by a spherical or pleomorphic AMN-107 morphology which differs significantly from the morphology of the parent cells [25], but as the shape of L-forms can vary considerably, this definition is not universal. They are most frequently defined as cell forms that have a deficient or absent cell wall and retain the ability to divide [26]. The ability of L-forms to form colonies on nutrient rich plates [26] helps to differentiate them from viable but non-culturable cells (VBNCs), another non-growth state AZD1152 which is often induced by starvation or unpermissive growth temperatures and in some cases shares many similar features with L-forms [27]. L-forms are selleck often classified in two categories, stable and unstable, which respectively refer to whether the L-form can revert back to the parent morphology or not [21]. Stressors that have been found to induce or promote the L-form morphology include treatment with β-lactam antibiotics with or without lysozyme[28, 29], cultivation in minimal media or exposure to nutrient limitation [30–32], exposure to extreme heat [30] and exposure

to high salt concentrations [33]. Following the observation that C. thermocellum strain ATCC 27405 develops L-forms Teicoplanin in addition to spores, we examine here the properties of these two non-growth cell states and the factors that trigger their formation in this organism. Results Evaluation of conditions under which spores were observed Several growth medium modifications were tested to evaluate impacts on sporulation of C. thermocellum strain ATCC 27405 as shown in Table 1. Only the absence of vitamins appeared to have any sporulation effect, with an average of 4% of the cells forming spores. Elevated amounts of acetate (3 g/L) and ethanol (0.2-10% v/v), the two

primary fermentation products formed by this organism, were also tested but a sporulation response was not observed. The effect of low pH was tested in C. thermocellum cultures allowed to drop below pH 6.0 during the course of normal fermentation, but sporulation was not observed. Likewise, a decrease in temperature below 48°C did not result in spore formation for exponential or stationary phase cells. Table 1 Percentage of resting cells formed after stress exposure Stress type Specific modification Percent spores Percent L-forms MTC media (control) No modifications 0 0 Nutrient limitation Reduced cellulose (1g L-1) 0 0 Nutrient limitation Low phosphorous 0 0 Nutrient limitation Low nitrogen 0 0 Nutrient limitation No vitamins 4.2 ± 2.8 0 Inhibitor Added ethanol 0 0 Inhibitor Added acetate 0 0 Oxidative stress Added oxygen 6.6 ± 4.

Overall

Overall survival was analyzed using the Kaplan-Meier method and evaluated by the log-rank test. Significant differences were considered at p < 0.05. The cutoff point was also p < 0.05 for univariate Selleckchem LY2603618 and multivariate Cox proportional hazard model analysis. Results p53AIP1 and survivin expression in primary non-small cell lung cancer (NSCLC) was evaluated by real-time

RT-PCR. All 47 samples were studied with paired histopathologically normal lung tissues which were far from the tumor margin. Table 1 shows a correlation between the clinicopathological status and p53AIP1 and survivin gene expressions. Although no relationship between the p53AIP1 gene expression and variables (age, sex, smoking index (SI), tumor size, nodal status, histological type) was not found, the survivin gene expression-MK-0457 mouse positive rates in the node metastasis-positive group were significantly selleck kinase inhibitor higher than in the negative group (p = 0.03). Table 1 Correlation between p53AIP1 or survivin expression

and clinicopathological characteristics Characteristics All patients p53AIP1 positive p Survivin positive p Age <70 19 11   14     ≥70 28 14 0.23 14 0.45 Sex male 14 6   11     female 33 19 0.36 17 0.08 Smoking <400 19 10   13   index ≥400 28 15 0.95 15 0.31 Tumor T1 27 16   18     T2 16 9   8     T3 4 0 0.08 2 0.52 Nodal status N0 33 12   10     N1 14 5 0.17 9 0.03* Histologic type Ad 27 12   19     Sq 16 10   7     others 4 3 0.34 2 0.22 Ad, adenocarcinoma; Sq, squarmous cell carcinoma * statistically significant Figure 1 shows the overall survival

Thymidylate synthase curves by Kaplan-Meier analysis for patients with non-small cell lung cancer classified according to p53AIP1 expression (positive, tumor/normal ratio ≥ negative, <1). Patients in the positive p53AIP1 expression group have a better prognosis than the negative expression group (p = 0.04). The median follow-up period was 5.4 years (1.2 to 8.4 years); however, the superiority of the survivin expression negative group to the positive group for overall survival was not significant (Figure 2). When we compared the prognosis according to the variable combination between p53AIP1 and survivin, the p53AIP (+) survivin (-) group had the best prognosis (Figure 3). In contrast, the p53AIP (-) survivin (+) group showed the worst prognosis and the other two groups were intermediate. In univariate analysis using age, tumor size, lymph node metastasis, histological type, survivin expression, p53AIP1 expression, and the combination of p53AIP1 and survivin, p53AIP1 and the combination were statistically significant (Table 2). Figure 1 Overall survival curves according to p53AIP1 gene expression. Differences are significant (p = 0.04). Number of patients in each group, positive, 22; negative, 25. Figure 2 Overall survival curves according to survivin gene expression. Differences are not significant (p = 0.36. Number of patients in each group, positive, 28; negative, 19.

Dietary amino acids are the major fuel for the small intestinal m

Dietary amino acids are the major fuel for the small intestinal mucosa as well as they are important substrates for the synthesis of intestinal proteins such as nitric oxide polyamines and other products with enormous biological activity [41]. Glutamine was one of the few free click here amino acid related compounds which was found at the highest level

in HC children. A low level of glutamine was also previously found in CD children and adults [22]. Specific amino acids and related compounds, including glutamine, were shown to possess a therapeutic role in gut diseases [41]. This study confirmed the hypothesis that CD is associated with intestinal and faecal dysbiosis, which is related to certain bacterial species. Recently, it was shown that potential celiac VX-689 in vitro subjects and overt celiac subjects show differences in the urine metabolites and a very similar serum metabolic profile [42]. Metabolic alterations

selleck inhibitor may precede the development of small intestinal villous atrophy and provide a further rationale for early institution of GFD in patients with potential CD [42]. As shown by both microbiology and metabolome analyses, the GFD lasting at least two years did not completely restore the microbiota and, consequently, the metabolome of CD children. Probably, the addition of prebiotics and probiotics to GFD might restore the balance of microbiota and metabolome of CD children. Conclusions As shown by the microbiology and metabolome studies, the gluten-free diet lasting at least two years did not completely restore the microbiota mafosfamide and, consequently,

the metabolome of CD children. Combining the results of this work with those from previous reports [9, 10, 16, 22, 27, 37], it seems emerge that microbial indeces (e.g., ratio between faecal cell density of lactic acid bacteria-Bifidobacterium vs. Bacteroides-Enterobacteria) and levels of some metabolites (e.g., ethyl-acetate, octyl-acetate, SCFA and glutamine) are signatures of CD patients. Further studies, using a major number of children and a complete characterization of all microbial groups, are in progress to find a statistical correlation between the microbiota and metabolome of T-CD compared to HC children. Methods Subjects Two groups of children (6 – 12 years of age) (Table 5) were included in the study: (i) nine-teen symptom-free CD patients, who had been on a GFD for at least 2 years (treated CD children, T-CD) (children numbered: 1 – 19 T-CD); and (ii) fifteen children without celiac disease and other known food intolerance undergoing upper endoscopy for symptoms related to functional dyspepsia and in whom endoscopy showed no signs of disease (non-celiac children) (children numbered: 20 – 34 HC). The pathology was diagnosed according to criteria given by the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition.

IEEE VLSI Symposium

2012, 151 13 Jung J, Cho W: Tunnel

IEEE VLSI Symposium

2012, 151. 13. Jung J, Cho W: Tunnel barrier engineering for non-volatile memory. J Semicond Tech Sci 2008, 8:No. 1, 33. 14. Woo J, Jung S, Siddik M, Cha E, Sadaf S, Hwang H: Effect of interfacial oxide layer on the switching uniformity of Ge2Sb2Te5-based resistive change memory devices. AIP Applied Physics Letters 2011, 99:162109. 10.1063/1.3656247CrossRef 15. Chen A: Switching control of resistive switching www.selleckchem.com/products/4egi-1.html devices. AIP Appl Phys Lett 2010, 97:263505. 10.1063/1.3532969CrossRef 16. Sriraman V, Chen Z, Li X, Wang X, Singh N, Lo G: HfO 2 based resistive switching non-volatile memory (RRAM) and its potential for embedded applications. International Conference Solid-State Integration Circuit 2012, 32. 17. Chen B, Lu Y, Gao B, Fu Y, Zhang F, Huang P, Chen Y, Liu L, Kang J, Wang Y, Fang Z, Yu H, Li X, Wang X, Singh N, Lo G, Kwong D: Physical mechanisms of endurance degradation in TMO-RRAM. PI3K Inhibitor Library solubility dmso IEEE International Electron Devices Meeting 2011, 283. Competing interests The Selleckchem Daporinad Authors declare that they have no competing interests. Authors’ contributions

SL had studied and analyzed behaviors of resistive random access memory (ReRAM) for high selectivity and switching uniformity. He observed that the TiOx tunnel barrier plays an important role in selectivity and switching uniformity. Firstly, JW observed the non-linear behavior of Flucloronide the ReRAM in our group. DL participated in the switching

uniformity analysis. EC participated in the study of the filament growth. Prof. HH comprehensively understands this work as an advisor. All authors have read and approved the final manuscript.”
“Background Nanotechnology is a rapidly advancing and key field of drug delivery. A great variety of nanoparticle (NP)-based therapeutic products have entered clinical development or been approved for clinical use [1]. As an excellent biocompatible and biodegradable nanomaterial with low toxicity and immunogenicity, chitosan (CS)-based nanocarriers presented great advantages for drug, protein, and gene delivery in therapeutics [2–5]. However, most CS-based nanocarriers were easily sequestered by macrophages in the mononuclear phagocyte system (MPS) after intravenous administration. To avoid the rapid clearance of the CS-NPs during circulation, PEGylation can be used to improve the physiological stability, reduce the opsonization, and increase the possibility reaching the tumor by the enhanced permeation and retention (EPR) effect (40 to 400 nm) [6–8]. Despite these advantages of the passive targeting, the main obstacle encountered with the clinical use of the PEGylated CS-NPs is how to facilitate their internalization in the target cells while reducing the unintended side effects. One strategy is the further functionalization of the PEGylated CS-NPs with active targeting agents.