Conclusions This report showed that the silencing of CD147 by RNA

Conclusions This report showed that the silencing of CD147 by RNAi inhibited the proliferation and invasion of human gastric cancer cell line SGC7901 in vitro and increased its chemosensitivity to the anti-tumor drug cisplatin. Our findings suggested that CD147 might be a promising target for gastric cancer treatment. Acknowledgements This work was supported by National Natural Science Foundation Decitabine cost of China (No. 30873022)

and Science and Technology Development Foundation of Nanjing Medical University (No. 09NJMUM070). References 1. Parker SL, Tong T, Bolden S, Wingo PA: Cancer statistics, 1997. CA Cancer J Clin 1997, 47:5–27.PubMedCrossRef 2. Parkin DM, Bray FI, Devesa SS: Cancer burden in the year 2000. The global picture. Eur J Cancer 2001,37(Suppl 8):S4-S66.PubMedCrossRef 3. Parkin DM: International variation. Oncogene

2004, 23:6329–6340.PubMedCrossRef 4. Tang Y, Kesavan P, Nakada Selleckchem Rapamycin MT, Yan L: Tumor-stroma interaction: positive feedback regulation of extracellular matrix metalloproteinase inducer (EMMPRIN) expression and matrix metalloproteinase-dependent generation of soluble EMMPRIN. Mol Cancer Res 2004, 2:73–80.PubMed 5. Kataoka H, DeCastro R, Zucker S, Biswas C: Tumor cell-derived collagenase-stimulatory factor increases expression of interstitial collagenase, stromelysin, and 72-kDa gelatinase. Cancer Res 1993, 53:3154–3158.PubMed 6. Nabeshima K, Iwasaki H, Koga K, Hojo H, Suzumiya J, Kikuchi M: Emmprin (basigin/CD147): matrix metalloproteinase modulator and multifunctional cell recognition molecule that plays a critical

role in cancer progression. Pathol Int 2006, 56:359–367.PubMedCrossRef 7. Tang Y, Nakada MT, Kesavan P, McCabe F, Millar H, Rafferty P, Bugelski P, Yan L: Extracellular matrix metalloproteinase inducer stimulates tumor angiogenesis by elevating vascular endothelial cell growth factor and matrix metalloproteinases. Cancer 3-mercaptopyruvate sulfurtransferase Res 2005, 65:3193–3199.PubMed 8. Tang Y, Nakada MT, Rafferty P, Laraio J, McCabe FL, Millar H, Cunningham M, Snyder LA, Bugelski P, Yan L: Regulation of vascular endothelial growth factor expression by EMMPRIN via the PI3K-Akt signaling pathway. Mol Cancer Res 2006, 4:371–377.PubMedCrossRef 9. Misra S, Ghatak S, Zoltan-Jones A, Toole BP: Regulation of multidrug resistance in cancer cells by hyaluronan. J Biol Chem 2003, 278:25285–25288.PubMedCrossRef 10. Yang JM, Xu Z, Wu H, Zhu H, Wu X, Hait WN: Overexpression of extracellular matrix metalloproteinase inducer in multidrug resistant cancer cells. Mol Cancer Res 2003, 1:420–427.PubMed 11. Marieb EA, Zoltan-Jones A, Li R, Misra S, Ghatak S, Cao J, Zucker S, Toole BP: Emmprin promotes anchorage-independent growth in human mammary carcinoma cells by stimulating hyaluronan production. Cancer Res 2004, 64:1229–1232.PubMedCrossRef 12.

Clin Immunol 2010,135(1):1–11 PubMedCrossRef 15 Aerts AM, Franco

Clin Immunol 2010,135(1):1–11.PubMedCrossRef 15. Aerts AM, Francois IE, Cammue BP, Thevissen K: The mode of antifungal action of plant, insect and human defensins. Cell Mol Life Sci 2008,65(13):2069–2079.PubMedCrossRef 16. Brogden KA: Antimicrobial peptides: pore formers or metabolic inhibitors in bacteria? Nat Rev Microbiol 2005,3(3):238–250.PubMedCrossRef 17. Storm DR, Rosenthal KS, Swanson PE: Polymyxin and related

peptide antibiotics. Annu Rev Biochem 1977, 46:723–763.PubMedCrossRef 18. Bechinger B: Structure and functions of channel-forming peptides: magainins, cecropins, melittin and alamethicin. J Membr Biol 1997,156(3):197–211.PubMedCrossRef 19. Toke O: Antimicrobial peptides: new candidates in the fight against bacterial infections. Biopolymers 2005,80(6):717–735.PubMedCrossRef 20. Sobieszczyk ME, Furuya BI6727 EY, Hay CM, Pancholi P, Della-Latta P, Hammer SM, Kubin CJ: Combination therapy with polymyxin AZD1152-HQPA research buy B for the treatment of multidrug-resistant

Gram-negative respiratory tract infections. J Antimicrob Chemother 2004,54(2):566–569.PubMedCrossRef 21. Jacob L, Zasloff M: Potential therapeutic applications of magainins and other antimicrobial agents of animal origin. Ciba Found Symp 1994, 186:197–216.PubMed 22. Zavascki AP, Goldani LZ, Li J, Nation RL: Polymyxin B for the treatment of multidrug-resistant pathogens: a critical review. J Antimicrob Chemother 2007,60(6):1206–1215.PubMedCrossRef 23. Ouderkirk JP, Nord JA, Turett GS, Kislak JW: Polymyxin B nephrotoxicity and efficacy against nosocomial infections caused by multiresistant gram-negative bacteria. Antimicrob Agents Chemother 2003,47(8):2659–2662.PubMedCrossRef 24. Falagas ME, Kasiakou SK: Toxicity of polymyxins: a systematic review of the evidence from old and recent studies. Crit Care 2006,10(1):R27.PubMedCrossRef 25. Macfarlane

EL, Kwasnicka A, Ochs MM, Hancock RE: PhoP-PhoQ homologues in Pseudomonas aeruginosa regulate expression of the outer-membrane protein OprH and polymyxin B resistance. Mol Microbiol 1999,34(2):305–316.PubMedCrossRef 26. Sohlenkamp C, Galindo-Lagunas KA, Guan Z, Vinuesa P, Robinson S, Thomas-Oates J, Raetz CR, Geiger O: The lipid Calpain lysyl-phosphatidylglycerol is present in membranes of Rhizobium tropici CIAT899 and confers increased resistance to polymyxin B under acidic growth conditions. Mol Plant Microbe Interact 2007,20(11):1421–1430.PubMedCrossRef 27. Tran AX, Lester ME, Stead CM, Raetz CR, Maskell DJ, McGrath SC, Cotter RJ, Trent MS: Resistance to the antimicrobial peptide polymyxin requires myristoylation of Escherichia coli and Salmonella typhimurium lipid A. J Biol Chem 2005,280(31):28186–28194.PubMedCrossRef 28. Stern A, Sorek R: The phage-host arms race: shaping the evolution of microbes. Bioessays 2011,33(1):43–51.PubMedCrossRef 29. Labrie SJ, Samson JE, Moineau S: Bacteriophage resistance mechanisms. Nat Rev Microbiol 2010,8(5):317–327.

25 Bernardet JF, Nakagawa Y: An Introduction to the Family Flavo

25. Bernardet JF, Nakagawa Y: An Introduction to the Family Flavobacteriaceae. In The Prokaryotes: A handbook on the biology of bacteria. 3rd edition. Edited by: Dworkin M, Falkow S, Rosenberg E, Schleifer KH, Stackebrandt E. New York:Springer-Verlag; 2006. 26. Horner-Devine MC, Bohannan BJ: Phylogenetic clustering and overdispersion in bacterial communities. Ecology 2006,87(7 Suppl):S100–108.PubMedCrossRef 27. Kraft NJ, Cornwell WK, Webb CO, Ackerly DD: Trait evolution, community assembly, and the phylogenetic structure of ecological communities. Am Nat 2007,170(2):271–283.PubMedCrossRef

28. Ley RE, Lozupone CA, Hamady M, Knigth R, Gordon JI: Worlds within worlds: evolution of vertebrate gut microbiota. Nat Rev Microbiol 2008,6(10):776–788.PubMedCrossRef 29. Fenchel T: Microbial ecology on land and sea. Phil Trans R Soc Lond B 1994, 343:51–56.CrossRef 30. Buckley DH, Schmidt TM: The Structure of Microbial selleck kinase inhibitor Communities in Soil and the Lasting Impact of Cultivation. Microb Ecol 2001,42(1):11–21.PubMed 31. Sogin ML, Morrison HG, Huber JA, Mark Welch D, Huse SM, Neal PR, Arrieta JM, Herndl GJ: Microbial

diversity in the deep sea and the unexplored “”rare biosphere”". Proc Natl Acad Sci USA 2006,103(32):15–20.CrossRef 32. Fierer N, Breitbart M, Nulton J, Salamon P, Lozupone C, Jones R, Robeson M, Edwards RA, Felts B, Rayhawk S, et al.: Metagenomics and small-subunit BAY 80-6946 solubility dmso rRNA analyses reveal isothipendyl the genetic diversity of bacteria, archaea, fungi, and viruses in soil. Appl Environ Microbiol 2007,73(21):7059–7066.PubMedCrossRef

33. Likens GE: Encyclopedia of Inland Waters. Oxford, New York: Academic Press-Elsevier; 2009. 34. Girvan MS, Bullimore J, Pretty JN, Osborn AM, Ball AS: Soil type is the primary determinant of the composition of the total and active bacterial communities in arable soils. Appl Environ Microbiol 2003,69(3):1800–1809.PubMedCrossRef 35. Hooper SD, Raes J, Foerstner KU, Harrington ED, Dalevi D, Bork P: A molecular study of microbe transfer between distant environments. PLoS ONE 2008,3(7):e2607.PubMedCrossRef 36. Santos SR, Ochman H: Identification and phylogenetic sorting of bacterial lineages with universally conserved genes and proteins. Environ Microbiol 2004,6(7):754–759.PubMedCrossRef 37. Lueders T, Friedrich MW: Evaluation of PCR amplification bias by terminal restriction fragment length polymorphism analysis of small-subunit rRNA and mcrA genes by using defined template mixtures of methanogenic pure cultures and soil DNA extracts. Appl Environ Microbiol 2003,69(1):320–326.PubMedCrossRef 38. Li W, Jaroszewski L, Godzik A: Clustering of highly homologous sequences to reduce the size of large protein databases. Bioinformatics 2001,17(3):282–283.PubMedCrossRef 39. Pignatelli M, Moya A, Tamames J: EnvDB, a database for describing the environmental distribution of prokaryotic taxa. Environ Microbiol Reports 2009, 1:191–197.CrossRef 40.

It is known that the obtained

fluorescence intensity, wit

It is known that the obtained

fluorescence intensity, with a few exceptions, is directly correlated with the growth rate of the target bacteria. The accessibility of the targets is controlled mainly by cell wall properties, which again require to get permeabilized by either the fixative or, in case of gram positive cells, lysozyme [25]. As P. intermedia and streptococci were readily stained at the base of the biofilms, a hindered diffusion of the probes or fixatives through the biofilms does not seem to be the problem. The accessibility of the cells can be sorted out as well, as the signal is very clear in the top layer of the biofilm. Careful examination of the images, by enhancing the contrast settings for the general DNA staining in our samples, Selumetinib mouse revealed structures

at the base of the biofilms that very much resembles the well-stained colonies of F. nucleatum observed in less thick biofilms. Combined with the high abundance detected by IF, it seems that F. nucleatum was in fact present in at the base of the biofilms, however, either in a non-viable- or at least non-active state. For future experiments, it might be worth investigating new methods to increase fluorescent signals, in order to obtain a bright staining throughout the whole biofilm. Catalysed reporter deposition (CARD)-FISH [26], the use of helper oligonucleotides [27], or designing probes targeting the 23S rRNA [28] might Alpelisib mw be solutions. Due to the large size of the horseradish peroxidase used with CARD-FISH, it seems unlikely

that this method would be appropriate, and the use of helper oligonucleotides or probes targeting the 23S rRNA seem more promising to reach stronger signals. One of the major differences to the in vivo situation is that the model biofilms Cediranib (AZD2171) grew without the presence of an epithelial cell layer. Some of the observed differences will be caused by the lack of interactions that occur in vivo. A future project will address this circumstance and aims to incorporate an epithelial cell layer into the model system. The main difficulty in maintaining such a co-culture system is that different growth conditions that are needed to cultivate either epithelial cells or biofilms. While the strict anaerobes in the consortium of the biofilms are very sensitive to oxygen, the epithelial cells do require oxygen for growth. Further, biofilms and epithelial cells do have very different nutritional requirements. In our co-culture experiments performed so far, cells and biofilms were cultured separately and incubated as co-culture after the development of both biofilms and epithelial cells [11]. Current experiments showed, that the biofilm consortium is still able to grow on agar plates after 48 h of co-culture, however, the viability of the bacteria was greatly reduced (data not shown).

32* -0 19 -0 27 –       Testing on doping 0 67* 0 25 0 31* -0 47*

32* -0.19 -0.27 –       Testing on doping 0.67* 0.25 0.31* -0.47* –     Doping in sailing 0.30 0.04 0.08 -0.15 -0.21 –   Penalties for doping 0.13 -0.03 0.07 0.10 0.12 -0.21 – Doping likelihood -0.04 0.16 0.16 -0.04 0.19 -0.05 -0.18 LEGEND: * denotes significant correlation coefficients at p < 0.05. A logistic regression analysis reveals that “crew number” is

the single significant predictor of DS usage among the factors, and this single-variable model is the only significant logistic model built (p < 0.05). The model MAPK inhibitor (Y = -1.042 + 1.841 * X) successfully classified 67% DS users and 32% DS nonusers, indicating that single crews as more inclined to DS usage (OR: 1.4-2.2). Discussion In the following text we will discuss the findings we have judged to be the most important with regard to study aims and topics that have not been previously investigated (i.e., types of DSs consumed, opinions about doping in sailing).

Therefore, the discussion will focus on DS use habits in conjunction with DS-related factors and doping likelihood. Our data revealing that 70% of sailing athletes are DS users support figures of other studies which have reported that the percentage of supplement users ranges from 60% to 93% [22–26, 44, 45]. Therefore, although the previous studies did not assess DS use the way we did (i.e., previous studies examined DS habits on a nominal “yes-no” scale, while we used a ordinal scale; see the tables for more details), our findings that BIBW2992 in vitro 38% of athletes used DSs occasionally and an additional 38% used them regularly are among the highest reported prevalence of DS use among athletes. Given the characteristics of sailing

and the associated training and competition (see Introduction and following text for details), such a relatively high incidence is expected. The reasons why vitamins, minerals and Selleck Tenofovir isotonic (electrolyte) drinks are consumed in most cases, and why most athletes use them regularly, are related to the characteristics of the sport of sailing. Both competitions and training of sailing often last for more than 5 hours. The athletes are regularly far away from the coast, and they wear sailing suits made of neoprene and latex materials that do not allow regular perspiration. It has already been noted that most of the sailing athletes are in a negative fluid balance after racing (mean loss for males: – 2.1%; for females: – 0.9%) [14]. In addition, Croatia is a Mediterranean country with a temperature ranging from 15 to 30 degrees Celsius (from March through the end of September, when most sailing occurs), and it is clear that adequate rehydration is difficult to achieve without isotonic drinks. Because hot-cold and dry-wet changes are common (i.e., weather conditions can change considerably during a single training session) and frequent travel is required (i.e.

campestris pv campestris This led already to the discovery of a

campestris pv. campestris. This led already to the discovery of an unexpected wealth of TonB-dependent receptors [62]. A detailed genomic analysis revealed now the presence of further genes coding for components of TonB systems (Figure 1A). In total, five copies of tonB, two copies of exbB and four copies Selleckchem KU-60019 of exbD were identified within the genome. Downstream of the previously characterized tonB-exbB-exbD1-exbD2 genes, which are located close to the chromosomal origin of replication, a third exbD gene was identified (Figure 1B). While the presence of different TonB-dependent receptors has been attributed

to their distinct binding specificities, where different molecules are bound at the outer cell surface to be either transported inside or to signal their presence to the cell interior, so far it has been assumed that only one set of tonB-exbB-exbD genes is required to build a TonB protein complex Decitabine cell line that interacts with all the different TonB-dependent receptors. Results of previous mutational analyses [64] suggest that the newly identified genes of TonB system core components are not involved in iron uptake. To shed more light on the multiplicity of these genes, we concentrated on analyzing the function of exbD2, which had already been shown to be involved in plant interaction, despite being not important for iron uptake [66]. A genomic comparison showed that this gene was present

and well conserved in all complete Xanthomonas genomes (Additional file 1). Figure 1 Genomic organization of the TonB-related genes in X. campestris pv. campestris B100. (A) A circular genome plot indicates the locations of the TonB-related genes on the chromosome. The core of the TonB system is encoded by the genes tonB, exbB and exbD. In X. campestris pv. campestris B100 multiple isoforms of these genes were identified. Their genomic

locations on the circular chromosome are indicated. So far, this multiplicity was only known for tonB genes in Pseudomonas[68] and for the exbD genes in Flavobacterium psychrophilum, where two paralogous Cytidine deaminase genes were found in tandem in a cluster combined with tonB and exbB[64] close to the chromosomal origin of replication (B). Size and direction of transcription is illustrated by arrows for this gene cluster. Genes that were predicted with convincing evidence are symbolized by shaded arrows, while an open arrow indicates a putative protein-coding sequence (CDS) that was predicted with less confidence. Now a third copy of exbD was found downstream of exbD2, separated from exbD2 only by a hypothetical gene for which nor functionality neither expression could be indicated. Further copies of tonB and the genes exbB-exbD were found at different chromosomal positions. To facilitate discriminating the individual genes, unique numbers were added to their names. The exbD2 gene is involved in pectate lyase activity X. campestris pv.

PubMedCrossRef 5 Baumann M, Krause M, Zips D, Petersen C, Dittma

PubMedCrossRef 5. Baumann M, Krause M, Zips D, Petersen C, Dittmann K, Dörr W, Rodemann

HP: Molecular targeting in radiotherapy of lung cancer. Lung Cancer 2004, 45:S187–197.PubMedCrossRef 6. Määttä AM, Tenhunen A, Pasanen T, Meriläinen O, Pellinen R, Mäkinen K, Alhava E, Wahlfors J: Non-small cell lung cancer as a target disease for herpes simplex type 1 thymidine kinase-ganciclovir gene therapy. Int J Oncol 2004, 24:943–949.PubMed 7. Nemunaitis Dabrafenib cell line J, Vorhies JS, Pappen B, Senzer N: 10-year follow-up of gene-modified adenoviral-based therapy in 146 non-small-cell lung cancer patients. Cancer Gene Ther 2007, 14:762–763.PubMedCrossRef 8. Lee SJ, Zhang Y, Lee SD, Jung C, Li X, Kim HS, Bae KH, Jeng MH, Kao C, Gardner T: Targeting prostate cancer with conditionally replicative adenovirus using PSMA enhancer. Mol Ther 2004, 10:1051–1058.PubMedCrossRef 9. Ulasov IV, Zhu ZB, Tyler MA, PD-0332991 molecular weight Han Y, Rivera AA, Khramtsov A, Curiel DT, Lesniak MS: Survivin-driven and fiber-modified oncolytic adenovirus exhibits potent antitumor

activity in established intracranial glioma. Hum Gene Ther 2007, 18:589–602.PubMedCrossRef 10. Strazisar M, Mlakar V, Glavac D: The expression of COX-2, hTERT, MDM2, LATS2 and S100A2 in different types of non-small cell lung cancer (NSCLC). Cell Mol Biol Lett 2009, 14:442–4569.PubMedCrossRef 11. Ji X, Zhang J, Cheng L, Wei F, Li H, Liu X, Chen X, Li C, Wang Y, Huang Q: Oncolytic adenovirus delivering herpes simplex virus thymidine kinase suicide gene reduces the growth of human retinoblastoma in an in vivo mouse model. Exp Eye Res 2009, 89:193–199.PubMedCrossRef 12.

Huang Q, Zhang X, Wang H, Yan B, Kirkpatrick J, Dewhrist MW, Li CY: A novel conditionally replicative adenovirus vector targeting telomerase-positive tumor cells. Pembrolizumab Clin Cancer Res 2004, 10:1439–1445.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions JFZ carried out most of the experiments and organized data for manuscript. FW, HPW, HML, XFC performed some experiments involving in viral construction, package, Western blot or cell culture. WQ and PKR participated in data organization and manuscript drafting. QH performed project design and manuscript writing. All authors read and approved the final manuscript.”
“Introduction Pancreatic cancer is one of the most virulent malignances, with an overall 5-year survival rate of only 3-5% and a median survival time after diagnosis of less than 6 months[1]. This highly lethal disease is usually diagnosed in an advanced stage, when there are few or no effective therapies[2]. Even among patients undergoing a potentially curative resection, the long-term outcome remains unsatisfactory because of early recurrence and metastatic disease[3]. Despite the immensity of the clinical problem, the biology of pancreatic cancer remains only poorly understood.

Feng P, Li TL, Guan ZX, Franklin RB, Costello LC: Effect of zinc

Feng P, Li TL, Guan ZX, Franklin RB, Costello LC: Effect of zinc on prostatic tumorigenicity in nude mice. Ann N Y Acad Sci 2003, 1010: 316–320.CrossRefPubMed 7. Costello LC, Franklin RB, Liu Y, Kennedy

MC: Zinc causes a shift toward citrate at equilibrium of the m-aconitase reaction of prostate mitochondria. J Inorg Biochem 2000, 78 (2) : 161–165.CrossRefPubMed 8. Franklin RB, Ma J, Zou J, Guan Z, Kukoyi BI, Feng P, Costello LC: Human ZIP1 is a major zinc uptake transporter for the accumulation of zinc in prostate PF-6463922 chemical structure cells. J Inorg Biochem 2003, 96 (2–3) : 435–442.CrossRefPubMed 9. Desouki MM, Geradts J, Milon B, Franklin RB, Costello LC: hZip2 and hZip3 zinc transporters are down regulated in human prostate adenocarcinomatous glands. Mol Cancer 2007, 6: 37.CrossRefPubMed

10. Habib FK, Mason MK, Smith PH, Stitch SR: Cancer of the prostate: early diagnosis by zinc and hormone analysis? Br J Cancer 1979, MAPK Inhibitor Library chemical structure 39 (6) : 700–704.PubMed 11. Costello LC, Franklin RB: Novel role of zinc in the regulation of prostate citrate metabolism and its implications in prostate cancer. Prostate 1998, 35 (4) : 285–296.CrossRefPubMed 12. Costello LC, Franklin RB, Feng P: Mitochondrial function, zinc, and intermediary metabolism relationships in normal prostate and prostate cancer. Mitochondrion 2005, 5 (3) : 143–153.CrossRefPubMed 13. Liang JY, Liu YY, Zou J, Franklin RB, Costello LC, Feng P: Inhibitory effect of zinc on human prostatic carcinoma cell growth. Prostate 1999, 40 (3) : 200–207.CrossRefPubMed Methamphetamine 14. Costello LC, Feng P, Milon B, Tan M, Franklin RB: Role of zinc in the pathogenesis and treatment of prostate cancer: critical issues to resolve. Prostate Cancer Prostatic Dis 2004, 7 (2) : 111–117.CrossRefPubMed 15. Gallus S, Foschi R, Negri E, Talamini R, Franceschi S, Montella M, Ramazzotti V, Tavani A, Dal Maso L, La Vecchia C: Dietary zinc and prostate cancer risk: a case-control study from Italy. Eur Urol 2007, 52 (4) : 1052–1056.CrossRefPubMed 16. Ronowska A, Gul-Hinc S, Bielarczyk H, Pawelczyk T, Szutowicz A: Effects of zinc on SN56 cholinergic neuroblastoma

cells. J Neurochem 2007, 103 (3) : 972–983.CrossRefPubMed 17. Dubi N, Gheber L, Fishman D, Sekler I, Hershfinkel M: Extracellular zinc and zinc-citrate, acting through a putative zinc-sensing receptor, regulate growth and survival of prostate cancer cells. Carcinogenesis 2008, 29 (9) : 1692–1700.CrossRefPubMed 18. Franklin RB, Costello LC: Zinc as an anti-tumor agent in prostate cancer and in other cancers. Arch Biochem Biophys 2007, 463 (2) : 211–217.CrossRefPubMed 19. Sobel RE, Sadar MD: Cell lines used in prostate cancer research: a compendium of old and
s – part 1. J Urol 2005, 173 (2) : 342–359.CrossRefPubMed 20. Yang M, Loda M, Sytkowski AJ: Identification of genes expressed differentially by LNCaP or PC-3 prostate cancer cell lines. Cancer Res 1998, 58 (16) : 3732–3735.PubMed 21.

M Gomila is the recipient of a postdoctoral contract from the Ju

M. Gomila is the recipient of a postdoctoral contract from the Juan de la Cierva Programme of the Spanish Ministerio de Ciencia e Innovación. Electronic VX-770 nmr supplementary material Additional file 1: Table S1. List of isolates analysed, their origin and sample type. External strains for comparison purposes have been included in the study: the type strains C. amycolatum CCUG 35685T and C. striatum ATCC 6940T, as well as two strains of C. striatum with different origins, CCUG 39137 (from a human wound) and CCUG 44705 (tobacco industry). (DOC 114 KB) Additional file 2: Table S2. Primers used for performing the molecular

analysis of the 56 Corynebacterium strains. (DOCX 16 KB) Additional file 3: Table S3. Phenotypic results of RapID CB Plus® tests for the different strains analysed. (DOC 169 KB) Additional file 4: Table S4. Antibiotic susceptibility pattern of each strain analysed. The antibiotics tested for all strains were penicillin (PEN), imipenem (IMI), erythromycin (ERI), rifampicin (RIF), tetracycline (TET), vancomycin (VAN), ciprofloxacin (CIP), gentamicin (GEN), cefotaxime (CEF), and trimethoprim-sulfamethoxazole (TRI). R, resistant; I, intermediate; S, susceptible. (DOC 98 KB) Additional file 5: Figure S1. ERIC-PCR patterns of the

different C. striatum clinical isolates analysed. The number on the top of the lane corresponds to the number of clinical isolate studied; CsT, C. striatum ATCC 6940T. find more M1, Marker λE/H; M2, marker 100 bp. (DOC 262 KB) Additional file 6: Figure S2. SARAMIS cluster analysis of all Corynebacterium strains isolated. (DOC 290 KB) References 1. Bolt F, Cassiday

P, Tondella ML, De Zoysa A, Efstratiou A, Sing A, Zasada A, Bernard K, Guiso N, Badell E, Rosso M-L, Baldwin A, Dowson C: Multilocus sequence typing identifies evidence for recombination and two distinct lineages of Corynebacterium diphtheriae . J Clin Microbiol 2010, 48:4177–4185.PubMedCrossRef 2. De Briel D, Langs JC, Rougeron G, Chabot P, Le Faou A: Multiresistant corynebacteria in bacteriuria: a comparative study of the role of Corynebacterium group D-2 and Corynebacterium jeikeium . J Hosp Infect 1991, 17:35–43.PubMedCrossRef 3. www.selleck.co.jp/products/Vorinostat-saha.html Riegel P, Ruimy R, Christen R, Monteil H: Species identities and antimicrobial susceptibilities of corynebacteria isolated from various clinical resources. Eur J Clin Microbiol Infect Dis 1996, 15:657–662.PubMedCrossRef 4. Riegel P, Ruimy R, de Briel D, Prevost G, Jehl F, Christen R, Monteil H: Genomic diversity and phylogenetic relationships among lipid-requiring diphtheroids from humans and characterization of Corynebacterium macginleyi sp. nov. Int J Syst Bacteriol 1995, 45:128–133.PubMedCrossRef 5. Funke G, Lawson PA, Bernard KA, Collins MD: Most Corynebacterium xerosis strains identified in the routine clinical laboratory correspond to Corynebacterium amycolatum . J Clin Microbiol 1996, 34:1124–1128.PubMed 6.

Acknowledgements This study was supported by Short-term grant (30

Acknowledgements This study was supported by Short-term grant (304/PPSP/6131535) from Universiti Sains Malaysia. We are grateful to Institute for postgraduate studies, Universiti Sains Malaysia for their Fellowship support, and Department of Medical Microbiology and Parasitology, Hospital Universiti Sains Malaysia, Kelantan, Malaysia; for providing the clinical isolates. References 1. Diekema DJ, Pfaller MA, Schmitz

FJ, Smayevsky J, Bell J, Jones RN, Beach M: Survey of infections due to Staphylococcus species: frequency of occurrence and antimicrobial susceptibility of isolates collected in the United States, Canada, Latin America, Europe, and the Western Pacific region for the SENTRY Antimicrobial Surveillance Program, 1997–1999. Clin Infect Dis 2001,32(Suppl

2):S114–132.CrossRefPubMed 2. Tiemersma EW, Bronzwaer SL, Lyytikainen O, Degener JE, Schrijnemakers P, Bruinsma N, BMN 673 in vitro Monen J, Witte W, Grundman H: Methicillin-resistant Staphylococcus aureus in Europe, 1999–2002. Emerg Infect Dis 2004,10(9):1627–1634.PubMed 3. Kluytmans-Vandenbergh MF, Kluytmans JA: Community-acquired methicillin-resistant Staphylococcus aureus: current perspectives. Clin Microbiol Infect 2006,12(Suppl 1):9–15.CrossRefPubMed 4. Vandenesch F, Naimi T, Enright MC, Lina G, Nimmo GR, Heffernan H, Liassine N, Bes M, Greenland T, Reverdy ME, et al.: Community-acquired methicillin-resistant Staphylococcus aureus carrying Panton-Valentine leukocidin genes: worldwide emergence. Emerg Infect Dis 2003,9(8):978–984.PubMed 5. Trametinib von Eiff C, Proctor RA, Peters G: Coagulase-negative staphylococci. Pathogens have major role in nosocomial infections. Postgrad Med 2001,110(4):63–64. 6. von Eiff C, Peters G, Heilmann C: Pathogenesis of infections due to coagulase-negative staphylococci. Lancet Infect Dis 2002,2(11):677–685.CrossRef

7. Patrick CC: Coagulase-negative staphylococci: pathogens with increasing clinical significance. J Pediatr 1990,116(4):497–507.CrossRefPubMed 8. Zhang K, Sparling J, Chow BL, Elsayed S, Hussain Z, Church DL, Gregson DB, Louie T, Conly JM: New quadriplex PCR assay for detection of methicillin and mupirocin resistance and simultaneous discrimination of Staphylococcus aureus from coagulase-negative staphylococci. J Clin Microbiol 2004,42(11):4947–4955.CrossRefPubMed 9. Perez-Roth E, Claverie-Martin F, Villar AMP deaminase J, Mendez-Alvarez S: Multiplex PCR for simultaneous identification of Staphylococcus aureus and detection of methicillin and mupirocin resistance. J Clin Microbiol 2001,39(11):4037–4041.CrossRefPubMed 10. Swenson JM, Tenover FC: Results of disk diffusion testing with cefoxitin correlate with presence of mecA in Staphylococcus spp. J Clin Microbiol 2005,43(8):3818–3823.CrossRefPubMed 11. Chambers HF: Methicillin resistance in staphylococci: molecular and biochemical basis and clinical implications. Clin Microbiol Rev 1997,10(4):781–791.PubMed 12.