This stemmed from a combined effort of the Trauma Group and Preventive Medicine Department to raise funds to develop a specific registry studying the mechanisms of RTCs and use of safety devices with detailed information of RTCs on a sound database. The RTC registry led to a better understanding of road traffic collisions and their impact on the country [9, 10]. Secondly, the equally alarming high rate of work-related injuries led to collaboration with a Preventive Medicine team who helped with refining of data elements of the trauma registry to include data important for research in trauma prevention [11–13]. This also led to an understanding that ongoing involvement of

researchers with specific interest in community medicine is an essential component of trauma prevention. The trauma selleck inhibitor registry helped to promote trauma awareness and management in the minds of clinicians. As a result of collaboration MG 132 with Preventive Medicine specialists,

the registry was modified to contain important information on injury prevention. In addition, several unnecessary variables related to management were removed. Furthermore, and as a result of extensive user needs analysis, the registry interface was also redesigned to be easier to navigate and more user-friendly in general. For data entry, the tabbed design was used to categorize related items of interest and this has proven tuclazepam to be the quickest and easiest data entry method. The relational database design was rechecked and modified accordingly. Discussion We were able to establish a Trauma Registry at Al-Ain Hospital. This was possible with support a research grant from the UAE University. Trauma registries need to be an integral part of health informatics data collection. Such Registries are valuable tools for identifying considerations that require implementation of quality improvement policy and are essential for much needed progress in the health care system [14]. Our

early analysis has shown that road traffic collisions caused 34.2% of the injuries while work-related injuries were responsible for 26.2% which has helped us to focus on these two important areas in our community. Several detailed analyses have emerged later from the registry related to RTC or occupational injuries. A study based on the RTC registry data regarding the driver’s pre-incident behavior and mechanism of injury defined the seatbelt compliance to be very low (25%). Front impact and rollover collisions were the most common mechanisms of injury, and only 16% of the drivers were distracted prior to having the crash [10]. Another RTC analysis on factors affecting mortality in RTC found that head injury is the major factor affecting mortality, followed by injury severity and hypotension [9].

The CsrA pathway and the mechanism of regulation have Tucidinostat supplier been studied extensively in the γ-proteobacteria and further studies of the

role of CsrA in various pathogens have extended its importance to the expression of virulence factors and the regulation of pathogenesis [22–26]. Despite these advances, very little is known about the mechanism of action of CsrA in the ε-proteobacteria. Examination of the C. jejuni genome [7, 27–29] suggests that this bacterium lacks several genes in the CsrA pathway, including apparent orthologs of the small RNA molecules csrB and csrC[30], the barA/uvrY two-component signal transduction system, and csrD which is responsible for csrB and csrC turnover [31]. One report describing the role of CsrA in the gastric pathogen Helicobacter pylori indicated that CsrA was required for motility, survival under oxidative stress, and host colonization, and plays a role in the expression of several virulence and oxidative stress related proteins [23]. It was also suggested that the H. pylori ortholog was unable to function when exogenously expressed in E. coli because it failed to complement the glycogen accumulation phenotype of an E. coli csrA mutant [23]. Considering these observations in H. pylori, the phenotypes of a C. jejuni csrA mutant, and the lack of knowledge concerning the functions of CsrA within the ε-proteobacteria, we examined the ability

of C. jejuni CsrA to complement the phenotypes of an E. coli csrA mutant with the hope of gaining further insight into the molecular mechanism of C. jejuni CsrA. Phylogenetic comparison revealed that C. jejuni CsrA exhibits selleck inhibitor variability in amino acids that constitute the published RNA binding domains, as well as in other residues that are important for CsrA-mediated regulation in E. coli. Surprisingly, although the C. jejuni ortholog was unable to complement the glycogen accumulation phenotype of E. coli, successful rescue of several other E. coli mutant phenotypes was achieved, demonstrating both similarities and

differences in the C. jejuni and E. coli Csr systems. Methods Bacterial strains and routine growth conditions All bacterial strains used in this Mephenoxalone study are listed in Table 1. Overnight cultures of E. coli strains were routinely carried out at 37°C on LB agar or in LB broth with shaking. One Shot® TOP10 chemically competent E. coli (Invitrogen, Carlsbad, CA) was used as a cloning host for TA-cloning procedures. E. coli MG1655 and TRMG1655 (csrA::Kan) were obtained from T. Romeo (University of Florida). When appropriate, E. coli strains were selected in LB medium using ampicillin (100 μg/ml) or kanamycin (50 μg/ml). Cloned genes were induced by the addition of 0.002% L-arabinose to the growth media. C. jejuni strain 81–176 was grown on MH agar at 42°C under microaerophilic contitions (10% CO2, 10% O2, and 80% N2) supplemented with 5% sheep’s blood (Remel, Lenexa, KS).

JAMA 2003, 290:2149–2158.PubMedCrossRef 14. Pirker R, Pereira JR, Szczesna A, von Pawel J, Krzakowski M, Ramlau R, Vynnychenko I, Park K, Yu CT, Ganul V, Roh JK, Bajetta E, YM155 cost O’Byrne K, de Marinis F, Eberhardt W, Goddemeier T, Emig M, Gatzemeier U, FLEX Study Team: Cetuximab plus chemotherapy in patients with advanced non-small-cell lung cancer (FLEX): an open-label randomised phase III trial. Lancet 2009, 373:1525–1531.PubMedCrossRef 15. Carlsson J, Forssell Aronsson E, Hietala SO, Stigbrand T, Tennvall J: Tumour therapy with radionuclides: assessment of progress and problems.

Radiother Oncol 2003, 66:107–117.PubMedCrossRef 16. Fontanini G, De Laurentiis M, Vignati S: Evaluation of epidermal growth factor-related growth factors and receptors and of neoangiogenesis in completely resected stage I-IIIA non-small-cell lung cancer: amphiregulin and microvessel count are independent prognostic indicators of survival. Clin Cancer Res 1998, 4:241–249.PubMed

17. Rusch V, Baselga J, Cordon-Cardo C, Orazem J, Zaman M, Hoda S, McIntosh J, Kurie J, Dmitrovsky E: Differential expression of the epidermal EVP4593 nmr growth factor receptor and its ligands in primary nonsmall cell lung cancers and adjacent benign lung. Cancer Res 1993, 53:2379–2385.PubMed 18. Milas I, Komaki R, Hachiya T, Bubb R, Ro J, Langford L, Sawaya R, Putnam J, Allen P, Cox J, McDonnell T, Brock W, Hong W, Roth J, Milas L: Epidermal Growth Factor Receptor, Cyclooxygenase-2, and BAX Expression Florfenicol in the Primary Non-Small Cell Lung Cancer

and Brain Metastases. Clinical Cancer Research 2003, 9:1070–1076.PubMed 19. Travis WD, Brambilla E, Muller-Hermelink HK, Harris CC: Pathology and Genetics of Tumors of the Lung, Pleura, Thymus and Heart. Lyon: IARC Press; 2004. 20. Sobin LH, Wittekind C: TNM Classification of Malignant Tumors. New York: Wiley-Liss; 2002. 21. Wei Q, Sheng L, Shui Y, Hu Q, Nordgren H, Carlsson J: EGFR, HER2, and HER3 expression in laryngeal primary tumors and corresponding metastases. Ann Surg Oncol 2008, 15:1193–1201.PubMedCrossRef 22. Shen L, Shui Y, Wang X, Sheng L, Yang Z, Xue D, Wei Q: EGFR and HER2 expression in primary cervical cancers and corresponding lymph node metastases: Implications for targeted radiotherapy. BMC Cancer 2008, 8:232.PubMedCrossRef 23. Wei Q, Chen L, Sheng L, Nordgen H, Wester K, Carlsson J: EGFR, HER2 and HER3 expression in esophageal primary tumours and corresponding metastases. Int J Oncol 2007, 31:493–499.PubMed 24.

Conservation plots and consensus sequences are shown at the bottom. Protein alignments were performed and represented using CLC-Bio sequence viewer [32]. Reference organisms: L. rhamnosus GG, L. casei ATCC 334, L. paracasei subsp. paracasei ATCC 25302, L. zeae (accession no. WP_010489923.1), L. buchneri CD034, L. plantarum WCFS1, L. helveticus R0052, L. delbrueckii subsp. lactis

DSM 20072, L. delbrueckii subsp. bulgaricus ATCC 11842, L. curvatus CRL 705, L. brevis ATCC 367, L. pentosus KCA1, L. coryniformis (ulaE, accession no. WP_010012151.1; xfp, WP_010012483.1). (ZIP 2 MB) References 1. Beresford TP, Fitzsimons NA, Brennan NL, Talazoparib in vivo Cogan T: Recent advances in cheese microbiology. Int Dairy J 2001, 11:259–274.CrossRef 2. Sgarbi E, Lazzi C, Iacopino check details L, Bottesini C, Lambertini F, Sforza S, Gatti M: Microbial origin of non proteolytic aminoacyl derivatives in long ripened cheeses. Food Microbiol 2013, 35:116–120.PubMedCrossRef 3. Cogan TM, Beresford TP, Steele J, Broadbent J, Shah NP, Ustunol Z: Invited review: advances in starter cultures and cultured foods. J Dairy Sci 2007, 90:4005–4021.PubMedCrossRef 4. Fox PF, McSweeney PLH:

Cheese: an overview. In Cheese: Chemistry, Physics and Microbiology. General Aspects. 3rd edition. Edited by: Fox PF, McSweeney PLH, Cogan TM, Guinee TP. London, UK: Elsevier; 2004:1–18.CrossRef 5. Settanni L, Moschetti G: Non-starter lactic acid bacteria used to improve cheese quality

and provide health benefits. Food Microbiol 2010, 27:691–697.PubMedCrossRef 6. de Dea Lindner J, Bernini V, de Lorentiis A, Pecorari A, Neviani E, Gatti M: Parmigiano Reggiano cheese: evolution of cultivable and total Chlormezanone lactic microflora and peptidase activities during manufacture and ripening. Dairy Sci Technol 2008, 88:511–523.CrossRef 7. Santarelli M, Bottari B, Lazzi C, Neviani E, Gatti M: Survey on the community and dynamics of lactic acid bacteria in Grana Padano cheese. Syst Appl Microbiol 2013, 36:593–600.PubMedCrossRef 8. Gatti M, de Dea Lindner J, de Lorentiis A, Bottari B, Santarelli M, Bernini V, Neviani E: Dynamics of whole and lysed bacterial cells during Parmigiano-Reggiano cheese production and ripening. Appl Environ Microbiol 2008, 74:6161–6167.PubMedCentralPubMedCrossRef 9. Neviani E, Bottari B, Lazzi C, Gatti M: New developments in the study of the microbiota of raw-milk, long-ripened cheeses by molecular methods: the case of Grana Padano and Parmigiano Reggiano. Front Microbiol 2013, 4:1–14.CrossRef 10. Neviani E, de Dea Lindner E, Bernini V, Gatti M: Recovery and differentiation of long ripened cheese microflora through a new cheese-based cultural medium. Food Microbiol 2009, 26:240–245.PubMedCrossRef 11. Bove CG, de Dea Lindner CG, Lazzi C, Gatti M, Neviani E: Evaluation of genetic polymorphism among Lactobacillus rhamnosus non-starter Parmigiano Reggiano cheese strains.

In F. pedrosoi, melanin confers structural integrity as a cell wall constituent and immune protection through antigen masking. F. pedrosoi melanin also has anti-phagocytic properties, and is overexpressed during infection [5]. Inside melanosomes, melanin plays a role in the intracellular storage and regulation of calcium and iron ions [11]. The anti-phagocytic properties of F. pedrosoi’s melanin were described after interaction with murine macrophages with or without

activation with lipopolysaccharide (LPS) and interferon-gamma (IFN-γ) [12, 13]. Temsirolimus In addition, conidia from F. pedrosoi cultures treated with 16 μg/ml of tricyclazole (TC), a DHN-melanin pathway inhibitor, showed a higher susceptibility to activated murine macrophages when compared to untreated fungus [12]. Macrophages are found in granulomas of chromoblastomycosis lesions and may participate in the antigen presentation and innate immune response against F. pedrosoi [14]. To contain the growth of pathogens, activated macrophages release oxygen and nitrogen reactive intermediates. NO released by the activated

macrophages are fungicidal against Histoplasma capsulatum [15], Cryptococcus neoformans and Sporothrix Apoptosis inhibitor schenkii [16, 17]. The anti-oxidative properties of fungal melanins [18, 19], their paramagnetism as revealed by ESR, and the melanin-iron (a known magnetic or paramagnetic metal depending on its oxidation state) association in F. pedrosoi raised the hypothesis; the trapping of free radicals by fungal melanin during interactions between macrophages and fungi is a mechanism of oxidative buffering. The aims of the present work were the following: (I) to characterise the melanin of F. pedrosoi by ESR; (II) to investigate the NO production of activated macrophages against F. pedrosoi conidia; (III) to detect i-NOS activity during macrophage interactions with fungi; (IV) to evaluate fungal growth after treatment

with NO and H2O2; and (V) STK38 to compare these approaches in conidia with or without TC treatment. Results ESR spectrometry and microwave power saturation of melanins The ESR spectra of the control-melanin and TC-melanin present strikingly similar signals with a peak of 3480 gauss (with respect to line width, line shape, and g value of 2.0023) (Fig. 1A). Progressive microwave power saturation shows that the paramagnetic centres in these melanins do not saturate under the experimental conditions. In addition, these experiments reveal that the control-melanin has a higher spin relaxation rate than the TC-melanin (Fig. 1B). These observations suggest that the control-melanin is a more compact polymer than TC-melanin. Figure 1 Electron spin resonance of melanins of F. pedrosoi. The ESR spectra (A) of control-melanin or TC-melanin present a single anisotropic line at g = 2.0023.

J Bone Miner Res 19:1059–1066PubMedCrossRef 8. Kanis JA, McCloskey EV, Johansson H, Cooper C, Rizzoli R, Reginster JY (2013) European guidance for the diagnosis and management of osteoporosis in postmenopausal women. Osteoporos Int 24:23–57PubMedCentralPubMedCrossRef 9. Orwoll E, Teglbjaerg CS, Langdahl BL, Chapurlat R, Czerwinski E, Kendler DL, Reginster HDAC inhibitor JY, Kivitz A, Lewiecki EM, Miller PD, Bolognese MA, McClung MR, Bone HG, Ljunggren O, Abrahamsen B, Gruntmanis U, Yang YC, Wagman RB, Siddhanti S, Grauer A, Hall JW, Boonen S (2012) A randomized, placebo-controlled

study of the effects of denosumab for the treatment of men with low bone mineral density. J Clin Endocrinol Metab 97:3161–3169PubMedCrossRef 10. Parthan A, Kruse

MM, Agodoa I, Tao CY, Silverman selleck screening library SL, Orwoll E (2013) Is denosumab cost-effective compared to oral bisphosphonates for the treatment of male osteoporosis (mop) in Sweden? Value Health 16:A223CrossRef 11. Rizzoli R, Burlet N, Cahall D, Delmas PD, Eriksen EF, Felsenberg D, Grbic J, Jontell M, Landesberg R, Laslop A, Wollenhaupt M, Papapoulos S, Sezer O, Sprafka M, Reginster JY (2008) Osteonecrosis of the jaw and bisphosphonate treatment for osteoporosis. Bone 42:841–847PubMedCrossRef 12. Ruggiera SL, Mehrotra B, Rosenberg TJ, Engroff SL (2004) Osteonecrosis of the jaws associated with the use of bisphosphonates: a review of 63 cases. J Oral Maxillofac Surg 62:527–534CrossRef 13. Subramanian G, Cohen HV, Quek SY (2011) A model for the pathogenesis of bisphosphonate-associated osteonecrosis of

the jaw and teriparatide’s potential role in its resolution. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 112:744–753PubMedCrossRef 14. Aghaloo TL, Felsenfeld AL, Tetradis S (2010) Osteonecrosis of the jaw in a patient on Denosumab. Resminostat J Oral Maxillofac Surg 68:959–963PubMedCentralPubMedCrossRef 15. Raylor KH, Middlefell LS, Mizen KD (2010) Osteonecrosis of the jaws induced by anti-RANK ligand therapy. Br J Oral Maxillofac Surg 48:221–223CrossRef 16. Diz P, Lopez-Cedrun JL, Arenaz J, Scully C (2012) Denosumab-related osteonecrosis of the jaw. J Am Dent Assoc 143:981–984PubMedCrossRef 17. Pichardo SE, Kuypers SC, Van Merkesteyn JP (2013) Denosumab osteonecrosis of the mandible: a new entity? A case report. J Craniomaxillofac Surg 41:e65–e69PubMedCrossRef 18. Qi WX, Tang LN, He AN, Yao Y (2013) Shen Z Risk of osteonecrosis of the jaw in cancer patients receiving denosumab: a meta-analysis of seven randomized controlled trials. Int J Clin Oncol (in press) 19.

However, there are other factors that intervene with the effect of calcium on bone quality and hip fractures, in particular vitamin D, which plays a crucial role in calcium absorption [51]. It has been shown that there was not much difference between calcium supplementation alone (almost the DRI) or calcium Selleck PRI-724 combined with vitamin D on reducing osteoporotic fractures [50, 53]. This is in line with

the conditions of use as determined by the European Food Safety Authority that indicate 1,200 mg of calcium per day, or 1,200 mg of calcium and 20 μg of vitamin D per day for women aged 50 years and older (http://​www.​efsa.​europa.​eu/​). However, if dietary calcium is a threshold nutrient, then that threshold for optimal calcium absorption may be achieved at a lower calcium intake when vitamin D levels are adequate [51]. In this respect, it should be mentioned that the occurrence of dairy mTOR cancer food fortification with vitamin D might have been of some influence on the results of our model. However, accurate information on the consumption of such products was not readily available. Besides such a fortification, dairy products themselves contain additional nutrients that are beneficial to bone health, e.g. high protein content

[54]. Unfortunately, the literature does not provide valid risk-estimates for osteoporotic fractures given the additional elements in dairy foods. In this regard, the results of this study might give an underestimation about the effect size of dairy calcium. Moreover, other factors mediate the effect of

calcium on bone health, and concomitantly on osteoporotic fractures. These factors include exposure to sunlight, level of exercise, and genetic predisposition [55]. Considering the foregoing, it may be expected that there are differences in the relative risk of hip fractures between the populations of different countries. MycoClean Mycoplasma Removal Kit Our analysis concentrated on the effects of dairy calcium on hip fractures. Two observations need to be made about this. First, we did not include osteoporotic fractures other than hip fractures, due to the unavailability of sufficient data. As a result, our model may have underestimated the beneficial effects of dairy calcium. On the other hand, a side effect of consuming more dairy products might be the intake of more saturated fat, considered a risk factor for vascular diseases. Although dairy products make a contribution to total fat consumption, this contribution is likely to be relatively small. Moreover, a review by Elwood et al. [5] showed that there was no convincing evidence of any increased risk of ischaemic heart disease or ischaemic stroke in subjects who have the highest milk consumption. For all countries in this study, the loss in quality of life following a hip fracture was based on data from a Swedish study [38] because country-specific data were not available.

Some gene variants are not included in

the microarray design as they were not identified in the first seven S. aureus whole 4EGI-1 manufacturer genome sequencing projects [25]. Figure 1 Microarray analysis. Microarrays show gene variants are conserved across unrelated lineages. Genes are listed in order by name and by their annotated gene number prefixed with the strain that was used as the template for the PCR probe on the microarray (R, MRSA252; N, N315; 8, 8325; M, MW2; U, Mu50). A black box indicates the gene or gene variant is present in that lineage. ‘*’ indicates the genome of a strain from this lineage has been sequenced. ‘+’ indicates ORFs from this lineage are included on the 7 strain microarray. C indicates community associated MRSA were included, and H indicates hospital associated MRSA were included. Strains from the following hosts were included: h, human, b, bovine, e, equine, p, pig. ‘v’ denotes a PCR product designed to a specific variant region. ‘u’ indicates variation in gene distribution for that lineage. Variation in host ligands of S. aureus proteins The SRT2104 location of and proportion of amino acid variable sites for human ligands are shown in Table 4. Variation is present in each of the ligands analysed. Notably, the proportion of variable residues is high (>0.0 15) in

the β-chain (FGB) and γ-chain (FGG) of fibrinogen, and in elastin (ELN). Lower levels of variation exist in the α-chain (FGA) of fibrinogen (0.0 10), promthrombin (PT) (0.006), vitronectin (VN) (0.006), fibronectin (FN-1) (0.006) and the von Willebrand factor (vWF) (0.008). This analysis shows that the amino acid sequence in S. aureus ligands varies in humans, and some of this variation is in domains interacting with ClfA, ClfB and FnBPA. This could provide a selective pressure for the evolution and adaptation of S. aureus adhesins in human populations. Table 4 Variation in human proteins Ligand Gene NCBIGeneID

Variable amino acid sites Proportion of variable sites Characterised interacting S. aureus protein(s) Elastin eln 2006 40, 71,165, 298, 311, 398, 422, 463, 494, 503, 544, 581, 651, 711 0.019 EbpS, FnBPA Fibrinogen/Fibrin fga 2243 6, 331 b , 392, 446, 456, 507, 729 0.010 ClfB, FnBPB, Ebh, IsdA,   fgb 2244 2, 86,100,170,192, 265, 398, 478 0.016 Efb,   fgg 2266 Methane monooxygenase 12,14, 25, 54, 77, 87, 89,113,114,132,140,177,191, 219, 410ac 0.033 ClfA, FnBPA Fibronectin fn-1 2335 15, 251 c , 352, 759, 817, 984,1044,1103,1558, 2195, 2212, 2261, 2275, 2281 0.006 FnBPA, FnBPB, Prothrombin f2 2147 165, 200, 272, 386 0.006 VWbp Vitronectin vtn 7448 122, 268, 400 0.006 Unknown protein [118] von Willebrand factor vwf 7450 137, 318, 325d, 471, 484, 653, 740, 817, 852, 885,1380,1381,1435,1472,1565,1569, 2126, 2178, 2281, 2342, 2561, 2705 0.008 VWbp Spa a residues located in ClfA binding region [61]. b residues located in ClfB binding region [64]. c residues located in FnBPA binding region [91, 92].

PLoS Biol 2007, 5: 2177–2189.PubMedCrossRef 73. Lupp C, Robertson ML, Wickham ME, Sekirov

I, Champion OL, Gaynor EC, Finlay BB: Host-mediated inflammation disrupts the intestinal click here microbiota and promotes the overgrowth of Enterobacteriaceae . Cell Host Microbe 2007, 2: 119–129.PubMedCrossRef 74. Artis D: Epithelial-cell recognition of commensal bacteria and maintenance of immune homeostasis in the gut. Nat Rev Immunol 2008, 8: 411–420.PubMedCrossRef 75. Kaser A, Zeissig S, Blumberg RS: Inflammatory bowel disease. Annu Rev Immunol 2010, 28: 573–621.PubMedCrossRef 76. Baron JH, Connell AM, Lennard-Jones JE: Variation between observers in describing mucosal appearances in proctocolitis. BMJ 1964, 5375: 89–92.CrossRef 77. DeSantis TZ, Hugenholtz P, Larsen N, Rojas M, Brodie EL, Keller K, Huber T, Dalevi D, Hu P, Andersen GL: Greengenes, a chimera-checked 16S rRNA gene database and workbench compatible with ARB. Appl Environ Microbiol 2006, 72: 5069–5072.PubMedCrossRef 78. Ludwig W, Strunk O, Westram R, Richter L, Meier H, Yadhukumar, Buchner A, Lai

T, Steppi S, Jobb G, Förster W, Brettske I, Gerber S, Ginhart AW, Gross O, Grumann S, Hermann S, Jost R, König A, Liss T, Lüssmann R, May M, VE-822 cost Nonhoff B, Reichel B, Strehlow R, Stamatakis A, Stuckmann N, Vilbig A, Lenke M, Ludwig T, et al.: ARB: a software environment for sequence data. Nucleic Acids Res 2004, 32: 1363–1371.PubMedCrossRef 79. Ashelford KE, Chuzhanova NA, Fry JC, Jones AJ, Weightman AJ: New screening software shows that most recent large 16S rRNA gene Gefitinib clone libraries contain chimeras. Appl Environ Microbiol 2006, 72: 5734–5741.PubMedCrossRef 80. Ashelford KE, Chuzhanova NA,

Fry JC, Jones AJ, Weightman AJ: At least 1 in 20 sequence records currently held in public repositories is estimated to contain substantial anomalies. Appl Environ Microbiol 2005, 71: 7724–7736.PubMedCrossRef 81. Schloss PD, Handelsman J: Introducing DOTUR, a computer program for defining operational taxonomic units and estimating species richness. Appl Environ Microbiol 2005, 71: 1501–1506.PubMedCrossRef 82. Johnson M, Zaretskaya I, Raytselis Y, Merezhuk Y, McGinnis S, Madden TL: NCBI BLAST: a better web interface. Nucleic Acids Res 2008, (36 Web server) : W5-W9. 83. Letunic I, Bork P: Interactive Tree Of Life (iTOL): an online tool for phylogenetic tree display and annotation. Bioinformatics 2007, 23: 127–128.PubMedCrossRef 84. Nadkarni MA, Martin FE, Jacques NA, Hunter N: Determination of bacterial load by real-time PCR using a broad-range (universal) probe and primers set. Microbiology 2002, 148: 257–266.PubMed Authors’ contributions AWW carried out the clone library construction, performed the sequence analysis and drafted the manuscript. CC co-ordinated the sequencing.

Proc Natl Acad this website Sci USA 2005,102(46):16819–16824.CrossRefPubMed 12. Boles BR, Thoendel M, Singh PK: Self-generated diversity produces

“”insurance effects”" in biofilm communities. Proc Natl Acad Sci USA 2004,101(47):16630–16635.CrossRefPubMed 13. Rice SA, Koh KS, Queck SY, Labbate M, Lam KW, Kjelleberg S: Biofilm formation and sloughing in Serratia marcescens are controlled by quorum sensing and nutrient cues. J Bacteriol 2005,187(10):3477–3485.CrossRefPubMed 14. Coetzee JN, Deklerk HC: Effect Of Temperature On Flagellation, Motility And Swarming Of Proteus. Nature 1964, 202:211–212.CrossRefPubMed 15. Kearns DB, Losick R: Swarming motility in undomesticated Bacillus subtilis. Mol Microbiol 2003,49(3):581–590.CrossRefPubMed 16. Givskov M, Ostling J, Eberl L, Lindum PW, Christensen AB, Christiansen G, Molin S, Kjelleberg S: Two separate regulatory systems participate in control of swarming motility of Serratia liquefaciens MG1. J Bacteriol 1998,180(3):742–745.PubMed 17. Overhage J, Lewenza S, Marr AK, selleck kinase inhibitor Hancock RE: Identification of genes involved in swarming motility using a Pseudomonas aeruginosa PAO1 mini-Tn5-lux mutant library. J Bacteriol 2007,189(5):2164–2169.CrossRefPubMed 18. Kaiser D: Bacterial swarming: a re-examination of cell-movement patterns. Curr Biol 2007,17(14):561–570.CrossRef 19. Wang Q, Frye JG, McClelland M, Harshey RM: Gene expression patterns during swarming

in Salmonella typhimurium: genes specific to surface growth and putative new motility and pathogeniCity genes. Mol Microbiol 2004,52(1):169–187.CrossRefPubMed 20. Connelly MB, Young GM, Sloma A: Extracellular proteolytic activity plays a central role in swarming motility in Bacillus subtilis. J Bacteriol 2004,186(13):4159–4167.CrossRefPubMed 21. Kim W, Surette MG: Prevalence of surface swarming behavior in Salmonella. J Bacteriol 2005,187(18):6580–6583.CrossRefPubMed

crotamiton 22. Kohler T, Curty LK, Barja F, van Delden C, Pechere JC: Swarming of Pseudomonas aeruginosa is dependent on cell-to-cell signaling and requires flagella and pili. J Bacteriol 2000,182(21):5990–5996.CrossRefPubMed 23. Shrout JD, Chopp DL, Just CL, Hentzer M, Givskov M, Parsek MR: The impact of quorum sensing and swarming motility on Pseudomonas aeruginosa biofilm formation is nutritionally conditional. Mol Microbiol 2006,62(5):1264–1277.CrossRefPubMed 24. Steil L, Hoffmann T, Budde I, Volker U, Bremer E: Genome-wide transcriptional profiling analysis of adaptation of Bacillus subtilis to high salinity. J Bacteriol 2003,185(21):6358–6370.CrossRefPubMed 25. Wang Q, Suzuki A, Mariconda S, Porwollik S, Harshey RM: Sensing wetness: a new role for the bacterial flagellum. Embo J 2005,24(11):2034–2042.CrossRefPubMed 26. Hall-Stoodley L, Costerton JW, Stoodley P: Bacterial biofilms: from the natural environment to infectious diseases.