campestris gum operon Appl Environ Microbiol 1999, 65:278–282 Pu

campestris gum operon. Appl Environ Microbiol 1999, 65:278–282.PubMed 81. Kovach ME, Elzer PH, Hill DS, Robertson GT, Farris MA, Roop RM, Peterson KM: Four new derivatives of the broad-host-range cloning vector pBBR1MCS, carrying LDE225 solubility dmso different

antibiotic-resistance cassettes. Gene 1995, 166:175–176.PubMedCrossRef Authors’ contributions MJ performed genetic analyses of the rosR mutants, carried out experiments concerning their phenotype characterization and plant experiments, and drafted the manuscript. JK conducted EPS and LPS analyses, TP performed microscope images and parameter analyses of biofilm. AS discussed the results and elaborated the final version of manuscript. All authors read and approved the final version of the manuscript.”
“Background Barasertib concentration Rhodocista centenaria, first described as Rhodospirillum centenum [1] is a thermotolerant phototrophic purple bacterium of the α-proteobacteria group isolated from

hot springs in Wyoming 1985. The slightly spiroid or vibrioid shaped cells are motile by means of a single long flagellum, their intracellular photosynthetic membranes are lamellar and their in vivo absorption spectra show features almost indistinguishable from those of Rhodospirillum rubrum [2]. However, 16S rRNA analysis elucidated considerable differences between the species, hence Rhodocista was separated into a new genus [3], now consisting of three

species [4, 5]. R. centenaria is closely related to the plant-associated genus Azospirillum [6]. As virtually all phototrophic organisms, R. centenaria exhibits a sensory response to light originally described as “”Schreckbewegung”" [7]. Engelmann and also Manten [8] found that R. rubrum cells accumulated in the most intense area of light gradients between wavelengths 800 and 900 nm. R. centenaria shows a particularly unique form of macroscopic phototactic behaviour, first described in 1994 by Gest and coworkers [9]. On solid media, the phototactic colonies Rolziracetam move towards longwave light and away from light with wavelengths less than 650 nm [10]. R. centenaria develops lateral flagella in viscous media or on solidified surfaces. These flagella consist of a distinct flagellin whose expression is controlled by specific mot and fli genes [11]. For R. centenaria, a close relationship between chemotaxis and the phototactic response has been found [12]. As seen with many other photosynthetic bacteria, R. centenaria has multiple chemotaxis operons with distinct functions [13–15]. The chemotaxis gene cluster has been well characterized and most of the genes are similar to those of other Gram negative bacteria like Escherichia coli. In brief, the histidine kinase CheA is linked to the chemotactic receptors (MCPs) by the CheW protein [16].

While Hoffman and colleagues [9] reported that a 2% level of dehy

While Hoffman and colleagues [9] reported that a 2% level of dehydration can decrease shooting percentages by 8% (results not statistically different), others have shown that a similar level of hypohydration can cause significant performance decrements in shooting accuracy [18] and that it can progressively decline with greater levels check details of fluid loss [8]. The results of this present investigation are consistent with these latter studies. The mechanism that may have contributed to a decrease in shooting percentage may be fatigue relating to the

hydration stress. However, considering that power outputs remained consistent between experimental trials and no difference in player load was observed between DHY and AG1, it is more likely that other factors contributed to the differences observed in shooting percentages between DHY and AG trials. A recent investigation has indicated that moderate levels of dehydration (4% body mass loss) can result in significant alterations in afferent neural processing [19]. This suggests that the ability to maintain fine motor control in performance, such as shooting a basketball, may become significantly impaired during a hypohydration stress. Additional research has also indicated that dehydration can increase lateral ventricle enlargement in the brain causing a higher level of neuronal activity

in the brain required to achieve the same performance level [20, 21]. This may explain in part the significant performance GDC-0199 clinical trial decrements observed in reaction time (both visual and in lower body) during DHY. When subjects were permitted to

rehydrate (regardless of W or AG) lower body reaction times were significantly improved. However, the ingestion of AG1 significantly enhanced basketball Celecoxib shooting performance to a greater extent (p < 0.05) than W only. In addition, AG1 improved visual reaction time during the competition, whereas no difference was observed between W and DHY. Although not statistically different, similar trends were seen between AG2 and shooting accuracy and visual reaction time (p = 0.09 and p = 0.08, respectively). The ability to enhance visual reaction time with AG1 does appear to have important implication for athletic performance. Mann and colleagues [22] have suggested the ability to process visual information provides critical information for enhancing the anticipatory response during athletic performance. Achieving excellence in basketball has been suggested to be related in part to an ability of the athlete to have a “”highly-tuned”" anticipatory ability that allows them to predict other’s actions ahead of their realization [23]. Rehydrating with AG during the rest breaks of the game may have contributed to a more efficient fluid and electrolyte uptake, minimizing the deleterious effects of dehydration.

Measurements were repeated at least four

times for each l

Measurements were repeated at least four

times for each leptospiral strain to achieve reproducible results. All Daporinad samples, including the non-pathogenic and intermediate strains, were correctly assigned at the species level. All reference strains of L. interrogans and the closely related strain of L. kirschneri serovar Grippotyphosa matched with the correct genomospecies at first place. In addition, 16 leptospiral field isolates (Table 2) were identified with the MALDI-TOF MS (Table 3). Field isolates belonging to one single L. borgpetersenii serovar and the seven L. interrogans strains matched with the correct genomospecies. Seven field isolates of the genomospecies L. kirschneri were also grouped within the correct species. One L. kirschneri isolate (LGL strain number 518) matched with the same score value of 2.18 in two different measurements with L. kirschneri and L. interrogans (marked with a in Table 3). 16S rRNA sequencing of all field isolates confirmed the MALDI-TOF results with a clear species identification

SRT1720 price of LGL strain 518 as L. kirschneri. Applying MALDI Biotyper TM identification it was not possible to differentiate the leptospiral strains below the species level. Table 3 Identification results of the 16 leptospiral field isolates by MALDI-TOF MS and 16S rRNA gene sequencing field isolate (LGL strain number) MALDI-TOF MS gene sequencing (16S rRNA) first match score value L. interrogans Canicola (87) L. interrogans Hebdomadis 2.62 L. interrogans L. interrogans Bratislava (538) L. interrogans Bratislava 2.37 L. interrogans L. interrogans Bratislava (540) L. interrogans Autumnalis 2.46 L. interrogans L. interrogans Australis (537) L. interrogans Hardjo 2.54 L. interrogans L. interrogans Icterohaemorrhagiae (113) L. interrogans Icterohaemorrhagiae

2.67 L. interrogans L. interrogans Icterohaemorrhagiae (471) L. interrogans Icterohaemorrhagiae 2.54 L. interrogans L. interrogans Icterohaemorrhagiae (535) L. interrogans Icterohaemorrhagiae 5.57 L. interrogans L. kirschneri Grippotyphosa a (518) L. kirschneri Grippotyphosa 2.18 L. kirschneri L. kirschneri Grippotyphosa a (518) L. interrogans Canicola 2.18 L. kirschneri L. kirschneri Grippotyphosa (517) L. kirschneri Grippotyphosa Vitamin B12 2.38 L. kirschneri L. kirschneri Grippotyphosa (533) L. kirschneri Grippotyphosa 2.09 L. kirschneri L. kirschneri Grippotyphosa (541) L. kirschneri Grippotyphosa 2.13 L. kirschneri L. kirschneri Grippotyphosa (112) L. kirschneri Grippotyphosa 2.54 L. kirschneri L. kirschneri Grippotyphosa (539) L. kirschneri Grippotyphosa 2.17 L. kirschneri L. kirschneri Pomona (532) L. kirschneri Grippotyphosa 2.28 L. kirschneri L. kirschneri Pomona (511) L. kirschneri Grippotyphosa 2.34 L. kirschneri L. borgpetersenii Saxkoebing (489) L. borgpetersenii Saxkoebing 2.49 L.

In the first case, the MLVA type remains identical In the case o

In the first case, the MLVA type remains identical. In the case of a reinfection, the MLVA type is likely to be different. Our MLVA scheme was used to study the course

of infection in seven patients. In six of these patients, sequential isolates belonged to a consistent MLVA Dabrafenib type in each case studied, suggesting in a persistent or relapse infection. Interestingly, the two clinical isolates Mh-2377 and Mh-2477 harboured the unique MLVA type 33 whereas previous PFGE analysis showed different migrations patterns when evaluated according to the interpretation guidelines of Tenover et al., and the total genome sizes of the two strains, deduced from the addition of the generated fragment lengths, were nearly identical [24]. These respiratory isolates were collected six months apart from a man with a chronic obstructive pulmonary disease who was treated several times with ciprofloxacin. As the M. hominis isolates were both resistant to fluoroquinolones, it would seem logical that the two

isolates were identical, as shown by MLVA typing. The observed differences in PFGE patterns may be due to restriction sites located in variable regions or to recombination. Indeed, results from previous analysis check details indicated that a high levels of intragenic and intergenic recombination occurred in M. hominis, and these recombination levels are presumably important for the adaptation potential of this species [11, 14]. Analysis of our results

suggests a new infection in a female patient, as the two sequential cervical isolates were of different MLVA types. A previous study investigated cervical isolates of M. hominis obtained before and after treatment by RAPD. In two of nine cases studied, the profile of amplification did not change, whereas in the rest of cases, RAPD patterns were different, suggesting that the patients were reinfected [10]. Nintedanib (BIBF 1120) We also performed molecular investigations of M. hominis isolates from two mother-neonate pairs. In each case studied, an identical MLVA type was found, confirming mother-to-child transmission. Our results are in agreement with those of Jensen et al. who reported that M. hominis isolates obtained from the cervices of pregnant women and from the ears or pharynges of their new-born infants yielded the same genomic profile by PFGE [7]. Similar results were obtained by Grattard et al., who showed that strains isolated within a mother-neonate pair exhibited an identical pattern by AP-PCR [25]. At the population level, MLVA typing assesses the genetic diversity of M. hominis strains. In this study, we described 40 MLVA types, revealing a genetic heterogeneity among this species. This finding is in agreement with the data obtained by studies using other molecular typing methods. Using RFLP, Busch et al. found a high heterogeneity among 20 isolates obtained from colonised women and women with various urogenital infections [8].

LCB arrangement was plotted in circular view as in [10] in CGView

LCB arrangement was plotted in circular view as in [10] in CGView [23]. As in [10], subset datasets were produced by randomly sampling nucleotides from concatenated LCB alignments for each chromosome

using BioPerl scripts. These subset datasets were 10,000 bp, 20,000 bp, 30,000 bp 40,000 bp, 50,000 bp, 100,000 bp, 200,000 bp, 300,000 bp, 400,000 bp, 500,000 bp, and 1,000,000 bp (only up to 300,000 bp for the small chromosome because the concatenated alignment was only just over 400,000 bp). These datasets were each also analyzed in TNT and Garli or RaxML (depending on length). 44-taxon dataset For this dataset, genomes were downloaded as detailed above or assembled de novo as detailed below. Because genome sequences that were present as multiple contigs were included, arrangement of these contigs was ignored and contigs were simply concatenated. Breakpoint analyses could not be Small molecule library high throughput completed on this dataset because the arrangement of gene and multi-gene fragments was not necessarily true to life after Imatinib contig concatenation. A different strategy was implemented in

Mauve in order to be able to include all 44 taxa. Concatenated contigs were grouped by two to three close relatives as determined in [9] as well the concatenated LCBs of closely related species from the Mauve results from the 19-taxon dataset. This was done because the de novo analysis in Mauve of all 44 concatenated genomes was computationally prohibitive. This strategy works because the Mauve results of interest are those LCBs common to all taxa. Since the 44-taxon dataset contains all the taxa of the 19-taxon dataset plus new taxa, one would expect the percent

of base-pairs to be homologized by Mauve to decrease as taxa are added. By running Mauve analyses that start with the LCBs generated by the 19-taxon dataset Mauve analysis, one expects to capture the same homologies that one would capture if all 44-taxa were analyzed in Mauve from scratch. The LCBs that resulted from the smaller runs for all 44-taxa were extracted. Since Mauve provides results that collinearize the LCBs, a final, simpler Mauve run was performed with all 44 taxa together. The above was done separately for the large and small chromosomes. Phylogenetic analyses in TNT and Garli were conducted on the resulting alignments for both the large and small chromosomes.V. brasiliensis was removed from Molecular motor small chromosome dataset because it caused Mauve to crash repeatedly. New genome sequences Salinivibrio costicola strain ATCC 33508, Vibrio gazogenes strain ATCC 43941, and Aliivibrio logei strain ATCC 35077 were ordered from the ATCC (American Type Culture Collection). They were grown on Difco Marine Agar. S. costicola was grown at 26 degrees C, V. gazogenes was grown at 26 degrees C and A. logei was grown at 18 degrees C. DNA was extracted using the Qiagen DNeasy DNA extraction kit and DNA concentration was measured using a Qubit 2.0 Fluorometer from Invitrogen.

tumefaciens chvI/G, Tcr Kmr [4] pKNG101 sacB + mobRK2 ori R6K, Sm

tumefaciens chvI/G, Tcr Kmr [4] pKNG101 sacB + mobRK2 ori R6K, Smr [51] pKD001 pTC190::pKNG101, Tcr This study Primer Sequence ( 5′-3′ )   LB5 atgcagaccatcgcgctt This study LB6 acatcgtgatccaacaagg This study LB61 gtaaaacgacggccagt This study Cloning of chvI for His•Tag-ChvI expression and purification S. meliloti Rm1021 chvI was PCR amplified using primers LB5 and LB6 (Table 3). The 800-bp PCR fragment was gel-purified and then cloned in pGEM®-T Easy vector. Plasmid pLB010 with the insert in the correct orientation for expression was verified by DNA sequence analysis. NotI chvI-containing fragment was then cut out of pLB010 and ligated to NotI-digested pET-30a,

generating a N-terminal His•Tag fusion pJF011. E. coli BL21(DE3)pLysS clones carrying the pJF011 plasmid were confirmed for His•Tag-ChvI production by western

blot using a His•Tag monoclonal antibody Selleck Fulvestrant from mouse (Novagen) and Alexa Fluor 488 goat anti-mouse IgG (H + L) (Invitrogen, Molecular Probes) as the secondary antibody. His•Tag-ChvI purification using nickel-affinity chromatography was performed in the laboratory of Professor Bi-Cheng Wang at University of Georgia (USA). Electrophoretic mobility shift assay using genomic DNA (GD.EMSA) To prepare samples, S. meliloti Rm1021 genomic DNA was digested to completion by overnight incubation with Bsp143I restriction enzyme (Sau3AI isoschizomer, Fermentas Life Sciences, Canada) and the reaction was then heat-inactivated. DMXAA ic50 Resminostat Purified His•Tag-ChvI protein was mixed with digested DNA in a solution of 9% glycerol, 3 mM acetyl phosphate, 0.8 mM Tris-acetate, 0.25 mM magnesium acetate, 1.65 mM potassium acetate, 2.5 μg ml-1 bovine serum albumin (BSA). For negative controls, ChvI protein was not added to samples. Incubations were carried out for 30 minutes at room temperature and loaded directly on gel without dye. To perform the electrophoresis, a sodium boric acid buffer (SB buffer) was made following the specifications of Brody and Kern [52]. 5% nondenaturing polyacrylamide gels

(14 cm × 16 cm) were cast using a Hoefer SE 600 gel electrophoresis unit and following the standard procedure for resolution of small DNA fragments [53] but using SB buffer instead of TBE buffer. Gels were run in 1X SB buffer between 25 to 40 mA for 3–6 hours. Gels were then stained for 1 hour in a 3X GelRed™ staining solution containing 0.1 M NaCl and following manufacturer’s recommendation for post gel staining (Biotium, USA, CA) prior to visualization on a UV transilluminator. Shifted DNA bands in the highest part of the gel were then excised and stored in 2-ml plastic tubes at −20°C. To recover DNA fragments from polyacrylamide gel, the method from Ausubel et al. (1992) [53] was used. The elution buffer used contained 0.

The voltage across the hybrid circuit was increased from 5 to 14,

The voltage across the hybrid circuit was increased from 5 to 14, 16, and finally 18 V. The light emitted varied in color, ranging from green, yellow, orange, and finally to red.

This was the result of electron transfer in the DNA hybrid molecule with increasing voltage [77]. Other important DNA-based nanoscale devices that have recently been developed include highly conductive nanowires [78], quantum dots with carbon nanotubules [79], and even radically advanced devices which detect single-nucleotide polymorphism and conduct nucleotide sequence mutation analysis [80]. With added progress in this field, it could be possible to use DNA-based electronics for both DNA-based diagnostics and sophisticated nanoscale electrical devices. DNA optoelectronics With recent advances BMS-777607 chemical structure in the field of biological electronics, there is great interest in developing problem-solving novel nanodevices for detection [81, 82], diagnosis [83], and discovery [84]. These devices may be used for

a variety of purposes. Nano-optoelectronics is the field of applying light to achieve or modify various biological functions at the DNA or protein level. Kulkarni and colleagues recently attempted to do just that by demonstrating the ability of photons to induce conductivity in two-dimensional DNA nanostructures with and without the help of graphene (Figure 11) [85]. They proved that the conductivity of DNA lattices lined with streptavidin protein could be further improved Selleckchem JQ1 by the addition of graphene sheet [85]. This optical pulse response of the DNA to graphene is very encouraging and may be exploited in the construction of biological sensors for immunological assays, DNA forensics, and toxin detection. Figure 11 Schematic of the biotinylated heptaminol DNA lattice structure layered onto a graphene sheet

connecting two gold electrodes, with streptavidin binding to the biotin protein [85]. In another study, Kim and colleagues attempted to construct a biosensor based on graphene and polydimethylsiloxane (PDMS) [86]. An evanescent field shift occurred in the presence of chemical or biological structures which were very sensitive in the refractive index. They were able to monitor the target analyte by attaching the selective receptor molecules to the surface of the PDMS optical waveguide resulting in a shift of the optical intensity distribution. Hence, they monitored the electrical characteristics of graphene in the dark and under PDMS wave-guided illumination. Changes in the resulting photocurrent through the graphene film showed that the fabricated graphene-coupled PDMS optical waveguide sensor was sensitive to visible light for biomolecular detection [86]. This finding can be used for the development of optical biosensor for the detection of various biological molecules in future biological assays. Correction of sequence mismatch The rise of DNA-based nanobiotechnology has led to an increase in demand for synthetic DNA.

Proc Natl Acad Sci USA 2001, 98: 13790–13795 CrossRefPubMed 31 T

Proc Natl Acad Sci USA 2001, 98: 13790–13795.CrossRefPubMed 31. Tibshirani R, Hastie T, Narasimhan B, Chu G: Class Prediction by Nearest Shrunken Centroids, with Applications to DNA Microarrays. Stat Sci 2003, 18: 104–117.CrossRef 32. Wang S, Zhu J: Improved centroids SB525334 cell line estimation for the nearest shrunken centroid classifier. Bioinformatics 2007, 23: 972–979.CrossRefPubMed 33. Cortes C, Vapnik V: Support-vector network. Mach Learn 1995, 20: 1–25. 34. Pirooznia M, Yang JY, Yang MQ, Deng Y: A comparative study of different machine learning methods on microarray gene expression data. BMC Genomics 2008, 9 (Suppl 1) : S13.CrossRefPubMed 35. Pirooznia

M, Deng Y: SVM Classifier-a comprehensive java interface for support vector machine classification of microarray data. BMC Bioinformatics 2006, 7 (Suppl 4) : S25.CrossRefPubMed 36. Campioni M, Ambrogi V, Pompeo E, Citro G, Castelli M, Spugnini

EP, Gatti A, Cardelli P, Lorenzon L, Baldi A, Mineo TC: Identification of genes down-regulated during lung cancer progression: a cDNA array study. J Exp Clin Cancer Res 2008, 27: 38.CrossRefPubMed 37. Al-Shahrour F, Díaz-Uriarte Vemurafenib supplier R, Dopazo J: Discovering molecular functions significantly related to phenotypes by combining gene expression data and biological information. Bioinformatics 2005, 21: 2988–2993.CrossRefPubMed 38. Huang D, Pan W: Incorporating biological knowledge into distance-based clustering analysis of microarray gene expression data. Bioinformatics 2006, 22: 1259–1268.CrossRefPubMed 39. Golub TR, Slonim DK, Tamayo P, Huard C, Gaasenbeek M, Mesirov JP, Coller H, Loh ML, Downing JR, Caligiuri MA, Bloomfield CD, Landers ES: Molecular classification of cancer: class discovery and class prediction

by gene expression monitoring. Science 1999, 286: 531–537.CrossRefPubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions PG conceived the study and drafted the manuscript. MRIP PG, DH, MH and BZ retrieved and reviewed the literature. PG and BZ attracted funding. All authors contributed to the writing of the final version of this paper.”
“Background Cancer is a genetic disease resulting from gradual accumulation of changes in the DNA that activate proto-oncogenes and inactivate tumour-suppressor genes leading to genetic instability which is further aggravated by DNA damage and errors made by the DNA maintenance and repair machinery [1]. Many cancers are heritable due to inheritance of specific variant allele/polymorphic variants [2–5]. Recent advancements in cancer research have provided increasing evidences that cancer acts through the interplay of high-risk variants in a set of low- and medium-penetrance genes rather than a few high penetrance genes [6, 7].

Rheumatology (Oxford) 44:iv33–iv35CrossRef 96 Kanis JA, McCloske

Rheumatology (Oxford) 44:iv33–iv35CrossRef 96. Kanis JA, McCloskey EV, Johansson H, Strom O, Borgstrom F, Oden A (2008) Case finding for the management of Proteasome inhibitor osteoporosis with FRAX—assessment and intervention thresholds for the UK. Osteoporos Int 19:1395–1408CrossRefPubMed 97. Kanis JA, Borgstrom

F, Zethraeus N, Johnell O, Oden A, Jonsson B (2005) Intervention thresholds for osteoporosis in the UK. Bone 36:22–32CrossRefPubMed”
“Erratum to: Osteoporos Int DOI 10.1007/s00198-010-1326-y Owing to an error by the authors, an inappropriate publication was cited as reference 71. The correct reference is: 71. Verdrengh M, Bokarewa M, Ohlsson C, Stolina M, Tarkowski A (2010) RANKL-targeted therapy inhibits bone resorption in experimental Staphylococcus aureus-induced Selleckchem p38 MAPK inhibitor arthritis. Bone 46(3):752–758″
“Introduction Osteoporosis is a disease associated with decreased bone mass and bone strength and leads to increased fracture risk. Due to its high prevalence worldwide [1], osteoporosis has become a major public health concern. The epidemiology of hip fractures has been intensively studied over the past few decades because of its expensive treatment cost and adverse outcomes. Although hip fractures are less prevalent in Asians [2], vertebral fractures are as frequent in Asian as in Caucasian women [3–5]. Indeed, vertebral

fractures Dichloromethane dehalogenase are the most common complication of osteoporosis, accounting for nearly 50% of all osteoporotic

fractures [6]. Besides physical deformity, vertebral fracture is associated with reduced mobility and quality of life [7, 8], and increased mortality [9, 10]. Previous studies have shown that vertebral fracture often occurs earlier than hip fractures in disease progression and that vertebral fracture is associated with an increased risk of both future vertebral and nonvertebral fractures [11–14]. Therefore, characterizing the prevalence of vertebral deformities and associated clinical risk factors would help physicians and policymakers to determine the appropriate amount of emphasis to be placed on diagnosis and prevention of osteoporosis. Although vertebral fractures are important as an independent risk factor for further fracture, they are not easy to diagnose as it has been estimated that only 30% of vertebral fractures come to medical attention [15]. Additionally, prevalence of vertebral fractures tends to vary across ethnic groups and geographic regions [6]. For example, studies in Europe have shown that the prevalence of vertebral fractures was higher in the UK [15] and Denmark [16] and lower in Finland [17]. On the contrary, in instances in which comparable methods and definitions have been used in studies, the prevalence of morphometric or radiographic vertebral fractures has been more similar across regions [5, 18, 19].

J Antimicrob Chemother 1990,26(2):247–259 PubMedCrossRef 3 Hanco

J Antimicrob Chemother 1990,26(2):247–259.PubMedCrossRef 3. Hancock RE: The bacterial outer membrane as a drug barrier. Trends Microbiol 1997,5(1):37–42.PubMedCrossRef 4. Wang Y, Ha U, Zeng L, Jin S: Regulation of membrane permeability by a two-component regulatory system in Pseudomonas aeruginosa . Antimicrob Agents Chemother 2003,47(1):95–101.PubMedCrossRef 5. Oliver A, Canton Birinapant chemical structure R, Campo P, Baquero F, Blazquez J: High frequency of hypermutable Pseudomonas aeruginosa in cystic fibrosis lung infection. Science 2000,288(5469):1251–1254.PubMedCrossRef 6. Costerton JW, Stewart PS, Greenberg EP: Bacterial biofilms: a common cause of persistent infections. Science 1999,284(5418):1318–1322.PubMedCrossRef 7. Fisher

JF, Meroueh SO, Mobashery S: Bacterial resistance to beta-lactam antibiotics: compelling opportunism, compelling opportunity. Chem Rev 2005,105(2):395–424.PubMedCrossRef 8. Lodge JM, Minchin SD, Piddock LJ, Busby JW: Cloning, sequencing and analysis of the structural gene and regulatory region of the Pseudomonas aeruginosa chromosomal

ampC beta-lactamase. Biochem J 1990,272(3):627–631.PubMed 9. Selleckchem BMN-673 Kong KF, Jayawardena SR, Del Puerto A, Wiehlmann L, Laabs U, Tummler B, Mathee K: Characterization of poxB , a chromosomal-encoded Pseudomonas aeruginosa oxacillinase. Gene 2005, 358:82–92.PubMedCrossRef 10. Kong KF, Jayawardena SR, Indulkar SD, Del Puerto A, Koh CL, Høiby N, Mathee K: Pseudomonas aeruginosa AmpR is a global transcriptional factor that regulates expression of AmpC and PoxB β-lactamases, proteases, quorum sensing, and other virulence factors. Antimicrob Agents Chemother 2005,49(11):4567–4575.PubMedCrossRef 11. Jacobs C: Pharmacia Biotech & Science prize. 1997 grand prize winner. Life in the balance: cell walls and antibiotic resistance. Science 1997,578(5344):1731–1732.CrossRef 12. Jacobs C, Frere JM, Normark S: Cytosolic intermediates for cell wall biosynthesis and degradation control inducible beta-lactam resistance in Gram-negative

bacteria. DNA Synthesis inhibitor Cell 1997,88(6):823–832.PubMedCrossRef 13. Jacobs C, Huang LJ, Bartowsky E, Normark S, Park JT: Bacterial cell wall recycling provides cytosolic muropeptides as effectors for beta-lactamase induction. EMBO J 1994,13(19):4684–4694.PubMed 14. Korfmann G, Sanders CC: ampG is essential for high-level expression of AmpC beta-lactamase in Enterobacter cloacae . Antimicrob Agents Chemother 1989,33(11):1946–1951.PubMed 15. Chahboune A, Decaffmeyer M, Brasseur R, Joris B: Membrane topology of the Escherichia coli AmpG permease required for recycling of cell wall anhydromuropeptides and AmpC beta-lactamase induction. Antimicrob Agents Chemother 2005,49(3):1145–1149.PubMedCrossRef 16. Cheng Q, Park JT: Substrate specificity of the AmpG permease required for recycling of cell wall anhydro-muropeptides. J Bacteriol 2002,184(23):6434–6436.PubMedCrossRef 17. Dietz H, Pfeifle D, Wiedemann B: The signal molecule for beta-lactamase induction in Enterobacter cloacae is the anhydromuramyl-pentapeptide.