First, the insider–outsider idea (standard vs. non-standard employment: Kalleberg 2003) stems from the aforementioned segmentation Cell Cycle inhibitor theories, which divide the labour market into core and peripheral workers (Atkinson 1984; Becker 1993; Hudson 2007). Core workers possess job-specific skills and are therefore hard to replace and thus important to their company. In order to tie these workers to their organisation, employers must offer them high-quality employment, including learning opportunities, job security and a proper salary (Hudson 2007). In contrast, employers do not need to tie the less important and more easily replaceable peripheral workers

to their organisation. Consequently, these workers receive less attractive working conditions and lower earnings than primary

segment workers. Secondly and related to segmentation theories, temporary employment is expected to include more adverse job Selumetinib concentration characteristics than permanent work (De Cuyper et al. 2008; De Witte and Näswall 2003). For example, temporary work has been associated with worse ergonomic conditions, lower earnings, less autonomy, less supervisory tasks, a higher dynamic work load, more repetitive tasks, monotonous work, less training opportunities and exposure to discrimination (Brown and Sessions 2003; De Cuyper et al. 2008; Goudswaard and Andries 2002; Kompier et al. 2009; Layte et al. 2008; Letourneux 1998; AP24534 mw Parent-Thirion et al. 2007); but also often with (indicators

of) lower task demands (De Cuyper and De Witte 2006; ID-8 Goudswaard and Andries 2002; Kompier et al. 2009; Letourneux 1998; Parker et al. 2002). Based on theories on well-designed ‘healthy’ work (Kompier 2003), it can be expected that such characteristics (e.g. combinations of high [but also low] demands and low control, low feedback, low support and high job insecurity) adversely impact workers’ health, well-being and work-related attitudes. Temporary employment and job insecurity A third perspective focuses on the impact of job insecurity on temporary workers’ health and well-being. Job insecurity, which increases with the temporality of the job (De Cuyper et al. 2008), implies uncertainty and thus unpredictability and uncontrollability. This can be linked to central elements of job stress theories (e.g. environmental clarity and lack of control) (De Witte 1999). Moreover, according to Jahoda’s (1982) latent deprivation model, employment is central to many people’s lives as it fulfils important needs as income, social contacts and opportunities for self-improvement. Threat and worry about job loss thus include potential loss of important resources and may therefore have many negative consequences for the worker involved (De Witte 1999).

Eighty-three percent of the mosquitoes ingesting a bloodmeal containing TE/3’2J/B2 were dead by day 21 versus 21% for mock, 11% for TE/3’2J, and 30% for TE/3’2J/GFP exposed mosquitoes (Figure

7A). Daily survival for mosquitoes that ingested TE/3’2J/B2 virus was significantly lower than mock, TE3’2J, or TE/3’2J/GFP-infected mosquitoes (P < 0.0001 for each comparison, Logrank test). Survival of TE/3'2J-infected mosquitoes was significantly different from TE/3'2J/GFP-infected mosquitoes (P = 0.0030). Survival of mosquitoes infected with TE/3'2J and TE/3'2J/GFP was not significantly different from mock-infected mosquitoes (P = 0.0623 this website and 0.2496, respectively). Figure 7 Virus associated mortality of Ae. aegypti HWE mosquitoes following infection by TE/3′J/B2 virus. A) Oral bloodmeal infection Mosquitoes were given an infectious oral bloodmeal containing 1 × 107 PFU of virus and kept at learn more optimal rearing conditions. Mortality was monitored daily for a total of 21 days. n = 200 mosquitoes per group. B) Infection via intrathoracic injection Mosquitoes were injected with virus stock diluted to 1 × 107 PFU/ml and mortality

was monitored daily. Day one mortality was not included. Black diamonds = Mock; Black circles = TE/3’2J; Black squares = TE/3’2J/GFP; Black triangles = TE/3’2J/B2. C) Determination of a mosquito 50 percent lethal dose for TE/3’2J-B2 infection. Groups of mosquitoes were

intrathoracically injected with TE/3’2J/B2 virus diluted ten-fold and mortality was monitored daily. n = 50 mosquitoes/group. White bar indicates 50% mortality. Because some mosquitoes that ingested a bloodmeal may not have become infected, individual mosquitoes were intrathoracically injected with virus to more accurately correlate infection with mortality. Female mosquitoes were injected with approximately 700 PFU of virus or cell culture medium and were monitored daily for mortality. At ten days post-infection, all mosquitoes injected with TE/3’2J/B2 virus were dead, whereas by day 13, at least 70% of mock-, TE/3’2J-, and TE/3’2J/GFP-injected mosquitoes survived (Figure 7B), suggesting that TE/3’2J/B2 virus infection caused the observed mortality in Ae. aegypti mosquitoes. To GW-572016 cost determine oxyclozanide if TE/3’2J/B2-associated mortality was dose-dependent, a 50% lethal dose at seven days post-injection was determined by mosquito intrathoracic injection (Figure 7C). Groups of 50 mosquitoes were injected with TE/3’2J/B2 virus diluted 10-fold in cell culture medium and monitored for mortality. TE/3’2J/B2 infection was extremely lethal, needing less than one PFU per mosquito to cause more than 50% mortality, and was dose-dependent. The median survival time for mosquitoes was five days at the highest dose (107 PFU/ml) and seven days at the lowest dose that caused more than 50% mortality (103 PFU/ml).

13C NMR (DMSO-d 6, δ ppm): 15.27 (CH3), 44.13 (CH2), 50.85 (CH2), 51.35 (2CH2), 56.10 (O–CH3) 61.53 (CH2), arC: [109.73 (d, CH, J C–F = 38.9 Hz), 114.98 (2CH), 118.72 (CH), 121.90 (d, CH, J C–F = 66.3 Hz), 129.12

(C), 131.24 (2CH), 132.53 (C), 138.35 (d, C, J C–F = 21.0 Hz), 147.24 (C), 154.40 (d, C, J C–F = 94.5 Hz), 160.10 (N=CH), 162.24 (C=O). Ethyl 4-(2-fluoro-4-[1H-indol-3-ylmethylene]aminophenyl)piperazine-1-carboxylate (4f) The solution of compound 3 (10 mmol) in absolute ethanol was refluxed with indol-3-carbaldehyde (10 mmol) for 6 h. On cooling the reaction content to room temperature, SP600125 a solid appeared. This crude product was filtered off and recrystallized from acetone. Yield: 82 %. M.p: 184–186 °C. FT-IR (KBr, ν, cm−1): 3484 (NH), 1678 (C=O),

1439 (C=N), 1220 (C–O). Elemental analysis for C22H23FN4O2 calculated (%): C, 66.99; H, 5.88; N, 14.20. Found (%): C, 66.76; H, 6.02; N, 14.01. 1H NMR (DMSO-d 6, δ ppm): 1.20 (brs, 3H, CH3), 3.01 (s, 4H, 2CH2), 3.53 (s, 4H, 2CH2), 4.06 (brs, 2H, CH2), 7.29 (brs, 5H, arH), 8.08 (s, 1H, arH), 8.38 (s, 2H, arH), 9.06 (s, 1H, N=CH), 9.29 (s, 1H, NH). 13C NMR (DMSO-d 6, δ ppm): 15.21 (CH3), 44.18 (CH2), 50.76 (CH2), 51.51 (2CH2), 62.46 (CH2), arC: [108.93 (d, CH, J C–F = 23.4 Hz), 113.47 (d, CH, J C–F = 34.4 Hz), 117.88 (CH), 118.82 (C), 120.71 (CH), 121.51 (CH), 121.84 (CH), 122.84 (CH), 123.76 (d, CH, J C–F = 41.0 Hz), 124.87 (C), 137.91 (d, C, J = 19.8 Hz), 139.24 find more Neratinib mouse (2C) 155.26 (d, C, J C–F = 4.0 Hz)], 153.18 (N=CH), 185.74 (C=O). Ethyl 4-(4-[(benzylamino)carbonyl]amino-2-fluorophenyl)piperazine-1-carboxylate (5) The mixture of compound 3 (10 mmol) and benzylisothiocyanate (10 mmol) in absolute ethanol was refluxed for 10 h. On cooling the reaction mixture to room temperature, a solid formed. This crude product was collected by selleckchem filtration and recrystallized from ethanol.

Yield: 93 %. M.p: 153–155 °C. FT-IR (KBr, ν, cm−1): 3346, 3284 (2NH), 3063 (ar–CH), 1694, 1638 (2C=O), 1236 (C–O). Elemental analysis for C21H25FN4O3 calculated (%): C, 62.99, H, 6.29; N, 13.99. Found (%): C, 62.78; H, 6.07; N, 14.04. 1H NMR (DMSO-d 6, δ ppm): 1.17 (t, 3H, CH3, J = 7.6 Hz), 2.85 (s, 4H, 2CH2), 3.40 (s, 4H, 2CH2 + H2O), 4.02 (q, 2H, CH2, J = 7.0 Hz), 4.26 (d, 2H, CH2, J = 6.0 Hz), 6.61 (brs, 1H, NH), 6.95 (s, 2H, arH), 7.21–7.31 (m, 6H, arH), 8.62 (s, 1H, NH). 13C NMR (DMSO-d 6, δ ppm): 15.27 (CH3), 41.39 (CH2), 43.39 (CH2), 44.15 (CH2), 51.23 (CH2), 60.45 (CH2), 61.52 (CH2), arC: [106.69 (d, CH, J C–F = 25.6 Hz), 114.19 (CH), 120.59 (CH), 127.42 (CH), 127.79 (2CH), 128.99 (2CH), 133.98 (d, C, J C–F = 9.55 Hz), 137.02 (d, C, J C–F = 9.85 Hz), 140.98 (C), 156.65 (d, C, J C–F = 137.5 Hz)], 155.83 (2C=O).

2%, 0.02%, 0.002%, and 0.0002%) to an OD600 of about 0.5, harvested the cells, and analyzed the protein profile of the lysate using SDS-PAGE. We examined the gels for a unique band that exists in the lysate from induced but not uninduced cultures. We obtained optimum induction using LB broth containing 0.002% arabinose (data not shown). LMG194/pAB4 was grown in RM minimal medium supplemented with glucose overnight and subcultured into fresh RM minimal medium. At an OD600 of 0.5, 0.002% arabinose was added to induce expression of PA2783 and incubation continued for 5 h. Initial examination of total proteins

from the whole cell lysate confirmed the overproduction of the protein. As shown in Figure 6B, SHP099 compared with proteins from the uninduced culture, a unique band that corresponds to the predicted 70.5-kDa recombinant PA2783 protein (rPA2783) was detected in the induced culture. We extracted the band and determined the amino acid sequence of an internal peptide. The sequence matched (100%) that of the predicted protein (data PD0325901 order not shown). Using the cold osmotic shock procedure [36, 42], we fractionated the cells into supernatant, periplasmic, cytoplasmic, and outer membrane fractions and separated the proteins by SDS-PAGE. Recombinant PA2783 was localized to the membrane fraction (data not shown). As overproduction of foreign

proteins in E. coli often results in their seclusion in inclusion bodies, which localize with the membrane fraction, we attempted to solubilize rPA2783. Despite trying numerous protocols, we failed to obtain a soluble protein with proteolytic activity. As an alternative, Phosphatidylinositol diacylglycerol-lyase we purified the outer membrane fraction of LMG/pAB4 and examined it for enzymatic activity [41, 42]. We detected the 70.5-kDa

rPA2783 within the outer membrane preparation of the arabinose-induced cells only (Figure 6C). This was confirmed by amino acid sequence analysis of an internal peptide obtained from the eluted protein (data not shown). Similarly, we detected the this website endopeptidase activity within the outer membrane of the arabinose-induced cultures only (Figure 6D). These results suggest that P. aeruginosa PA2783 encodes a membrane-bound 65-kDa protein with endopeptidase activity. We propose the name Mep72 for this protein that belongs to the metalloendopeptidase family M72.001, and mep72 for the gene encoding it. Vfr regulates mep72 expression by specifically binding to its upstream region Vfr is a DNA binding protein that regulates the expression of several genes including lasR, toxR, pvdS, and ptxR by binding to the promoter region of these genes [15, 16, 18, 43]. Thus, Vfr may regulate mep72 expression directly by binding to the upstream region of the PA2782-mep72 operon. Analysis of the upstream region revealed the presence of a potential Vfr-binding sequence located from −58 to −38 bp 5′ of the PA2782 GTG codon and between the −10 and −35 sequences (Figure 7A) [18].

Case report. J Gastrointestin Liver Dis 2006, 15:297–299.PubMed 2. Oida Y, Motojuku M, Morikawa G, Mukai M, Shimizu K, Imaizumi T, Makuuchi H: Laparoscopic-assisted resection of gastrointestinal stromal tumor in small Paclitaxel manufacturer intestine. Hepatogastroenterology 2008, 55:146–149.PubMed 3. Miettinen M, Sobin LH, Lasota J: Gastrointestinal stromal tumors presenting

as omental masses–a clinicopathologic analysis of 95 cases. Am J Surg Pathol 2009, 33:1267–1275.PubMedCrossRef 4. Sornmayura P: Gastrointestinal stromal tumors (GISTs): a pathology view point. J Med Assoc Thai 2009, 92:124–135.PubMed 5. Steigen SE, Bjerkehagen B, Haugland HK, Nordrum IS, Løberg EM, Isaksen V, Eide TJ, Nielsen TO: Diagnostic and prognostic markers BVD-523 solubility dmso for gastrointestinal stromal tumors in Norway. Mod Pathol 2008, 21:46–53.PubMedCrossRef 6. Wilson SL, Wheeler WE: Giant leiomyoma of the small intestine with free PKC inhibitor perforation into the peritoneal cavity. South Med J 1992, 85:667–668.PubMedCrossRef 7. Shah SN: Malignant gastrointestinal stromal tumor of intestine: a case report. Indian J Pathol Microbiol 2007, 50:357–359.PubMed 8. Huang CC, Yang CY, Lai IR, Chen CN, Lee PH, Lin MT: Gastrointestinal stromal tumor of the small intestine: a clinicopathologic study of 70 cases in the postimatinib era. World J Surg 2009, 33:828–834.PubMedCrossRef 9. Kingham TP, DeMatteo RP: Multidisciplinary treatment of gastrointestinal stromal tumors. Surg Clin North Am 2009, 89:217–233.PubMedCrossRef

10. Annaberdyev S, Gibbons J, Hardacre JM: Dramatic response of a gastrointestinal stromal tumor to neoadjuvant imatinib therapy. World J Surg Oncol 2009, 7:30.PubMedCrossRef Competing interests The authors

declare that they have no competing interests. Authors’ contributions UD participated in the conception, design of the study, sequence alignment and drafted the manuscript. SD carried out the immunohistochemical studies. DK participated in the clinical and surgical management. KKD helped to draft the manuscript. All authors read and approved the final manuscript.”
“Introduction Intra-abdominal infections (IAIs) include a wide spectrum of pathological conditions, ranging from uncomplicated appendicitis to fecal Urease peritonitis. In the event of complicated IAI [1], the infection proceeds beyond a singularly affected organ and causes either localized peritonitis (intra-abdominal abscesses) or diffuse peritonitis. Effectively treating patients with complicated intra-abdominal infections involves both source control and antimicrobial therapy [2, 3]. Study design The aim of the CIAO Study was to describe the epidemiological, clinical, microbiological, and surgical treatment profiles of community-acquired and healthcare-associated complicated intra-abdominal infections (IAIs) based on data collected over a 6-month period (January-June 2012) from 68 medical institutions throughout Europe (see Figure 1). Figure 1 Geographic distribution of the CIAO Study.

References 1. Cullen WR: Is Arsenic an Aphrodisiac? The Sociochemistry of an Element. UK: Royal Society of Chemistry Publishing; 2008. 2. Nordstrom DK: Worldwide occurrences

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7 vs 17.9 months, p = 0,02) [45]. So a real standard strategy regarding bevacizumab administration through several lines of treatment of mCRC patients is still not defined. In this sense, to date, there are no phase III trial comparing the bevacizumab rechallenge strategy (bevacizumab readministration after buy 3-deazaneplanocin A a treatment holiday) with bevacizumab-alone maintenance

and with a de-escalated chemotherapy and bevacizumab maintenance. The ongoing AIO study could suggest which is the better strategy applying to bevacizumab administration. Moreover, clinical trials evaluating predictive factors of response to chemotherapy and biologic agents rechallenge or to intermittent therapies are warranted in order to select patients, avoid possible side effect and useless waste of resources. In addition, randomized trials should be performed to understand the clinical impact of rechallenge and intermittent treatment strategies in advanced CRC patients. References 1. Coco C, Zannoni GF, EGFR inhibitor Caredda E, Sioletic S, Boninsegna A, Migaldi M, Rizzo G, Bonetti LR, Genovese G, Stigliano E, Cittadini A,

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putida strain PaW85 [26] which is isogenic to fully sequenced KT2440 [27]. Bacteria were grown on Luria-Bertani (LB)

medium [28] or on minimal medium [29] containing either 0.2% glucose, 0.2% Na-benzoate or 0.2% gluconate. Some experiments were performed with bacteria grown on media with glucose concentrations of 0.4 and 0.8%. To enhance the lysis of the colR mutant, in some experiments 1 mM phenol was added into the solid minimal medium. Congo Red at 0.0005% was added to the medium for visual evaluation of cell lysis. When selection was necessary, the growth medium was supplemented with ampicillin (100 μg/ml), streptomycin (20 μg/ml) or gentamicin (10 μg/ml) for E. coli and with carbenicillin (1500 μg/ml), kanamycin (50 μg/ml), streptomycin (300 μg/ml), tetracycline (20 μg/ml) or gentamicin (10 μg/ml) for P. putida. P. putida was incubated BMS202 cost at 30°C and E. coli at 37°C. Bacteria were electrotransformed following Sharma and Schimke [30]. Table 1 Bacterial strains and plasmids Strain or plasmid Genotype or construction Source or reference E. coli     CC118

λpir Δ(ara-leu) araD ΔlacX74 galE galK phoA20 thi-1 rpsE rpoB argE(Am) recA1 λpir phage lysogen [64] P. putida     PaW85 Wild-type, isogenic to KT2440 [26] PaWcolR PaW85 colR::Kmr [22] PaWoprB1 PaW85 oprB1::Smr [23] PaWcolR-oprB1 PaWcolR oprB1::Smr [23] PaWoprB1-tacB1 PaWoprB1 + oprB1 under the control of tac promoter and lacI q repressor (Smr Gmr) This study PaWcolR-oprB1-tacB1 PaWcolR-oprB1 + oprB1 under the control of tac promoter and lacI q repressor (Smr Gmr) This study PaWcrc PaW85 crc::Tetr This Resminostat study PaWoprB1-tacB1-crc PaWoprB1-tacB1 crc::Tetr (Smr Gmr Tetr) This AG-881 study Plasmids     mTn5SSgusA40 Delivery plasmid for mini Tn5 Sm (Apr Smr) [65] pRK2013 Helper plasmid for conjugal transfer of mTn5SSgusA40 (Kmr) [66] pKTlacZS/C Promoter probe plasmid pKTlacZ containing tnpA promoter of Tn4652 fused with lacZ [35]

p9TTBlacZ Promoter probe plasmid (Cmr Apr) [23] p9TT1015 p9TTBlacZ containing gtsA promoter fused with lacZ (Cmr Apr) This study pBRlacItac Expression vector containing Ptac promoter and lacI q repressor in pBR322 (Apr) [67] pBRlacItac/oprB1 pBRlacItac containing oprB1 as a HindIII-XbaI fragment under the Ptac promoter (Apr) This study pUCNotKm pUC18Not derivative with Kmr gene instead of Apr (Kmr) R. Teras pUCNotKm/tacoprB1 pUC18NotKm containing BamHI fragment with lacI q-Ptac-oprB1 cassette (Kmr) This study pBK-miniTn7-ΩGm pUC19-based delivery plasmid for miniTn7-ΩGm (Apr Gmr) [68] pminiTn7Gm/tacoprB1 pBK-miniTn7-ΩGm containing NotI fragment with lacI q-Ptac-oprB1 cassette (Apr Gmr) This study pCRC10 pKNG101 containing sucB and crc interrupted with tetracycline resistance gene (Smr Tetr) [32] Selection of the suppressors of the lysis of the colR-deficient P. putida For the identification of genes LY333531 concentration implicated in cell lysis, the colR-deficient strain was subjected to mutagenesis using a Tn5 based mini-transposon that contains a streptomycin resistance marker.

Curr Opin Nephrol Hypertens. 2005;14(6):543–9.PubMedCrossRef 5. Wabel P, et al. Importance of whole-body bioimpedance spectroscopy for the management of fluid balance. Blood Purif.

2009;27(1):75–80.PubMedCrossRef 6. Koziolek MJ, et al. Bioimpedance analysis and intradialytic hypotension in intermittent hemodialysis. Clin Nephrol. 2006;66(1):39–50.PubMed 7. Chertow GM, et al. Vintage, nutritional status, and survival in hemodialysis patients. Kidney Int. 2000;57(3):1176–81.PubMedCrossRef 8. Evofosfamide price Chazot C, Wabel P, Chamney P, Moissl U, Wieskotten S, Wizemann V. Importance of normohydration for the long-term survival of haemodialysis patients. Nephrol Dial Transplant. 2012; 27:2404–10. 9. Katzarski KS, et al. Fluid state and blood pressure control in patients treated with long and short haemodialysis. Nephrol Dial Transplant. 1999;14(2):369–75.PubMedCrossRef 10. Cheigh JS, et al. Hypertension Selleckchem OSI 906 is not adequately controlled in hemodialysis patients. Am J Kidney Dis. 1992;19(5):453–9.PubMed 11. Zhu F, et al. Estimation of normal hydration in dialysis patients using

whole body and calf bioimpedance analysis. Physiol Meas. 2011;32(7):887–902.PubMedCrossRef 12. Cheriex EC, et al. Echography of the inferior vena cava is a simple and reliable tool for estimation of ‘dry weight’ in haemodialysis patients. Nephrol Dial Transplant. 1989;4(6):563–8.PubMed”
“Introduction IgA nephropathy (IgAN), a major component of chronic glomerulonephritis, causes end-stage renal disease in up to 50 % of affected patients [1]. Although proteinuria AMN-107 datasheet has been considered one of the most important predictors of renal outcome [2–6], few studies have clarified what degree of proteinuria at an early phase after initial treatment predicts renal survival. Donadio et al. [7] showed a lower amount of proteinuria at 1 year after the introduction of treatment to be associated with a better renal survival. However, they did not define the proteinuria level predicting a favorable renal outcome. Among the many clinical trials demonstrating the efficacy of steroid therapy

for IgAN [8–10], a randomized controlled trial by Pozzi Selleck Decitabine et al. [11, 12] clearly demonstrated that 6 months of steroid therapy significantly reduced the risk of a 100 % increase in serum creatinine from the baseline compared to conventional therapy during a 5- or 10-year follow-up. They demonstrated that the steroid therapy induced the lowest level of proteinuria at 1 year of follow-up. We herein aimed to define the target level of proteinuria at 1 year after initiating steroid therapy to establish a prognostic threshold for a favorable renal survival of IgAN patients. Subjects and methods Patients and study design We collected the medical records from 169 patients with IgAN who received 6 months of steroid therapy between 2004 and 2010 in four affiliated hospitals of Jikei University School of Medicine, employing a historical cohort design.

These high-coverage contigs indicate that this strain harbors one or more multi-copy plasmids. Table 1 Genome statistics for strains sequenced in this study Strain Cluster # 1 Contig # Contig N50 FRAX597 chemical structure scaffold # Scaffold N50 Genome size ORFs PavBP631 43 M2 38 bp PE 1,613 6,420 297 79,231 6,628,588 4816   38 M 38 bp MP             PavVe013 59 M 82 bp PE 389 30,917 66 297,710 6,165,792 5136   43 M 40 bp MP             PavVe037 35 M 82 bp PE 220 61,365 61 263,756 6,050,967 5078   45 M 40 bp MP             1. PE: paired-end (ca. 200 bp insert). MP: mate-pair

(3–5 kb insert). STAT inhibitor 2. Millions of reads. Figure 1 Coverage plots for contigs generated for each Pav strain. Read coverage vs. contig length, plotted on log scales. Box and whisker boxes indicate median, quartiles, and range for each strain, with values more than 2.5 times the interquartile range above or below the median plotted as points. Data were plotted using the car package in R [18, 19]. When the contigs were scaffolded using 38–45

million mate-pairs, the N50 improved to 79 kb for Pav BP631 and to 264–298 kb for the other strains (Table 1). The total genome sizes were 6.6 megabases (Mb) for Pav BP631 and 6.1 to 6.2 Mb for the other two strains, consistent with the presence of extra-chromosomal plasmids in Pav BP631. Pav Ve013 Dibutyryl-cAMP supplier and Pav Ve037 are largely colinear with the phylogroup 2 reference strain Psy B728a, while Pav BP631 displays substantially more rearrangement relative to Pto DC3000,

the reference strain for phylogroup 1 (Figure 2). There is a 95 kb scaffold in Pav BP631 that is made up of high-coverage contigs and is colinear with plasmid A from Pto DC3000 over about half of its length. Figure 2 Whole-genome alignments of Pav scaffolds to the most closely related reference sequences. A. PavBP631 contigs aligned to Pto DC3000 reference sequence. Inset: Alignment of scaffold 88 to plasmid A from Pto DC3000 (this was done as a separate analysis). B. Pav Ve013 and Pav Ve037 contigs aligned to Psy B728a reference sequence. Each colored block represents a local colinearity block that can be aligned PLEKHM2 between strains without any rearrangements. White spaces within blocks indicate regions of low sequence conservation. Vertical red lines indicate scaffold breaks for Pav sequences or boundaries between chromosomes/plasmids in the case of the Pto DC3000 reference sequence. Alignments were generated using progressiveMauve [20]. Ortholog analysis The RAST annotation sever predicted between 4816 and 5136 open reading frames (ORFs) per strain (Table 1) which were grouped into between 4710 and 4951 ortholog groups by orthoMCL (Figure 3a). There were 3967 ortholog families shared among the three Pav strains, all of which were also found in other strains. Of these, 1856 were found in all 29 P. syringae strains, comprising the operational P. syringae core genome.