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44. Duffy MF, Noormohammadi AH, Baseggio N, Browning GF, Markham PF: Immunological and biochemical characterization of membrane proteins. In Methods in Molecular Biology. Edited by: Miles R, Nicholas R. Humana Press, Totowa, New Jersey; 1998:279–298. vol. 104 45. Ladefoged SA, Christiansen G: Mycoplasma hominis expresses two variants of a cell-surface protein, one a lipoprotein, and one not. Microbiology 1998,144(Pt 3):761–770.PubMedCrossRef 46. Inukai M, Takeuchi M, Shimizu K, Arai M: Mechanism of action of globomycin. J Antibiot (Tokyo) 1978,31(11):1203–1205.CrossRef 47. Inukai M, Ghrayeb J, Nakamura K, Inouye M: Apolipoprotein, an intermediate in Repotrectinib the processing CBL0137 of the major lipoprotein of the Escherichia coli outer membrane. J Biol Chem 1984,259(2):757–760.PubMed 48. O’Brien-Simpson NM, Pathirana RD, Paolini RA, Chen YY, Veith PD, Tam V, Ally N, Pike RN, Reynolds EC: An immune response directed to proteinase and adhesin functional epitopes protects against Porphyromonas gingivalis-induced periodontal bone loss. J Immunol 2005,175(6):3980–3989.PubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions I.S.P designed the study, performed the experiments and

data analysis, and drafted the manuscript, AK helped with the experiments, CC contributed the ltuf siglac construct, P.D.V and M.D.G performed mass Carnitine dehydrogenase spectrometry identification and analysis and provided suggestions about the manuscript. G.F.B and P.F.M contributed to the study design, analysis, drafting and review of the manuscript. All authors have read and approved the manuscript.”
“Background Enterococci are normal constituents of the gastro-intestinal flora of humans and other animals [1–3]. Although they only occasionally cause infections in healthy individuals,

they are the third most commonly isolated gram positive organisms from hospital-associated (HA) infections in the United States and are increasingly reported in other countries [4, 5]. Enterococcal infections are often difficult to treat due to the number of antibiotics to which these organisms are resistant. Some antibiotic resistances are intrinsic, such as resistances to cephalosporins, while other antibiotic resistances are acquired through mutations or horizontal gene transfer, most notably the van systems that encode vancomycin Navitoclax molecular weight resistance [6–12]. Several recent studies also confirmed that enterococci can transfer their resistance to even more virulent organisms, such as Staphylococcus aureus[13]. Enterococcus faecalis is the most common enterococcal species recovered from infections. However, in the last decade, infections with Enterococcus faecium have been on the rise in the United States, Europe, and South America [2–5, 14]. In the US, isolates of E. faecium now account for ca.

2A, the proliferation of SKOV-3

was inhibited significantly on 3rd d while there was no difference after 7d’s incubation. As for the proliferation of ES-2 cells, there has no significant difference after incubation under hypoxia. The proliferation of HUVEC cells were inhibited by incubation under hypoxia for 3 d and further inhibited after 7 d’s incubation. Figure 2 The proliferation, cell cycle, apoptosis, invasion of SKOV-3, ES-2 and HUVEC cells induced by hypoxia. The SKOV-3, ES-2 and HUVEC cells were cultured for 3 or 7 d in normoxia or hypoxia Screening Library clinical trial conditions before proliferation, cell cycle (S-phage), apopotosis and invasion detected by MTT, FCM (for cell cycle and apoptosis) and Transwell as shown in methods. BGB324 manufacturer A. The proliferation of three cells by MTT. B. The S-phase ratio in three cells by FCM. C. The apoptosis of three cells detected by FCM. D and E. The numbers of cells invasion through the membrane indicated by Transwell after incubated for 3 days (D) or 7 days (E). Data were shown in Mean ± S.D. from three separate experiments with the similar result. * and ** indicates P < 0.05 and P < 0.01 vs. Normoxia. The percent of cells in S-phase and apoptosis after incubation for 3 or 7 d under hypoxia were shown in Fig. 2B and 2C. As they shown, in the case of SKOV-3

CHIR98014 manufacturer and ES-2 cells, the percent in S-phase were decreased and those of apoptosis were increased after 3 d’s incubation, however, there had no difference in S-phase and apoptosis after 7 d’s incubation of the two cell lines. On the other hand, the percent of S-phase of HUVEC cells was decreased and that of apoptosis was increased after both 3 and 7 d’s incubation. The numbers of cell migrated through basement membrane of the transwell chamber were shown in Fig. 3D (after 3 d’s incubation) and 3E (after 7 d’s incubation). Compared to normoxia control, the numbers decreased significantly in SKOV-3 after 3 and 7 d’s incubation under hypoxia while it decreased significantly in ES-2 only after 3 d’s incubation. The numbers of HUVEC cells were decreased significantly after both

3 and 7 d’s incubation. Figure 3 The genes expression in SKOV-3, ES-2, ELs from cancer cells and HUVEC induced by hypoxia. The SKOV-3, ES-2 and oxyclozanide HUVEC cells were cultured for 7 d in normoxia or hypoxia conditions before harvested for the expression of HIF-1a, VEGF, Flk-1, CyclinD1, p53 and V-src genes detected by Real-time PCR. A. The genes expression in SKOV-3 and relative cells by Real-time PCR. B. The genes expression in ES-2 and relative cells by Real-time PCR. SKOV-3 EL: the endothelial-like cells induced from SKOV-3 cells; SKOV-3+Si: the SKOV-3 cells treated by Sirolimus under hypoxia; ES-2 EL: the endothelial-like cells induced from ES-2 cells; ES-2+Si: the ES-2 cells treated by Sirolimus under hypoxia; *, ^, and & indicates that P < 0.05 vs.HUVEC, SKOV-3 (or ES-2) and SKOV-3+Si (or ES-2+Si); **, ^^, and && indicates that P < 0.01 vs.HUVEC, SKOV-3 (or ES-2) and SKOV-3+Si (or ES-2+Si).

Colorectal Dis

2011,13(12):396–402.CrossRef 66. Lee EC, Murray JJ, Coller JA, Roberts PL, Schoetz DL Jr: Intraoperative colonic lavage in nonelective surgery for diverticular disease. Dis Colon Rectum 1997, 40:669–674.selleck compound PubMedCrossRef 67. Herzog T, Janot M, Belyaev O, Sülberg D, Chromik AM, Bergmann U, Mueller CA, Uhl W: Complicated sigmoid diverticulitis–Hartmann’s procedure or primary anastomosis? Acta Chir Belg 2011,111(6):378–383.PubMed 68. Myers E, Winter DC: Adieu to Henri Hartmann? Colorectal Dis 2010, 12:849–850.PubMedCrossRef 69. Trenti L, Biondo S, Golda T, Monica M, Kreisler E, Fraccalvieri D, Frago R, Jaurrieta E: Generalized peritonitis due to perforated diverticulitis: Hartmann’s procedure or primary anastomosis? Int J Colorectal Dis 2011,26(3):377–384.PubMedCrossRef 70. Biondo S, Jaurrieta E, Martí Ragué J, Ramos E, Deiros HMPL-504 research buy M, Moreno P, Farran L: Role of resection and primary anastomosis of the left colon in the presence of peritonitis. Br J Surg 2000,87(11):1580–1584.PubMedCrossRef

71. Salem L, Flum DR: Primary anastomosis or Hartmann’s procedure for patients with diverticular peritonitis? A systematic review. Dis Colon Rectum 2004, 47:1953–1964.PubMedCrossRef 72. Zorcolo L, Covotta L, Carlomagno N, Bartolo DCC: Safety of primary anastomosis in emergency Colo-rectal surgery. Colorectal Dis 2003, 5:262–269.PubMedCrossRef 73. Kreis ME, Mueller MH, Thasler WH: Hartmann’s Procedure or primary anastomosis? Dig Dis 2012,30(1):83–85.PubMedCrossRef 74. Tabbara M, Velmahos GC, Butt MU, Chang

Y, Spaniolas K, Demoya M, King DR, Alam HB: Missed opportunities for primary repair in complicated acute diverticulitis. buy PLX3397 Surgery Molecular motor 2010,148(5):919–924.PubMedCrossRef 75. Masoomi H, Stamos MJ, Carmichael JC, Nguyen B, Buchberg B, Mills S: Does primary anastomosis with diversion have Any advantages over Hartmann’s procedure in acute diverticulitis? Dig Surg 2012,29(4):315–320.PubMedCrossRef 76. Taylor CJ, Layani L, Ghusn MA, White SI: Perforated diverticulitis managed by laparoscopic lavage. ANZ J Surg 2006, 76:962–965.PubMedCrossRef 77. Myers E, Hurley M, O’Sullivan GC, Kavanagh D, Wilson I, Winter DC: Laparoscopic peritoneal lavage for generalized peritonitis due to perforated diverticulitis. Br J Surg 2008, 95:97–101.PubMedCrossRef 78. Favuzza J, Frield JC, Kelly JJ, Perugini R, Counihan TC: Benefits of laparoscopic peritoneal lavage for complicated sigmoid diverticulitis. Int J Colorectal Dis 2009, 24:799–801.CrossRef 79. Karoui M, Champault A, Pautrat K, Valleur P, Cherqui D, Champault G: Laparoscopic peritoneal lavage or primary anastomosis with defuctioning stoma for Hinchey 3 complicated diverticulitis: results of a comparative study. Dis Colon Rectum 2009, 52:609–615.PubMedCrossRef 80. Rogers AC, Collins D, O’Sullivan GC, Winter DC: Laparoscopic lavage for perforated diverticulitis: a population analysis. Dis Colon Rectum 2012,55(9):932–938.PubMedCrossRef 81.

The inhibition of NFκB is relevant to both apoptotic processes and inflammation, as discussed further below. NFκB and cell proliferation NFκB, a transcription factor represented by a series of subunits harbouring discrete DNA binding and transactivational

functionality, is implicated in both intrinsic and extrinsic apoptotic pathways (see [36] for review) and has been shown to prevent apoptosis as well as promote transformation in epithelial-derived cancers [37]. Mechanistically, in the absence of NFκB signalling, inhibitor-of-apoptosis proteins (IAPs) fail to suppress assembly of the death-inducing complex II, which allows for the TRADD-mediated activation of caspase-8 Elafibranor in vitro and subsequent apoptosis [36, 38]. Furthermore, IAPs can directly promote the ubiquitin-mediated degradation of the NFκB-inducing serine/threonine kinase (NIK), ultimately resulting in NFκB activation [39]. Although

a detailed discussion on this topic is out of scope, it is well established PF-04929113 research buy that activated NFκB is associated with an anti-apoptotic pro-survival advantage which is relevant given our data showing that GTA+ve extracts reduced NFκB expression. These this website observations are consistent with the reported biological activity of the resolvins and protectins, which have been shown to exert both pro-apoptotic effects [40] and the resolution of inflammation by attenuating cytokine levels in an NFκB-dependent manner [41]. One limitation of our study was that we were unable to determine NFκB levels in RAW264.7 cells, which will require further investigation upon ever the generation of sufficient quantities

of either enriched extract, or more preferably, purified synthetic GTAs. However, the dramatic reduction of NFκB upon GTA treatment in colon tumor cells is highly relevant given the reduced levels of circulating GTAs in CRC patients [17, 18] and the well-established inflammatory component of this disease [42]. NFκB and inflammation Besides its anti-apoptotic role, NFκB represents a key link between inflammation and cancer (see [43] for review), and in particular, is considered a master regulator of intestinal immunological function and activator of factors involved in driving intestinal inflammation [44–46]. NFκB activation has been observed in numerous GI-related conditions including inflammatory bowel disease [47], Crohn’s disease [48], ulcerative colitis [35], inflamed intestinal mucosa [49] as well as CRC [50–53]. It has been shown that the NFκB transcriptional activity in gastric mucosa is induced during aging [53], that positive NFκB expression as assessed through immunohistochemistry is observed in 73.

Vaccine 2009, 28:329–337.PubMedCrossRef 40. Goto Y, Bogatzki LY, Bertholet S, Coler RN, Reed SG: Protective immunization Ro 61-8048 datasheet against visceral leishmaniasis using Leishmania sterol 24-c-methyltransferase formulated in adjuvant.

Vaccine 2007, 25:7450–7458.PubMedCrossRef 41. Nagill R, Kaur S: Enhanced selleck chemical efficacy and immunogenicity of 78 kDa antigen formulated in various adjuvants against murine visceral leishmaniasis. Vaccine 2010, 28:4002–4012.PubMedCrossRef 42. Bhardwaj S, Vasishta RK, Arora SK: Vaccination with a novel recombinant Leishmania antigen plus MPL provides partial protection against L. donovani challenge in experimental model of visceral leishmaniasis. Exp Parasitol 2009, 121:29–37.PubMedCrossRef 43. Dietrich J, Billeskov R, Doherty TM, Andersen P: Synergistic effect of bacillus calmette guerin and a tuberculosis subunit vaccine in cationic liposomes: increased immunogenicity and protection. J Immunol 2007, 178:3721–30.PubMed 44. Ghosh A, Zhang WW, Matlashewski G: Immunization with A2 protein results in a mixed Th1/Th2 and a humoral response which protects mice against Leishmania donovani infections. Vaccine 2001, 20:59–66.PubMedCrossRef 45. Cui Y, Choi IS, Koh YA, Lin XH, Cho YB, Won YH: Effects of combined BCG and DHEA treatment in preventing the development of asthma. Immunol Invest 2008, 37:191–202.PubMedCrossRef 46. Oscherwitz J,

Hankenson FC, Yu F, Cease K: Low-dose intraperitoneal Freund’s adjuvant: toxicity and immunogenicity in mice using an immunogen

targeting amyloid-beta peptide. Vaccine 2006, 24:3018–3025.PubMedCrossRef 47. Bhowmick S, Mazumdar T, Ali N: Vaccination route that induces Selleck Belnacasan transforming growth factor beta production fails to elicit protective immunity against Leishmania donovani infection. Infect Immun 2009, 77:1514–1523.PubMedCrossRef 48. Wijburg OL, van den Dobbelsteen GP, Vadolas J, Sanders A, Strugnell RA, van Rooijen N: The role of macrophages in the induction and regulation of immunity elicited by exogenous antigens. Eur J Immunol 1998, 28:479–487.PubMedCrossRef 49. Lowry OH, Rosebrough NJ, Farr AL, Randall RJ: Protein measurement with the Folin phenol reagent. J Biol Chem 1951, 193:265–275.PubMed 50. Stewart JC: Colorimetric determination of phospholipids with ammonium ferrothiocyanate. Anal Biochem 1980, either 104:10–14.PubMedCrossRef 51. Stauber LA, Franchino EM, Grun J: An eight day method for screening compounds against Leishmania donovani in the golden hamster. J Protozool 1958, 5:269–273. Authors’ contributions RR performed all the experiments of this study. SB and NA have contributed in designing of the paper. SB and AD wrote the draft of the manuscript. NA conceived the study, coordinated it and revised the manuscript. All authors read and approved the final manuscript.”
“Background Catheter-associated urinary tract infection (CAUTI) is the most common nosocomial infection in the United States and a frequent cause of bacteremia [1].

CrossRef 22. Cao X, Li X, Gao X, Yu W, Liu X, Zhang Y, Chen L, Cheng X: Forming-free colossal resistive switching effect in rare-earth-oxide Gd 2 O 3 films for memristor applications. Appl #Danusertib in vivo randurls[1|1|,|CHEM1|]# Phys Lett 2009, 106:073723. 23. Kinoshita K, Tamura T, Aoki

M, Sugiyama Y, Tanaka H: Bias polarity dependent data retention of resistive random access memory consisting of binary transition metal oxide. Appl Phys Lett 2006, 89:03509.CrossRef 24. Janousch M, Meijer GI, Staub U, Delley B, Karg SF, Andreasson BP: Role of oxygen vacancies in Cr-doped SrTiO 3 for resistance-change memory. Adv Mater 2007, 19:2232.CrossRef 25. Panda D, Dhar A, Ray SK: Nonvolatile and unipolar resistive switching characteristics of pulsed laser ablated NiO films. Appl Phys Lett 2011, 108:104513. 26. Lin CY, Wang SY, Lee DY, Tseng TY: Electrical properties and fatigue behaviors

of ZrO 2 resistive switching thin films. J Electrochem Soc 2008, 155:H615-H619.CrossRef 27. Lin CY, Wang SY, Lee DY, Tseng TY: Ti-induced recovery phenomenon of resistive switching in ZrO 2 thin films. J Electrochem Soc 2010, 157:G167-G169. 28. Esch F, Fabris S, Zhou L, Montini T, Africh C, Fornasiero this website P, Comelli G, Rosei R: Electron localization determines defect formation on ceria substrates. Science 2005, 309:752–755.CrossRef 29. Chen MC, Chang TC, Huang SY, Chen SC, Hu CW, Tsai CT, Sze M: Bipolar resistive switching characteristics of transparent indium gallium zinc oxide resistive random access memory. Electrochem Solid State Lett 2010, 13:H191-H193.CrossRef 30. Chang WY, Ho YT, Hsu TC, Chen F, Tsai MJ, Wu TB: Influence of crystalline constituent on resistive switching properties of TiO 2 memory films. Eletrochem Soild-State Lett

2009, 12:H135-H137.CrossRef 31. Liu Q, Guan W, Long S, Jia R, Liu M, Chen J: Resistive switching memory effect of ZrO 2 films with Zr + implanted. J Appl Phys 2008, 92:012117. 32. Guan W, Long S, Liu Q, Liu M, Wang W: Nonpolar non-volatile resistive switching in Cu doped ZrO 2 . IEEE Trans Elec Lett 2008, 29:434–437.CrossRef 33. Liu Q, Long S, Wang W, Zuo Q, Zhang S, Chen J, Liu M: Improvement of resistive Chloroambucil switching properties in ZrO 2 -based RRAM with implanted Ti ions. IEEE Trans Elec Lett 2009, 30:1335–1337.CrossRef 34. Long S, Cagli C, Lelmini D, Liu M, Sune J: Analysis and modeling of resistive switching characteristics. J Appl Phys 2012, 111:074508.CrossRef 35. Long S, Cagli C, Lelmini D, Liu M, Sune J: Reset statistics of NiO-based resistive switching memory. IEEE Trans Elec Lett 2011, 32:1570–1572.CrossRef 36. Long S, Cagli C, Lelmini D, Liu M, Sune J: A model for the set statistics of RRAM inspired in the percolation model of oxide breakdown. IEEE Trans Elec Lett 2013, 34:999–1001.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions The manuscript was written through the contributions of all authors, MI, CYH, DP, CJH, TLT, JHJ, CAL, UC, AMR, EA, IT, MYN, and TYT.

We adjusted urine samples to pH 7 with 1 M NaOH or 1 M HCl. We performed the LC/MS analyses through a Waters find more Acquity ultra-performance liquid chromatography (UPLC) system connected with a high performance Quattro Micro triple quadruple mass spectrometer designed for LC/MS-MS operation. We performed the analytical separations on the UPLC system using an Acquity UPLC BEH C18 1.7 μm column (1 × 100 mm) at a flow rate of 0.15 ml/min. We then moved the elutions from the UPLC column to the Quattro

Micro mass spectrometer. The ionization method used for MS analysis was Electrospray ionization (ESI) in both the positive ion (PI) and negative ion (NI) mode with an ESI-MS capillary voltage of 3.0 kV, an extractor cone voltage of 3 V, and a detector voltage GSI-IX nmr of 650 V. We performed the MS-MS in the multiple reaction monitoring (MRM) mode to produce structural information about the analytes by fragmenting the BKM120 purchase parent ions inside the mass spectrometer and identifying the resulting daughter/fragment

ions. We processed the resulting data and quantified the estrogen metabolites using the QuanLynx software (Waters). To calculate limits of detection, we injected various concentrations of the analytes to LC/MS-MS. The detection limit was considered to be the injected amount that resulted in a peak with a height at least two or three times higher than the baseline. The detection limits of 2-OHE1 and 16α-OHE1 were 18 fmol and 349 fmol, respectively. Intra-assay cAMP coefficients of variation for 2-OHE1 and 16α-OHE1 were 3.2% and 3.0%, respectively. Inter-assay coefficients of variation were 1.9% and 3.5%, respectively. We had previously measured the intra- and inter-individual variability for 2-OHE1, 16α-OHE1 determinations and their ratio over a one year period [13]. The intra-class correlation coefficients (ICCs) and lower limit

of 95% CI (in parentheses) were 0.70 (0.46), 0.63 (0.35) and 0.78 (0.62), respectively. We had previously provided a detailed description of the procedures related to the reliability assessment [13]. Systematic Review We conducted a systematic search of the literature to identify additional studies published up to August 2009 which examined the association between estrogen metabolites and Pca risk using our standard methods [19–22]. We searched MEDLINE (January 1966 onwards) and EMBASE (January 1980 onwards). An expert librarian designed a search strategy combining terms for estrogens, estrogen metabolites and prostate specific antigen (PSA) with terms for Pca (available upon request). We screened titles and abstracts in duplicate using the following inclusion criteria: observational studies investigating prostate cancer risk in relation to estrogen metabolism. We included studies providing at least one measure of either urinary or circulating levels of 2-OHE1, 16α-OHE1 and the 2-OHE1 to 16α-OHE1 ratio.

Typhi strains, both ΔrecF mutations resulted in approximately 10-fold decrease in recombination frequency (P < 0.01), while the ΔrecA and ΔrecJ mutations resulted in a 2-3-fold reduction (P < 0.01). In the complementation

test, the recombination frequency of plasmid pYA4463 in S. Typhi χ11053 was restored to 2.52 ± 0.18 × 10-3 and 1.71 ± 0.68 × 10-3 by introduction of plasmid pYA5005 encoding S. Typhimurium recF gene and pYA5006 encoding the S. Typhi recF gene, respectively (Table 3). Table 3 Plasmid recombination frequency (Mean ± STD, × Cytoskeletal Signaling inhibitor 10- 3) Strain rec deletion pYA4463a pYA4590b pYA4464+pYA4465c S. Typhimurium         χ3761 None 1.55 ± 0.31 2.40 ± 0.54 2.88 ± 0.85 χ9833 ΔrecA62 1.07 ± 0.24 0.22 ± 0.07** 0.27 ± 0.07** χ9070 ΔrecF126 1.14 ± 0.15 0.52 ± 0.07** 0.33 ± 0.09** χ9072 ΔrecJ1315 1.87 ± 0.44 2.37 ± 0.21 1.10 ± 0.20** selleck kinase inhibitor χ9081 ΔrecJ1315 ΔrecF126 NAd NA 0.35 ± 0.08** χ9939 ΔrecF126 ΔrecA62 NA 0.41 ± 0.09** 0.35 ± 0.08** χ9833(pYA5002) ΔrecA62 (RecA+) NA 2.50 ± 0.42 NA χ9070(pYA5005) ΔrecF126 (RecF+) NA 2.00 ± 0.24 NA S. Typhi Ty2

        χ3769 None 4.69 ± 0.26 11.59 ± 2.61 4.20 ± 1.44 χ11159 ΔrecA62 1.32 ± 0.27** 0.60 ± 0.19** 3.37 ± 0.96 χ11053 ΔrecF126 0.51 ± 0.06** 0.57 ± 0.09** 6.19 ± 2.71 χ11134 ΔrecF1074 0.45 ± 0.05** 0.52 ± 0.17** 16.28 ± 2.64** χ11194 ΔrecJ1315 1.69 ± 0.26** 4.88 ± 1.56** 2.31 ± 0.90 χ11053(pYA5005) ΔrecF126 (RecF+) 2.52 ± 0.18 NA NA χ11053(pYA5006) ΔrecF126 (RecF+) 1.71 ± 0.68 NA NA χ11159(pYA5002) ΔrecA62 (RecA+) NA 14.35 ± 2.44 NA χ11053(pYA5006) ΔrecF126 (RecF+) NA 2.86 ± 0.59 NA S. Typhi ISP1820         χ3744 None 4.93 ± 0.67 13.10 ± 1.23 4.22 ± 0.25 χ11133 ΔrecF1074 0.65 ± 0.26** 0.71 ± 0.06** 5.38 ± 0.58 S. Paratyphi A         χ8387 None 2.70 ± 0.39 3.32 ± 0.61 1.03 ± 0.15 χ11243 ΔrecA62 1.91 ± 0.69** 0.55 ± 0.20** 0.13 ± 0.03** Ribose-5-phosphate isomerase χ11244 ΔrecF126 5.00 ± 0.70 1.16 ± 0.21** 0.34 ± 0.04** χ11245 ΔrecJ1315 2.56 ± 0.41 1.83 ± 0.99** 0.64 ± 0.15** aIntraplasmid recombination without selleck compound intervening sequence (5′tet-3′tet). b Intraplasmid recombination with a 1041-bp intervening sequence (5′tet-kan-3′tet).

c Interplasmid recombination. d Not assayed. ** P < 0.01, relative to the parental rec + strain. The results with plasmid pYA4590 were also variable among strains. The recombination frequency in Rec+ S. Typhimurium and S. Paratyphi A strains was approximately 2-3 × 10-3 and in both S. Typhi strains, the frequency was 3-fold higher, at 1.16 × 10-2 (Ty2) and 1.31 × 10-2 (ISP1820). In S. Typhimurium and S. Typhi Ty2, the Δ recA and ΔrecF mutations reduced the recombination frequency of plasmid pYA4590 by 5-20-fold (P < 0.01; Table 3). The results were similar for S. Paratyphi A, though the ΔrecF mutation only led to 3-fold lower plasmid pYA4590 recombination (P < 0.01).

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