Am J Emerg Med 2005, 23:911–2.CrossRef 5. Çil BE, Türkbey B, Canyiğit M, Geyik S, Yavuz K: An usual complication of carotid stenting: spontaneous this website rectus sheath hematoma and its endovascular management. Diagn Interv Radiol

2007, 13:46–8.PubMed 6. Tomoe N, Tatsuyuki I, Daihiko E, Kinya Y, Daisuke T, Katsumi S, Hiromu H, Hidetaka AICAR supplier M: Spontaneous internal oblique hematoma successfully treated by transcatheter arterial embolization. Radiat Med 2008, 26:446–9.CrossRef 7. Lohle PN, Puylaert JB, Coerkamp EG, Hermans ET: Nonpalpable rectus sheath hematoma clinically masquerading as appendicitis: US and CT diagnosis. Abdom Imaging 1995, 20:152–4.CrossRefPubMed 8. Moreno Gallego A, Aguayo JL, Flores PD-1/PD-L1 Inhibitor 3 research buy B, Soria T, Hernandez Q, Ortiz S, Gonzalez-Costea R, Parrilla P: Ultrasonography and computed tomography reduce unnecessary surgery in abdominal rectus sheath haematoma. Br J Surg 1997, 84:1295–7.CrossRefPubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions NF wrote this manuscript and revised it. SI, JS and KS performed the operation and recommended me to write this case and advised me to revise it. All authors read and approved the final manuscript.”
“Background Percutaneous transhepatic biliary drainage (PTHBD)

is one of the most therapeutic options for the menagement of biliary obstructive disorders, but the use of interventional procedures is associated with

an increased incidence of arteriovenous shunting, hepatic artery pseudoaneurysm and vascular stenoses that result in hemobilia[1]. The diagnosis of hemobilia may be difficult because of a variety of clinical manifestations and sometimes can be fatal. Its management aims to stopping the bleeding and resolve obstruction. Actually the development of interventional radiology, such as transarterial embolization, has been recognized the first line of procedure to stop hemobilia with a success rate of about 80%-100%, by ensuring that the classic surgery interventions, GPX6 such as ligation of bleeding vessels or excisions of aneurysms, should be considered fails and burdened by high mortality [2, 3]. Case Report A 60-year-old man came to our observation with intermittent pain localized to upper quadrants of the abdomen, fever (39°C) preceded by thrill, vomiting and signs of peritoneal interesting. Laboratory tests revealed leucocytosis (18300 WBC), and the increment of cholestasis markers, while US scan demonstred an acute cholecystitis with lithiasis, without biliary tree dilatation, and a small liquid flap next to gallbladder. Because of poor conditions, we decided to perform a surgical operation.

In this study we described six NDM-4-producing buy ARS-1620 E.coli isolates obtained from two patients admitted to an Italian hospital. We also present data on the localization and the genetic environment of the bla NDM-4 gene. Methods Bacterial strains Six E.coli isolated from urine samples of two inpatients at the San Martino-IST University Hospital (Genoa, Italy)

were studied. Isolates were taken as part of standard patient care and informed consent for the use of clinical data has been obtained by both patients. Strain identification, antibiotic susceptibility testing and phenotypic screening for MBL production Routine identification and antibiotic susceptibility testing were carried out using the Vitek-2 automated system (BioMérieux, Marcy-L’etoile, France). In vitro activity of carbapenems, aztreonam, fosfomycin and nitrofurantoin was further determined by the broth microdilution method and interpreted according to the of European Committee on Antimicrobial Susceptibility Testing (EUCAST ) guidelines (Version 4.0, 2014) [6]. To detect metallo-β-lactamase (MBL) production,

a synergy test using imipenem and EDTA discs was used [7]. Pulsed-field gel electrophoresis (PFGE) Genomic DNA was prepared, digested with XbaI (New England Biolabs Inc., MA, USA) and subjected to PFGE with the CHEF DRII device (Bio-rad, Milan, Italy), as described previously [8]. Fingerprinting pattern was interpreted ISRIB ic50 according to the method of Tenover et al. [9]. Multilocus sequence typing (MLST) MLST was carried out using protocols and conditions described on the E.coli MLST website (http://​mlst.​warwick.​ac.​uk/​mlst/​dbs/​Ecoli/​documents/​primersColi_​html).

Sequence types were assigned using the website BAY 1895344 in vitro interface. Molecular analysis techniques Polymerase chain reaction (PCR) amplification of the bla NDM gene and direct sequencing of the PCR products was performed as previously described [10]. Screening for resistance genes was carried out using primers and conditions previously described [11–13]. Phylogenetic analysis using multiplex PCR method as described previously [14] was used. PCR experiments were performed to identify the upstream- and downstream-located regions of the bla NDM-4 gene [15]. Mapping of the variable region of class 1 integron was performed by PCR as described previously [16]. The genetic environment of bla NDM-4 was studied by PCR mapping and sequencing GSK-3 inhibitor as described previously [13]. Conjugation assay and plasmid study Plasmid transfer was attempted by conjugation, using E.coli J53 as the recipient, as described previously [17]. Plasmid DNA, isolated from E.coli, was obtained by the alkaline lysis method and was used as a template in PCR analysis with primers that are specific for bla NDM and bla CTX-M[18]. To rule out chromosomal DNA contamination the template was used to amplify an internal fragment of the house-keeping recA gene. A PCR-based replicon typing method was used to identify the incompatibility group [19].

In contrast, in case of GI5 we were not able to detect a circular intermediate neither with the originally predicted borders nor with the additional genes suggested by the microarray experiments (Bpet3771–3779), although the microarray data of the phenotypic https://www.selleckchem.com/products/JNJ-26481585.html variants f, g, and k definitely revealed the deletion of this element from their genomes. As shown above, we were

able to detect circular intermediates of most genomic islands by PCR amplification, although the microarray experiments with the phenotypic variants clearly demonstrated the deletion events. Possible explanations for this fact could be that the excised islands are diluted during growth of the bacteria since they cannot replicate. Moreover, the experimental protocols for the two methods are different and PCR amplification is much more sensitive as compared to cy3/cy5 labeling by

Klenow polymerisation. Stability of genomic island GI3 The frequent appearance of phenotypic variants involving the genomic islands present in the B. petrii genome and the detection of circular intermediates of these islands under standard growth conditions indicates that these genomic islands are rather unstable and active at least in terms of excision. To assess the stability of one of these islands (GI3) by homologous recombination we integrated a tetracycline resistance cassette in GI3 between the genes Bpet1523 and Bpet1524 coding for a putative transposase and a glycosyltransferase, respectively. Under standard growth conditions, the resulting strain B. petrii GI3::tetR

did not show any change in its maximum specific growth rate as compared to the wild type (data not shown). This strain was then used for Histone Methyltransferase inhibitor growth experiments without selective pressure in which the bacteria were cultivated for about 150 consecutive generations. Exponentially growing B. petrii Lepirudin has a generation time of about 90 min (data not shown). Figure 5 shows the time course of loss of GI3::tetR determined by differential counting of tetracycline resistant and sensitive bacteria plated out on the respective agar plates. GI3 was stably present in the B. petrii population for about 40 generations, then the proportion of tetracycline resistant bacteria declined steadily and virtually no tetracycline resistant bacteria were found in the population after about 100 generations. Lack of the entire GI3 was confirmed by Southern blotting in representatives of these bacteria (data not shown). Although we cannot exclude a destabilizing effect of the tetracycline cassette on the island, it is likely that GI3 is highly unstable and gets lost with a high Salubrinal price incidence when no selective pressure for its persistence is present. Figure 5 Stability of the genomic island GI3 in the genome of B. petrii during culture grown without selective pressure. On the x-axis the number of consecutive generations of the bacteria culture and on the y-axis the proportion of tetracycline resistant bacteria in the culture is shown.

TrAC Trends Anal Chem 2013, 43:14–23.CrossRef 14. Chigome S, Torto N: Electrospun nanofiber-based solid-phase extraction. AMPK inhibitor TrAC Trends Anal Chem 2012, 38:21–31.CrossRef 15. Chigome S, Torto N: A review of opportunities for electrospun nanofibers in analytical chemistry. Anal Chim Acta 2011, 706:25–36. 10.1016/j.aca.2011.08.021CrossRef 16. Chigome S, Darko G, Torto N: Electrospun nanofibers as sorbent material for solid phase extraction. Analyst 2011, 136:2879–2889. 10.1039/c1an15228aCrossRef 17. Xu Q, Wu S-Y, Wang M, Yin X-Y, Wen

Z-Y, Ge W-N, Gu Z-Z: Electrospun Nylon6 nanofibrous membrane as SPE adsorbent for the enrichment and determination of three estrogens in environmental water samples. Chromatographia 2010, 71:487–492. 10.1365/s10337-009-1453-9CrossRef

18. Xu Q, Wang M, Yu S, Tao Q, Tang M: Trace analysis of diethylstilbestrol, dienestrol and hexestrol in environmental water by Nylon 6 nanofibers mat-based solid-phase extraction coupled with liquid chromatography-mass spectrometry. Analyst 2011, 136:5030–5037. 10.1039/c1an15494jCrossRef 19. Wu SY, Xu Q, Chen TS, Wang M, Yin XY, Zhang NP, Shen YY, Wen ZY, Gu ZZ: Determination of bisSelleckchem Doramapimod phenol A in plastic bottled drinking water by high performance liquid chromatography with solid-membrane extraction based on electrospun Nylon 6 nanofibrous membrane. Chin J Anal Chem 2010, 38:503–507. 10.1016/S1872-2040(09)60035-9CrossRef 20. Xu Q, Yin X, Wu S, Wang M, PLX-4720 solubility dmso Wen Z, Gu Z: Determination of phthalate esters in water samples using Nylon6 nanofibers mat-based solid-phase extraction coupled to liquid chromatography. Microchim Acta 2010, 168:267–275. 10.1007/s00604-010-0290-8CrossRef 21. Xu Q, Yin X, Shen Y, Zhang N, Wang M: Detection of phthalate esters in environmental SPTLC1 water samples – comparison of Nylon6 nanofibers mat-based solid phase extraction and other conventional extraction methods. Chin J Chem 2011, 29:567–574. 10.1002/cjoc.201190124CrossRef 22. Wang J, Pan K, He Q, Cao B: Polyacrylonitrile/polypyrrole core/shell nanofiber mat for the removal of hexavalent chromium from aqueous

solution. J Hazard Mater 2013, 244–245:121–129.CrossRef 23. Boparai HK, Joseph M, O’Carroll DM: Kinetics and thermodynamics of cadmium ion removal by adsorption onto nano zerovalent iron particles. J Hazard Mater 2011, 186:458–465. 10.1016/j.jhazmat.2010.11.029CrossRef 24. Taqvi SI, Hasany SM, Bhanger MI: Sorption profile of Cd(II) ions onto beach sand from aqueous solutions. J Hazard Mater 2007, 141:37–44. 10.1016/j.jhazmat.2006.06.080CrossRef 25. Wu F-C, Tseng R-L, Juang R-S: Initial behavior of intraparticle diffusion model used in the description of adsorption kinetics. Chem Eng J 2009, 153:1–8. 10.1016/j.cej.2009.04.042CrossRef 26. Jiang JQ, Cooper C, Ouki S: Comparison of modified montmorillonite adsorbents – part I: preparation, characterization, and phenol adsorption. Chemosphere 2002, 47:711–716. 10.1016/S0045-6535(02)00011-5CrossRef 27.

The tubes were placed into a FastPrep (Bio 101) homogenizer and agitated twice at 6 m/s for 40 s. with 1 min-interval on ice. The next steps were performed according to manufacturer’s instructions. Finally, RNA samples were dissolved in 30 μl of RNase-free water. RNA integrity was tested with electrophoresis on 1% agarose gel. RNA quantification was performed measuring the absorbance at 260 nm. Nucleic acid purity was assessed measuring A260/A280 ratio (acceptable ratio was between 1.8 and 2.0). cDNA synthesis Reverse transcription was performed with the use of commercially available QuantiTect Reverse Transcription kit (QIAgen,

Hamburg, Germany). Firstly, 100 ng of total RNA was incubated with 2 μl of Wipeout buffer (QIAgen, Hamburg, Germany), containing RNase-free DNase, for

Luminespib cell line 5 min. at 42°C. cDNA synthesis reaction was performed in a final volume of 20 μl, containing 100 ng of total RNA, 50 ng of random hexamer primers and the QuantiTect Reverse Transcriptase in RT buffer (QIAgen, Hamburg, Germany) according to the manufacturer’s instructions for the first-strand cDNA synthesis. Quantitative real-time PCR conditions The expression level of sodA and sodM genes were quantified using real-time RT-PCR (LightCycler® FastStart DNA Master SYBR Green I; Roche Diagnostics). Two μl of cDNA were subjected to amplification in a 20-μl volume containing 5 μM concentration of each primer (Table 3), 3 mM of MgCl2 and 2 μl of ready-to-use Light Cycler® DNA Master SYBR Green I (Roche Diagnostics). Pre-incubation step (95°C for 10 min.) was initially selleck products performed to activate FastStart DNA polymerase and to denature the template DNA. The following cycling conditions were used in the reaction: amplification and quantification program repeated 50 times

(95°C for 5 s, 66°C for 15 s and 10 s extension at 72°C with a single fluorescence measurement), melting curve program (65-95°C with a heating rate of 0.2°C per second and a continuous fluorescence measurement) and finally a cooling step to 40°C. Specificity of the PCR products was confirmed by analysis of the dissociation Galeterone curves. Expression levels of sodA and sodM genes were measured using an absolute quantification method that allows to determine the exact copy concentration of target gene by relating the Ct value to a standard curve. Ct value is see more defined as the point at which the fluorescence rises appreciably above the background fluorescence. Standard curve was constructed by amplifying known amounts of target DNA. Standard curves for sodA and sodM genes were generated using serial dilutions of a standard sample (calibrator): 1×, 0.5×, 0.2×, 0.1×. As a calibrator, genomic DNA extracted from RN6390 strain (12.34 ng/μl) was used. In the case of sodA transcript quantification, amplification of sodA gene fragment was used, and similarly, to quantify sodM transcript level, sodM gene fragment from genomic DNA was used as calibrator.

Comparison of metabolite and gene expression profiles of C. perfringens grown with cystine or homocysteine To obtain new insights into the regulation in response to sulfur availability, we compared the metabolome and the transcriptome of C. perfringens after growth in the presence of 0.5 mM cystine or 1 mM homocysteine. The doubling time was about two-fold higher for C. perfringens strain 13 grown in the presence of homocysteine than in the presence #Selleck Nec-1s randurls[1|1|,|CHEM1|]# of cystine. Cystine allows efficient growth while homocysteine is a poor sulfur source for C. perfringens. This suggests that some metabolites are limiting during growth with homocysteine. So, we measured the

intracellular concentration of several sulfur compounds and amino acids by HPLC in crude extracts of strain 13 grown in the presence of cystine or homocysteine

(Fig. 3). The intracellular concentration of methionine remained undetectable SU5402 solubility dmso in both growth conditions. This suggests that methionine biosynthesis is not very efficient and/or that methionine requirements are high. Homocysteine can be detected only during growth with this compound suggesting that homocysteine was mainly taken up from outside under these conditions. Cystine, cysteine but also proline pools were below the threshold of detection during growth with homocysteine while their intracellular concentrations Astemizole were 325 μM, 236 μM and 80 μM, respectively during growth with cystine. This strongly suggests that growth in the presence of homocysteine mimics conditions typically associated with cysteine limitation.

The concentration of alanine, lysine and serine and/or threonine differed to a lesser extent in these two conditions. Figure 3 Intracellular concentration of sulfur compounds (A) and amino acids (B) in strain 13 grown in the presence of cystine or homocysteine. Grey or white boxes indicate the metabolite concentrations extracted from strain 13 grown in the presence of 0.5 mM cystine or 1 mM homocysteine, respectively. The mean value of three independent experiments is presented. # indicates that the metabolite is not detectable. We further compared gene expression profiles of strain 13 grown in the presence of cystine or homocysteine. For this purpose, we designed a microarray containing oligonucleotides representative of 2706 genes of C. perfringens. For each condition, eight data sets generated with RNAs extracted from four independent cultures were used to perform statistical analysis (see Methods). A total number of 177 genes were differentially expressed in these two conditions. Most of them (122 out of 177) were up-regulated in the presence of homocysteine. Some of the controlled genes including those associated with sulfur metabolism, redox functions, carbon metabolism and virulence are presented in Table 1.

Furthermore, delayed gastric emptying, which results from diabetic neuropathy, hypothyroidism, and connective tissue diseases, forms a basis for the development of gastrointestinal phytobezoars[9–11]. Chisholm et al. retrospectively examined 13 patients with phytobezoars, and found that all the patients had a history of persimmon consumption, whereas 11 (84,6%) had a history of gastric surgery [12]. Krausz et al., in their retrospective study on 113 patients, showed that 106 (93,8%) patients CB-839 ic50 had undergone gastric surgery, whereas 103 (91,1%) had a history of persimmon

consumption [10]. In the present study, all 13 patients (100%) had a history of Diospyros Lotus consumption, whereas four (30,7%) had a history of previous gastric surgery. Furthermore, four (30,7%) patients had diabetes mellitus and three (23%) had a history of using dental implants. The main clinical symptoms are abdominal pain, epigastric distress, nausea and vomiting. In addition, sensation Selleckchem AZD3965 of fullness, dyspepsia, dysphagia, anorexia, weight loss, and gastrointestinal bleeding may be seen [1,

13–15]. Decreased bowel sounds, rebound tenderness, rigidity, distension, diarrhea, constipation, nausea and vomiting may be seen in complicated cases [10]. Small bowel obstruction is the most common major complication of phytobezoars. Moreover, gastritis, ulcer, and gastric perforation may be seen. Small bowel phytobezoars usually occur due to the extension of gastric phytobezoars [10, 16]. Guanylate cyclase 2C However, small intestinal phytobezoars may also be seen in patients with underlying diseases, such as diverticulitis, stricture, and tumor [17–19].

Small bowel obstructions due to phytobezoars usually occur in the terminal ileum and jejunum, which are the narrowest parts of the small intestine [20]. Chisholm et al. identified phytobezoars in the stomach in two (12,5%), in the jejunum in four (25%), in the ileum in nine (56,2%), and in more than one region of the small intestine in two (12,5%) patients[12]. Krausz et al. detected phytobezoars in the stomach in 13 (11,5%), in the small intestine and stomach in 20 (17,6%), and in the small intestine in 80 (70,7%) patients[10]. In the present study, phytobezoars were selleck products located in the stomach alone in three (23%), in the jejunum and stomach in two (15,3%), in the jejunum alone in two (15,3%), and in the ileum alone in six (46,1%) patients.

These preliminary biochemical and kinetic analyses of Dictyostelium FAAH supports the identification of [GenBank: XM_638290] as a functional homolog of mammalian FAAH. N-acylphosphatidylethanolamines (NAPEs) and its hydrolysed product N-acylethanolamines (NAEs) have been previously reported in Dictyostelium [31]. Identification of FAAH in Dictyostelium #selleck kinase inhibitor randurls[1|1|,|CHEM1|]# indicates FAAH may be a potential regulator of NAEs produced in Dictyostelium cells. Among many established physiological roles for anandamide in mammalian cells, recently a role in neutrophil chemotaxis was identified [32] and therefore we predict a similar kind of role for NAEs that may exist in Dictyostelium.

As recent advances are made to develop FAAH inhibitors for potential novel therapeutics, having a mammalian FAAH homolog in Dictyostelium should offer an additional and moreover simple eukaryotic model system to screen any relevant drugs for their pharmacological influence at the molecular and cellular level. Conclusions Our study indicates that Dictyostelium produces GSK1210151A order anandamide hydrolysing enzyme throughout its development life cycle. This is the first report on the identification of anandamide hydrolyzing enzyme in

Dictyostelium, suggesting the potential of Dictyostelium as a simple eukaryotic model system to study the mechanisms of action of any FAAH inhibitors as drug targets. Methods Anandamide, arachidonoyl p-nitroaniline, decanoyl p-nitroaniline and methyl arachidonoyl fluorophosphonate (MAFP) were purchased from Cayman Chemicals (Ann Arbor, MI, USA). Phenylmethylsulfonyl fluoride (PMSF) Dimethyl sulfoxide (DMSO), isopropyl-1-thio-β-D-galactopyranoside (IPTG), p-nitroaniline, and Freund’s complete and incomplete adjuvant were purchased from Sigma-Aldrich Canada (Oakville, ON, Canada). All media were obtained from Tangeritin Difco Laboratories (Detroit, MI). All restriction endonucleases were obtained from New England Biolabs (Mississauga, ON, Canada). T4 DNA ligase, Taq polymerase and G418 were purchased

from Invitrogen (Burlington, Ontario, Canada). PCR amplification reactions were performed with a GeneAmp PCR system 9700 thermocycler (Applied Biosystems Canada, Streetsville, ON, Canada). PWO polymerase was purchased from Roche Applied Science (Laval, Quebec, Canada). Dictyostelium strain growth and development Dictyostelium discoideum AX3 cells were grown either with Klebsiella aerogenes on SM agar plates or in Sorensen’s phosphate buffer (2 mM Na2HPO4, 14.6 mM KH2PO4, pH 6.0). Cells were grown axenically in liquid nutrient medium [33] with shaking of the suspension at 150 rpm at 22-24°C. AX3FAAH cells were cultured in axenic liquid nutrient medium containing 10 μg ml-1 G418 for selection of the recombinant protein producing cells.

05 in A and C; P < 0.01 in D and E). Effects of PDCD4 on MHCC-97H cell migration and invasion In the migration assay, the average

number of migrated cells per field of the MHCC-97H -PDCD4 group (Group1) was 27.20 ± 7.26, which was much lower than that of the MHCC-97H -vector group (Group2) (161.80 ± 17.06) or the MHCC-97H group (Group3) (194.60 ± 30.83) (Fig. 3D). The average number of migrated cells in the invasion assay was 19.0 ± 3.18, 64.40 ± 9.61 and 69.80 ± 12.32 for the Group1, Group2 and Group3, respectively (Fig. 3E). The difference was significant AZD6094 in vitro between Group1 and Group2 or Group3 (n = 5, P < 0.01). There is no difference between Group2 and Group3. Discussion PDCD4 was originally found to be an apoptosis-associated gene in mouse cells. PDCD4 expression was found to be up-regulated in cells treated with various apoptosis-inducing agents such as topoisomerase inhibitors, corticosteroids and cytokine deprivation[29]. The function

of PDCD4 in the course of programmed cell death remains unclear. Later studies showed that PDCD4 was a suppressor of tumor cell transformation. The expression levels of PDCD4 were reduced in many human progressed carcinomas[7]. A study on human HCC showed that expression level of PDCD4 protein was much lower in HCC tissues tested than that of the corresponding noncancerous liver[30]. In this study, we showed that higher metastatic potential HCC cells expressed lower level of PDCD4. The expression levels of PDCD4 were inversely correlated with the metastasis potentials of HCC cells. This result is consistent with the previous JNK-IN-8 research buy BCKDHA findings. We also demonstrated that the MHCC-97H cell proliferation

rate was remarkably decreased and the cell apoptosis rate was significantly increased after transfection with the PDCD4 gene. Cell cycle analysis showed that transfection of PDCD4 gene increase the percentage of both G1 and G2. Data of our results suggest that PDCD4 might promote cell cycle arrest in phase of G1 and in G2 and further block the cell proliferation. It is known that PDCD4 is a binding partner of the eukaryotic Omipalisib clinical trial translation initiation factor 4A (eIF4A). By binding to eIF4A, PDCD4 can directly inhibit translation initiation and then delay the process of protein synthesis. A study on Bon-1 carcinoid cells showed that PDCD4 not only suppressed the transcription of the mitosis-promoting factor cyclin-dependent kinase 1(CDK1)/cdc2, but also decreased the expression of CDK4/6[31]. CDK1 and CDK4/6 are are directly involved in cell cycle control. Decrease of CDK1 or CDK4/6 promotes cell cycle arrest in G1 or G2 phase and further inhibits proliferation of cells[32]. PDCD4 inhibits the activity of c-Jun N-terminal kinase (JNK), blocks the JNK signaling pathway and consequently decreases the activation of c-Jun and AP-1-dependent transcription[8]. Many genes regulated by AP-1 are important modulators of invasion and metastasis.

PubMed 4. Saslaw S, Eigelsbach HT, Wilson HE, Prior JA, Carhart S: Tularemia vaccine study. I. Intracutaneous challenge. Arch Intern Med 1961, 107:689–701.PubMed 5. Eigelsbach HT, Downs CM: Prophylactic effectiveness of live and killed tularemia vaccines. I. Production of vaccine and evaluation in the white mouse and guinea pig. J Immunol 1961, 87:415–425.PubMed 6. Larsson P, Oyston PC, Chain P, Chu MC, Duffield M, Fuxelius HH, Garcia E, Halltorp G, Johansson D, Isherwood KE, et al.: The complete genome sequence of Francisella tularensis find more , the causative agent of tularemia. Nat Genet 2005,37(2):153–159.PubMedCrossRef 7. Gallagher LA, Ramage E, Jacobs MA, Kaul R, Brittnacher M, Manoil C: A comprehensive transposon

mutant library of Francisella novicida , a bioweapon surrogate. Proc Natl Acad Sci USA 2007,104(3):1009–1014.PubMedCrossRef 8. Su J, Yang J, Zhao D, Kawula TH, Banas JA, Zhang JR: Genome-wide identification of Francisella tularensis virulence determinants. Infect Immun 2007,75(6):3089–3101.PubMedCrossRef 9. Anthony LD, Burke RD, Nano FE: Growth of Francisella spp. in rodent macrophages. Infect Immun 1991,59(9):3291–3296.PubMed 10. Clemens DL, Lee BY, Horwitz MA: Virulent and avirulent strains of Francisella tularensis prevent acidification and maturation of

their phagosomes and escape into the cytoplasm in human macrophages. Infect Immun 2004,72(6):3204–3217.PubMedCrossRef 11. Golovliov I, Baranov V, Krocova Z, Kovarova H, Sjostedt A: An attenuated strain of the facultative intracellular bacterium Francisella tularensis can escape the phagosome of monocytic cells. Infect Immun Regorafenib 2003,71(10):5940–5950.PubMedCrossRef 12. Santic M, Molmeret M, Klose KE, Jones S, Kwaik YA: The Francisella tularensis pathogenicity island protein IglC and its regulator MglA are essential for modulating phagosome biogenesis and subsequent bacterial escape into the cytoplasm. Cell Microbiol 2005,7(7):969–979.PubMedCrossRef 13. Qin A, Scott DW, Thompson JA, Mann BJ: Identification of an essential Francisella tularensis subsp.

tularensis virulence factor. Infect Immun 2009,77(1):152–161.PubMedCrossRef 14. Gil H, Platz GJ, Forestal CA, Monfett M, Bakshi CS, BI 10773 molecular weight Sellati TJ, Furie MB, Benach JL, Thanassi DG: Deletion of TolC orthologs L-NAME HCl in Francisella tularensis identifies roles in multidrug resistance and virulence. Proc Natl Acad Sci USA 2006,103(34):12897–12902.PubMedCrossRef 15. Bina XR, Lavine CL, Miller MA, Bina JE: The AcrAB RND efflux system from the live vaccine strain of Francisella tularensis is a multiple drug efflux system that is required for virulence in mice. FEMS Microbiol Lett 2008,279(2):226–233.PubMedCrossRef 16. Mohapatra NP, Soni S, Bell BL, Warren R, Ernst RK, Muszynski A, Carlson RW, Gunn JS: Identification of an orphan response regulator required for the virulence of Francisella spp. and transcription of pathogenicity island genes. Infect Immun 2007,75(7):3305–3314.PubMedCrossRef 17.