BMC Surg 2006, 28:6–15. 29. Yokoyama S, Takifuji K, Hotta T, Matsuda K, Nasu T, Nakamori M, Hirabayashi N, Kinoshita H, Yamaue H: C-Reactive protein is an independent surgical indication marker for appendicitis: a retrospective study. World J Emerg Surg 2009, 4:36.PubMedCrossRef 30. Lee SL, Walsh AJ, Ho HS: Computed tomography and ultrasonography do not improve and may delay the diagnosis and treatment of acute appendicitis. Arch Surg 2001,136(5):556–562.PubMedCrossRef 31. Gronroos JM: Do normal leucocyte count and

C-reactive protein value exclude acute appendicitis in children? Acta Paediatr 2001,90(6):649–651.PubMedCrossRef 32. Khan MN, Davie E, Irshad K: The role of white cell count and C-reactive protein Galunisertib mw in the diagnosis of acute appendicitis. J Ayub Med Coll

Abbottabad 2004,16(3):17–19.PubMed 33. Gulzar S, Umar S, Dar GM, Rasheed R: Acute Selleck Protease Inhibitor Library appendicitisrole of clinical examination in making a confident diagnosis. Pak J Med Sci 2005,21(2):125–132. 34. Bener A, Suwaid MH, Ghazawi IE: Diagnosis of appendicitis. Can J Rural Med 2002, 7:26–29. 35. de Carvalho BR, Diogo-Filho A, Fernandes C, Barra CB: Leukocyte count, C-reactive protein, alpha-1 acid glycoprotein and erythrocytes sedimentation rate in acute appendicitis. Arq Gastroenterol 2003,40(1):25–30.PubMedCrossRef 36. Körner H, Söreide JA, Söndenaa K: Diagnostic accuracy of inflammatory markers in patients operated on for suspected acute appendicitis: a receiver operating characteristic curve analysis. Eur J Surg 1999,165(7):679–685.PubMedCrossRef 37. Rodríguez-Sanjuán JC, Martín-Parra JI, Seco I, García-Castrillo L, Naranjo A: C-reactive protein and leukocyte count in the diagnosis of acute appendicitis in children. Dis Colon Rectum 1999,42(10):1325–1329.PubMedCrossRef 38. Andersson RE, Hugander AP, Ghazi SH, Ravn H, Offenbartl SK, Nyström PO, Olaison GP: Diagnostic value of disease history, clinical parameters, and inflammatory parameters of appendicitis. World J Surg 1999,23(2):133–140.PubMedCrossRef 39. Guss DA, Richards C: Normal

Selleckchem Ibrutinib total WBC and operative delay in appendicitis. Cal J Emerg Med 2000,1(2):7–8.PubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions ZA carried out the design the study, collection and analysis of data, drafting and approved the final manuscript for publication.”
“Introduction Gastric cancer is the second most common cause of cancer death worldwide [1], being responsible for 650 000 deaths annually. In the UK in 2007, there were 5,236 deaths from stomach cancer, making it the seventh most common cause of cancer death and responsible for over 3% of all cancer related mortality [2]. In 2007 the age-standardised rate of gastric carcinoma in the UK was 5.7 per 100 000 population. The majority of the patients present with non-acute symptoms but gastric cancer can also manifest as an emergency with haematemesis, visceral perforation, or gastric outlet obstruction.

Precleared serum was incubated at 4°C for 1 h with 10 μl of HMFG1 MAb. Fifty μl protein A-Sepharose CL-4B was added to immune complexes and shook on a rotator at 4°C for 1 h. After spinning, the supernatant CB-839 cell line was removed and the pellet was washed with lysis buffer (1% NP40, 1 mM phenyl methyl sulphonyl fluoride, 150 mM NaCl, 50 mM Tris-HCl, pH 8.0) (SIGMA, St. Louis, MO, USA). Then, 50 μl of Laemmli buffer (2% SDS, 5% 2-mercapoethanol, 10% glycerol) was added and heated to 90–100°C for 10 min. After spun down, the supernatant was loaded on the gel for SDS-PAGE analysis. SDS-PAGE and Western blot (WB)

of IP Supernatants were analyzed under reducing conditions in SDS-PAGE in a discontinuous buffer system according to Laemmli [22]. After electrophoresis, gels were either stained with Coomassie blue (SIGMA, St. Louis, MO, USA) or they were electrophoretically CP-690550 concentration transferred to nitrocellulose membranes [23] which were blocked with PBS/5% skimmed milk

(blocking buffer). After washing with PBST, sheets were incubated with either HMFG1 MAb or C14 MAb diluted in blocking buffer. HMFG1 MAb was employed undiluted while C14 MAb was diluted 1/100 in blocking buffer. Sheets were incubated overnight at 4°C and rinsed with PBST buffer. A final incubation with 1/400 peroxidase-conjugated anti-human immunoglobulins was performed according to the manufacturer’s instructions (SIGMA, St. Louis, MO, USA). Nitrocellulose sheets were developed with 3,3′-diaminodiazobenzidine in PBST containing 30% H2O2. Immunohistochemistry (IHC) In all samples,

the technique was performed following standard procedures: paraffin embedded specimens were treated with 10 mM sodium citrate buffer pH: 6.0 at 100°C for 10 min and incubated overnight at 4°C with mouse anti-Lewis y and anti-MUC1 MAbs. Negative controls were incubated with PBS instead of Methane monooxygenase MAb. A final incubation with 1/400 peroxidase-conjugated goat anti-mouse IgM immunoglobulins (SIGMA, St. Louis, MO, USA) was performed. The chromogen employed was 3,3′-diaminodiazobenzidine (SIGMA, St. Louis, MO, USA) in 1%BSA/PBS containing 30% H2O2. Sections were examined by light microscopy and the antibody staining patterns were scored in a semiquantitative manner. Staining intensity was graded as negative (-), low (+), moderate (++), or strong (+++). The number of optical fields in a specimen that were positively stained was expressed as a percentage of the total number of optical fields containing tissue. The staining of cytoplasm, plasma membrane and nucleus was evaluated; cells were considered positive when at least one of these components was stained. The pattern of reaction was classified as linear (membrane reaction), cytoplasmic, or mixed (cytoplasmic and membrane) and the positive reaction in gland lumen content was identified as cellular debris or secretion. Apical and non-apical reactions were also considered [24].

Also, due to a sort of ionic contribution into the B-N chemical bonding and preferential B-N-B-N stacking across the tubular multilayers, a BNNT has a characteristically straight shape (opposed to CNTs, which are usually waved, entangled, and curled) which makes it easy to achieve effective BNNT dispersion and/or texturing in any given matrix. For more than a decade, our group has been working on such tubes and various composites made of them. Successfully fabricated polymer or ceramic-BNNT composites had indeed been reported [8–11]. Also, as the first try merging Al and BNNT functional

properties, we succeeded in the fabrication of the so-called ‘Al-BNNTs nanocomposites’ Ku-0059436 mouse using ion implantation and magnetron sputtering and carried out pioneering in situ tensile and bending tests on individual Al-BNNT composite structures in a high-resolution transmission electron microscope equipped with a piezo-driven manipulator [12]. As an outcome of these experiments, at least a nine-time increase in the tensile strength at room temperature was achieved on such nanocomposites compared

to non-reinforced Al samples. The regarded nanomaterials consisted of a single BNNT core (20 to 50 nm in diameter) covered with a rather thick Al shield (up to 300 nm). Thus, the next logic-driven step would be a try to design and to realize such lightweight BNNT-containing composites with meaningful dimensions (e.g., dozens of centimeter ranges) in which BNNTs are somehow distributed in a real crystalline Al matrix. As the initial step toward this goal, here, we report the first-time utilization of a melt-spinning technique to prepare BNNT-loaded Staurosporine cell line lightweight Al composite ribbons. Methods Multiwalled BNNTs were synthesized at a high yield (approximately 1 g per single Adenosine triphosphate experimental run) through the so-called boron oxide-assisted CVD (BOCVD) method, as was reported in our previous publications [9, 10, 12–14]. Figure 1 depicts low- and

high-resolution TEM images of the prepared BNNTs. The length of BNNTs was 1 to 5 μm, and their average external diameter was 40 to 50 nm. Figure 1 TEM characterization of synthesized BNNTs. (a) Representative low-magnification image of a BNNT ensemble. (b) High-resolution TEM image of an individual BNNT. After subsequent high-temperature purification in argon atmosphere, the nanotubes were dispersed in ethanol. The Al-BNNT composites were cast using a melt-spinning technique in argon atmosphere. Figure 2 shows a sketch of the fabrication procedure. Figure 2 Fabrication procedure of Al-BNNT composite ribbons. To disperse BNNTs well within an Al powder, the tubes were kept in ethanol during their mixing with the powder (50 to 150 μm, purity 99.5%). It was a very important step as some tube clustering may occur under powder mixing and further formed Al-BNNT pellets cannot be electrically conductive (BNNT fraction is an electrical insulator).

For instance, wpgrp1 and tollip genes are good regulator candidates and they could play a crucial role in this inhibition [76, 84]. Recently, Ryu et al. [75] have reported that the Drosophila homeobox gene caudal also regulates the commensal-gut bacteria by repressing the nuclear factor Kappa B-dependent AMP genes. Ongoing RNAi experiments will provide more information about the function and the regulation of these pathways in the Sitophilus system. The high accumulation of transcripts from Rab7, Hrs and SNARE genes could be viewed as being due to intense endosomal trafficking

within the bacteriocyte. These genes are certainly very involved in vesicle synthesis and fusion [62–64]. Moreover, intense vesicle trafficking has already been observed by electronic Neratinib microscopy within Sitophilus bacteriocytes [30]. Vesicle trafficking may aid in metabolic component exchanges between the host and the symbiont, or it may help in endosome fusion, with late endosomes and lysozomes, to favor autophagy. For the latter, we can speculate about the possibility that autophagy could serve as an additional host mechanism to regulate symbiont density. In support of this hypothesis, in silico cDNA comparison between symbiont-full and symbiont-free ovaries has shown

that vesicle trafficking is also highly represented in the presence of Wolbachia in the isopod Armadillidium vulgare [35]. Moreover, receptors of innate immunity have been identified on vertebrate endosome membranes [57, 87] and autophagy has been described as a possible means of eliminating intracellular pathogens [61]. To permanently sequester the Wnt tumor endosymbiont within the

bacteriome, and to avoid bacterial invasion into insect tissues, bacteriocyte cells need to maintain homeostasis and to survive during insect developmental stages. While apoptosis has been observed as a response to infection by a wide range of animal and plant pathogens [88, 89], very limited data are available on invertebrate symbiotic systems [70]. To tackle Dapagliflozin this question in the Sitophilus system, we have analyzed genes potentially involved in apoptosis inhibition (iap2 and iap3) and apoptosis execution (caspase-like). We have shown that the high expression of apoptosis inhibitor genes paralleled the low amount of caspase-like gene transcripts in the bacteriome. In addition to the upregulation of genes involved in cell growth, such as Ras and leonardo 14-3-3, these preliminary data suggest that weevil bacteriocytes manage to survive an endosymbiont infection by inhibiting the apoptosis pathway. Inhibition of apoptosis can also be mediated by the expression of the FK506BP gene (or FKBP). In vertebrates, the FKBP38 gene inhibits apoptosis by interacting with Bcl-2 [90]. Moreover, we cannot exclude the possibility that apoptosis inhibition is manipulated by the symbiont for its own survival.

4315 ± 1.2301 1.3524 ± 0.7102 0.001 GADD45β 3.2564 ± 1.5201 2.3472 ± 1.0526 0.056 GADD45γ 2.9562 ± 1.3458 2.0561 ± 1.0210 0.062 Table 4 The result of immunohistochemistry Tissue GADD45α-IRS > 5 GADD45α-IRS < 5 Tumor 18/20 2/20 Normal 0/20 20/20 The correlation between Selleck Galunisertib GADD45α mRNA and clinical pathological stages We evaluated the correlation between GADD45α mRNA expressions in the ESCC tissues with clinical pathological stages. We found that the relative GADD45a mRNA level was 1.8672 ± 1.26732 in ESCC tissues from clinical stages I. Moreover, in tissues from stages II, III and IV, the relative GADD45a mRNA levels were 4.0800 ± 1.30220,4.4936 ± 1.25856 and 4.3292 ± 2.69446

respectively. (Table 5 and Figure 1D). The presence of lymph node metastasis, and poor differentiation were associated with mRNA expression levels of GADD45a in ESCC (P = 0.007, P = 0.006, P = 0.010 and P = 0.005, respectively Table 6). Table 5 Correlation between the expression level of GADD45α mRNA and pTNM staging TNM stage Relative GADD45a mRNA P value I 1.8672 ± 1.26732 0.026 a 0.031b 0.029c II 4.0800 Lapatinib cost ± 1.30220 0.082 d 0.091e   III 4.4936 ± 1.25856 0.90 f     IV 4.3292 ± 2.69446       a was the result of compare between

stage I and II. b was the result of compare between stage Iand III.c was the result of compare between stage Iand IV. d was the result of compare between stage IIand III. e was the result of compare between stage II and IV. f was the result of compare between stage III and IV Table 6 Correlation between the expression level of GADD45α mRNA and clinic pathological factors   Total Relative GADD45a mRNA P Depth of invasion    T1/2 23 2.1683 ± 1.06534 0.007    T3/4

17 4.0265 ± 1.20145   Lymph node metastasis    N0 18 1.5682 ± 0.76238 0.006 a    N1 14 3.8326 ± 1.25123 0.010 b    N2/N3 8 4.8352 ± 1.81245. 0.005 c a was the result of compare between N0 and N1. b was the result of compare betweenN1 and N2/N3 c was the result of compare between stage N0 and N2/N3 Hypomethylation in promoter of GADD45α in ESCC We detected the methylation status of CG pairs in 181 bp (position-190 to -165) of GADD45α gene. Amplified fragments HSP90 were cloned and five clones were sequenced for each amplification product from each subject. Figure 2 A and B show the average methylation of each 11 CG pairs within the promoter region. The mean methylation status of most CG pairs was decreased in the tumor group; there were statistically significant difference in the overall combined mean methylation status between two groups (0.0545 ± 0.03067 vs 0.0255 ± 0.01788, P = 0.000). (Figure 2C). Figure 2 A and B show the mean methylation status of each CG pairs in the promoter region upstream of GADD45α gene in tumor tissue and adjacent normal tissue. Compared with adjacent normal tissue, the promoter region with 11 CG pairs (-158,-146,-135,-122,-116,-110,-104,-96,-91,-84, and-64 bp) upstream of GADD45α gene were hypomethylation in tumor tissue.

Each promoter has a control lane (-) that contains no protein, a binding reaction that contains either Ma or Mth MsvR (200 nM) in the absence of DTT (non-reduced, +), and a binding reaction that contains either Ma or Mth MsvR (200 nM) in the presence of 5 mM DTT (reduced, R). (c) EMSA assay (10 nM Ma P msvR DNA) with decreasing concentrations of reduced MaMsvR (5 mM DTT) [monomer] 1 μM, 500 nM, 250 nM, 125 nM, 62.5 nM, 31.3 nM, 15.6

nM, 7.8 nM, and 3.9 nM. (d) EMSA assay (10 nM Mth P msvR/fpaA DNA) with decreasing concentrations of reduced MaMsvR (5 mM DTT) [monomer] 1 μM, 500 nM, 250 nM, 125 nM, 62.5 nM, 31.3 nM, 15.6 nM, 7.8 nM, and 3.9 nM. (e) EMSA assay (10 nM Epigenetics inhibitor Mth P msvR/fpaA DNA) with decreasing concentrations of reduced MthMsvR (5 mM DTT) [monomer] 1 μM, 500 nM, 250 nM, 125 nM, 62.5 nM, 31.3 nM, 15.6 nM, 7.8 nM, and 3.9 nM. The observed promoter binding behavior of MaMsvR is consistent with the hypothesis that MaMsvR acts as a transcription repressor of Ma P msvR under reducing conditions. An oxidizing environment inhibits Ma P msvR binding, likely leading to derepression. A mechanism for MthMsvR is less clear. Under reducing conditions, BTK pathway inhibitors MthMsvR functions

as a transcription repressor in vitro, yet MthMsvR binds the promoter under both reducing and non-reducing conditions. To reconcile this apparent discrepancy, it has been proposed that MthMsvR follows a mechanism reminiscent of the well-characterized redox regulator, OxyR, which binds DNA irrespective Branched chain aminotransferase of redox status but has different effects on transcription under varying redox conditions [9, 26]. These effects would likely be regulated by conformational changes in MthMsvR between the oxidized and reduced states. However, addressing this experimentally has been problematic because of

both the limitations of the M. thermautotrophicus in vitro transcription system, which requires reducing conditions, and the complexity of the divergent promoter structure within Mth P msvR/fpaA . MaMsvR exhibits different DNA binding patterns than MthMsvR MaMsvR appears to produce higher molecular weight complexes on Mth P msvR/fpaA as movement of the DNA is further retarded in the gel compared to the shifted complex seen on Ma P msvR (Figure 2a, c, and d). Consistent with previously published data, MthMsvR binding to Mth P msvR/fpaA produced two distinct multiple shifted complexes, suggesting that varying stoichiometries of MthMsvR bound to Mth P msvR/fpaA (Figure 2b) [9]. In contrast, only one shifted complex was seen with MaMsvR (Figure 2a, c, and d). To determine if MaMsvR was capable of producing complexes of varying stoichiometry, increasing concentrations of MaMsvR were incubated with Ma P msvR (Figure 2c) or Mth P msvR/fpaA (Figure 2d). Even at concentrations of one hundred-fold excess MaMsvR over DNA, only a single shifted complex was observed for either promoter.

The forward primer Arch21F was shortened to match Sirolimus the new annealing temperature of the reverse primer. The cycle profiles had an initial 5 min at 95°C for Taq polymerase activation followed by denaturation at 94°C for 1 min, annealing at 58°C for 30 s and elongation at 72°C for 1 min. The annealing temperature was decreased 1°C every 3 cycles until reaching 55°C where the number of cycles was 30. The reactions were ended with a final elongation step

at 72°C for 7 min. Cloning The PCR-products of nine PCR replicates, generated from two DNA extraction replicates, were pooled and purified using Qiagen MinElute PCR Purification Kit (Qiagen). 8 ng and 15 ng of purified PCR-product were ligated into the plasmid vector pCR 4 TOPO (Invitrogen) in duplicate reactions. One Shot DH5alpha-T1R competent Escherichia coli cells (Invitrogen) were transformed with the vector constructs according to the manufacturer’s instructions in two separate reactions. The transformed cells were plated on LB-agar plates with 50 μg/ml Kanamycin

and incubated at 37°C over night. 95 cloned sequences were amplified directly from transformed single colonies from the two cloning reactions by PCR using the vector specific primers T3 (ATTAACCCTCACTAAAGGGA) and T7 (TAATACGACTCACTATAGGG). The bacterial cells were lysed by five minutes incubation at 94°C followed by PCR-cycles as described above but with a starting annealing temperature of 57°C. Sequencing and sequence analysis Cloned sequences were sequenced from see more both ends using Big Dye Sequencing Kit (Applied Biosystems) and primers T3 and T7 as sequencing primers. Sequence data was generated by capillary gel electrophoresis (3730 DNA analyzer, Applied Biosystems). Raw data sequences were manually inspected using SeqScape (Applied Biosystems). Sequences sequenced from different ends of the PCR-product were aligned using BioEdit (version 5.0.9) [61]. Consensus sequences were generated for 82 clones with overlaps between the 5’ and 3’ end sequences ranging from 80 to 496 bases. The sequences were aligned using the alignment tool of the SILVA rRNA database [26]

and checked for PDK4 chimeras using the Bellerophon server [62]. The sequences were also aligned with a reference E. Coli sequence, accession number U00096, and checked for chimeras using Mallard [63]. No chimeric sequences were detected with either of the two methods. The similarity between the 16S rRNA gene sequences was determined by generating a similarity matrix using the DNADIST program in the PHYLIP package [64]. The sequences were then assigned to OTUs based on different similarity thresholds. For Bacteria, 16S rRNA gene sequence similarities of 80%, 90%, 95% and 98.7% approximately represent the division in phylum, family/class, genus and species levels, respectively [23, 24], and we use the same criteria for Archaea.

s. is likely a synapomorphy Trichostatin A cost (Seitzman et al. 2011), though the fungus may not be entirely beneficial to its host (Agerer 2012). The habit of parasitizing bryophytes and different types of algae (i.e., in bryophilous and lichen-forming species) is likely involved in several adaptive radiations within subfamily Lichenomphalioideae, though the most basal group, (Arrhenia, tribe Arrheniae) is apparently free-living (Lawrey et al. 2009). The trophic habits for many Hygrophoraceae remains unknown, but circumstantial evidence from environmental sequencing projects suggests the possibility that Hygrocybe s.l.

and Cuphophyllus may obtain recent plant carbon as rhizosphere or endophytic symbionts. Fungal systematists, parataxonomists and fungal conservationists use named subgenera, sections and subsections in Hygrocybe s.l. Many authors, but especially PLX4032 chemical structure Donk (1962), Clémençon

(1982), Redhead et al. (1995, 2002, 2011), Kovalenko (1988, 1989, 1999, 2012), Candusso (1997) and Lawrey et al. (2011) were instrumental in verifying and publishing correct generic and infrageneric names and combinations in the Hygrophoraceae, and we hope we have corrected most of the remaining errors. Some systematists and many conservationists and parataxonomists primarily use infrageneric names in Hygrocybe rather than the segregate genera recognized in this paper. With the exception of Cuphophyllus, the use of Hygrocybe s.l. is not incorrect as long as Hygroaster is assigned an infrageneric rank in Hygrocybe, so we provide a dual nomenclature of Hygrocybe s.l. for all user groups. Cuphophyllus appears at the base of the Hygrophoraceae near the backbone of the Agaricales whereas Hygrocybe is terminal, so placing these in the same genus would require using the oldest genus name, Hygrophorus, for the entire family. Further work remains to be done in making new combinations, especially recombining species of Camarophyllus, Hygrocybe and Hygrophorus in Cuphophyllus. Many species previously believed to be amphi-Atlantic were found to not be conspecific Hydroxychloroquine manufacturer as they

belong to separate clades, and those that are not from the same region as the type locality will need new or resurrected names. Predominantly arctic-alpine taxa (e.g., Lichenomphalia spp.) likely are exceptions to this general trend, as they apparently are capable of frequent dispersals on a circumpolar scale (Geml et al. 2012). Sequencing more gene regions and new genes are needed to provide the basis for further higher level revisions, especially in Hygrocybe subg. Pseudohygrocybe, Gliophorus and Neohygrocybe in tribe Humidicuteae, and Cuphophyllus. Sequencing of more species is also needed in undersampled groups such as Humidicutis, Gliophorus, Neohygrocybe and Cuphophyllus, especially species from Australasia. The most basal species in several clades in our analyses are from the Australasian region, e.g., Porpolomopsis lewelliniae, Gliophorus graminicolor from Tasmania and a G.

However, consistent with our present data, a previous study on bladder cells suggested that adherence mediated by the PapG did not result bacteria internalisation [9]. Notably, the percentage Acalabrutinib ic50 of isolates expressing type 1 fimbriae is much lower in bacteraemia isolates than in urinary isolates (33% versus 56%). In contrast a higher percentage expressing P fimbriae was seen (60% versus 12.5%) in bacteraemia isolates. It is likely that ‘crosstalk’ occurs between the regulators of the different fimbrial systems in pathogenic E. coli. Classically pyelonephritis strains are more likely to contain and express P fimbrial gene clusters and therefore down-regulate type 1 fimbriae expression [23]. This may explain the

different patterns of clinical

infection caused by different strains of E. coli. Conclusion Type 1 fimbriae mediated-binding is essential for C3-dependent internalisation. We do not know whether this is a co-operative, synergistic action or the additive activities of two factors. Since, FimH alone can mediate intra-cellular invasion, we suggest that the C3 opsonisation augments the signalling initiated by FimH-mediated Selleckchem RXDX-106 binding (Figure 5). Studies to analyse the mechanism by which C3 receptor(s) (CD46) and the receptors for FimH interact are important to fully understand invasion of human urinary tract by pathogenic E. coli. Figure 5 Diagram showing possible involvement of both CD46 and type 1 fimbrial receptor signalling in the internalisation of E. coli by PTECs. Internalisation of E. coli is initiated by type 1 fimberiae mediated adhesion to epithelium mannosylated glycoproteins receptor. This may be sufficient to induce internalisation Epothilone B (EPO906, Patupilone) alone. However, during UTI, E. coli can be opsonised by urine C3 in urinary tract space. C3b bound on bacteria surface interact with cell surface expressed CD46. This C3b-CD46 interaction could activate host cells and augments the direct interaction of fimH with manosylated receptor resulting in a high internalisation. Inhibition and FimH mutant experiments indicate that non-opsonic

interactions are necessary for E. coli adherence to and invasion of PTECs. Acknowledgements This work was founded by a Wellcome Trust grant and the Welton Foundation. Cystitis isolate NU14 and the isogenic mutant were kindly provided by Dr. Scott Hultgren. We also thank Dr. Jonathan Edgeworth for providing E. coli isolates. References 1. Foxman B, Barlow R, D’Arcy H, Gillespie B, Sobel JD: Urinary tract infection: self-reported incidence and associated costs. Ann Epidemiol 2000, 10:509–515.CrossRefPubMed 2. Foxman B: Recurring urinary tract infection: incidence and risk factors. Am J Public Health 1990, 80:331–333.CrossRefPubMed 3. Ivanyi B, Rumpelt HJ, Thoenes W: Acute human pyelonephritis: leukocytic infiltration of tubules and localization of bacteria. Virchows Arch A Pathol Anat Histopathol 1988, 414:29–37.CrossRefPubMed 4.

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