CrossRef 30. Graf BL, Raskin I, Cefalu WT, Ribnicky DM: Plate-derived therapeutics for the treatment of metabolic syndrome. Curr Opin Investig Drugs 2010, 11:1107–1115.PubMedCentralPubMed 31. Harris RC, Soderlund K, Hultman E: Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Clin Sci (Lond) 1992, 83:367–374. Competing interests Martin Bauer Group, Finzelberg GmbH & Co. KG. provided funding for this study through a research grant to Texas A&M University. CX-6258 datasheet All researchers
involved independently collected, analyzed, and interpreted the results from this study and have no financial interests concerning the outcome of this investigation. RBK has received grants as Principal Investigator through EPZ015938 price institutions with which he has been affiliated to conduct exercise and nutrition related research, has served as a legal and scientific consultant, and currently serves Nutlin-3a research buy as a scientific consultant for Woodbolt International (Bryan, TX). MP, IP, and RJ have been named as inventors on pending patents by the Martin Bauer Group. Remaining co-authors have no competing interests to declare. Data from this study have been presented at the International Society of Sports Nutrition Annual meeting and have not been submitted for publication to any other journals. Publication of these findings should not be viewed
as endorsement by the investigators or their institutions of the nutrients investigated. Authors’ contributions JMO served as the study coordinator, oversaw all testing, and assisted in data analysis and writing of the manuscript. ARJ assisted in data collection and statistical analysis. IP, RJ, and MP assisted in the experimental design, data analysis, and manuscript preparation. AS assisted with data collection JF and SR supervised the biopsy procedures. MG assisted Ergoloid in experimental design, data analysis, and manuscript preparation. KK supervised muscle assays
and CM served as a collaborating scientist. CR served as lab coordinator and oversaw data collection and quality control of the study. RBK served as Principal Investigator and contributed to the design of the study, statistical analysis, manuscript preparation, and procurement of external funding. All authors read and approved the final manuscript.”
“Background Hepatocellular carcinoma (HCC) is a leading cause of cancer death worldwide, and the presense of intraheptatic metastases at the time of surgery has been regarded as the main causes of recurrence . The cancer cells readily disseminate via portal venous branches and patients with multiple tumor nodules in liver are proved to have poor prognosis . Multiple hepatocellular carcinoma is usually regarded as HCC with multiple tumor nodules, clinically classified as either intrahepatic metastasis or multicentric carcinogenesis .
We noticed that her ankle pain disappeared Alpelisib molecular weight once she had resumed walking. Radiography and computed tomography images revealed that union of the ankle had been achieved (Fig. 2c, d). No side effects attributable to the drug were observed during treatment, and her subsequent laboratory findings continued to be normal. At 6 months, the patient could walk without a brace and without any pain. Plain images taken at this time revealed complete healing of the fractured and nonunion sites. Discussion A major problem for patients with chronic diabetes mellitus is the development of peripheral neuropathy. Sensory loss leads to
neuropathic ulceration, which is aggravated in the presence of foot and ankle deformities and causes excessive pressure on deformed areas, a condition that is known as Charcot arthropathy or diabetic ankle [5, 6]. The main aims when treating Charcot arthropathy of the foot and ankle
are to correct the deformity so that there is an appropriate distribution of pressure for healing and to prevent skin ulceration . Surgical correction with internal fixation for Charcot arthropathy is associated with a high rate of complications and failure because of infection, bone softening, resorption, fragmentation, and breakage of the implant . Our patient with severe Type selleck inhibitor I diabetes mellitus and Charcot arthropathy had undergone two failed operations. Ankle union was not achieved even after the second operation, and the patient sustained a femoral shaft fracture. Nonunion is a severe complication and has a negative impact on the quality of life; undoubtedly, a second intervention is therefore necessary, but it is not exempt from further risks and potential
complications . It is therefore important that some treatment that can resolve this problem should be undertaken, but a third surgery to fix nonunion is extremely difficult as the ankle needs to be stabilized and the bone needs to be strengthened. Teriparatide (rhPTH 1–34) is an anabolic agent that is administered subcutaneously. Its anabolic effect is attributable to the stimulation of osteoblasts, which causes a net increase in both cancellous Janus kinase (JAK) and cortical bone, thus improving the bone architecture [10, 11]. Teriparatide has different effects on trabecular and cortical bone. Because of the high degree of PRI-724 nmr remodeling and apoptosis of trabecular bone osteoblasts, teriparatide has a more profound effect on trabecular than on cortical bone, which has a lower degree of osteoblastic apoptosis . Teriparatide also accelerates fracture healing by improving the biomechanical properties of the fracture callus and by increasing endochondral ossification and bone remodeling in animal models . This effect has also been observed in several other clinical case reports [12–14].
These patterns (SB1763–1767) reveal BB-94 supplier deletion events that could have lead to new spoligotype patterns evolving, as was the case in Portugal . However, more detailed studies need to be conducted to fully ascertain this assertion. The sharing of grazing land in the Kafue Basin in Zambia between cattle and Kafue lechwe antelopes (Kobus leche Kafuensis), considered as wildlife biological reservoir hosts for BTB, might explain
the high prevalence levels found in this setting [3, 4, 6, 33]. Underlying factors in sustaining the infectious agent depend on the temporal and spatial distribution between the source of infection and the susceptible animals, which also are a function of the duration of interaction between the agent, the susceptible host and its environment . The underlying factors for BTB transmission between the Lechwe antelopes and cattle are reported to be optimal in the Kafue Basin [3, 6], although further investigations at molecular level will be necessary
to elucidate this relationship. The tracing of livestock movement patterns from their areas of origin to major abattoirs is important in understanding selleck compound possible disease dispersion patterns. Cattle traders trek for days from areas within and around the Kafue Basin to abattoirs in the nearby districts. In our study, we observed that identical and closely related strains were also found in other districts. These Thiamet G findings PRI-724 suggest the sharing of strains between districts, a finding which is important when determining BTB localization or spread. Namwala district (the only district right in the Kafue Basin)  was found to have more
isolates than any other district. The practice of allowing trekking animals to spend one or more nights in different kraals during the journey to abattoirs may partially be responsible for the dissemination of the infectious organisms. This pattern of animal movements may to a greater extent be responsible to the observed dispersion of spoligotype patterns suggestively, based on our results from the Namwala district zones to other surrounding districts. However, these results need to be interpreted with caution considering limitations related to the survey period and sample size related to limited resources and time constraints. This makes the results a bit difficult to interpret when inferring to the entire region given the representativeness of the sample size. In addition, the spoligotyping technique has weaknesses in that it has a low discriminatory power  which may result in low specificity of some patterns with a possibility of grouping strains that might not be identical when typed by other methods. However, the results obtained in this study give an indication of M. bovis strains in cattle with an insight in the likely role that cattle movements have on the dissemination of the disease.
Conjugation was carried out on LB agar plates overnight with a bacterial proportion of 4:1 of E. coli containing conjugative plasmid (donor) and V. cholerae as recipient strain. Bacterial cultures (mixed E. coli and V. cholerae) were plated on LB agar plate containing Carb (100 μg/ml) and Km (30 μg/ml) for selection of V. cholerae transconjugants carrying the plasmid. The removal of vector backbone from V. cholerae genome was achieved by favoring the homologous recombination Sapanisertib and use of lethal sacB gene while passaging the transconjugants in sodium chloride free LB medium supplemented with 10% sucrose. Attempts for construction of a kdpD knockout mutant using V. cholerae
strain NM06-058 The gene VC_A0531 encodes for the histidine kinase KdpD in V. cholerae and is flanked by the genes VC_A0530 encoding ��-Nicotinamide pyruvate-flavoredoxin oxidoreductase and VC_A0532 encoding response regulator KdpE homologue S3I-201 solubility dmso of E. coli. To generate a VC_A0531 deletion mutant, two fragments were amplified from the small chromosome of the wild type strain NM06-058 using two primer
pairs (i) kdpD_del_forw_1 / kdpD_del_rev_1 and (ii) kdpD_del_forw_2 / kdpD_del_rev_2. Using the first primer pair an approximately 600 pb fragment of gene VC_A0530 was amplified with a 24 bp homolog overhang to the start region of the VC_A0532 at the C-terminus. The second primer pair was used to amplify an approximately 400 bp fragment of the gene VC_A0532 with a 16 bp overhang homolog to the end region of the VC_A0530 at the N-terminus. Both amplicons were mixed together at equimolar ratio and a re-PCR was carried out with a combination of primers learn more kdpD_del_forw_1 and kdpD_del_rev_2 to generate an amplicon with a size of approximately 1,000 bp. The restriction of vector pEX18Ap and the insert was carried out with XbaI and PstI. After ligation and transformation into E. coli S17-1, a conjugation into the wild type V. cholerae strain NM06-058 was mediated according to the protocol described above. The cloning strategy was successful until transconjugation according selection on Carb / Km agar plates and sequencing, but homolog recombination attempts
with V. cholerae strain NM06-058 did not yield viable strains with deleted kdpD gene. Acknowledgments Authors thankfully acknowledge helpful technical assistance from Subhasis Barik. We thank the Indian Council of Medical Research (ICMR), Govt. of India and for funding support through the Indo-German Science Centre (Sanction No. TDR/491/2008-ECD-II). SR is recipient of a Junior Research Fellowship from the Council of Scientific and Industrial Research (CSIR), Govt. of India (Sanction No. 09/482(0054)/2010-EMR-I). References 1. WHO: Cholera. Fact sheet No 107 2011. http://www.who.int/mediacentre/factsheets/fs107/en/ 2. Kitaoka M, Miyata ST, Unterweger D, Pukatzki S: Antibiotic resistance mechanisms of Vibrio cholerae. J Med Microbiol 2011,60(4):397–407.PubMedCrossRef 3.
Incubation proceeded for 1 h at 37°C. After three washings with PBS – T, 100 μL of a 1:5,000 dilution of HRP – conjugated goat anti – mouse IgG (Sigma) in PBS was added per well for 1 h at 37°C. The wells were washed three times, and o – phenylenediamine (OPD) (1 mg/mL) in citrate phosphate buffer (pH 5.0) plus 1 μL/mL H2O2 was added (100 μL per well). The reaction proceeded for 10 min and was interrupted by the addition of 50 μL of 4 N H2SO4. The absorbance at 492 nm was determined in a microplate reader (TP – reader, Thermo). For statistical analyses, the binding of recombinant proteins to ECM macromolecules
A-1210477 chemical structure and to serum components were compared to its binding to gelatin and by Student’s two – tailed t test. Metaperiodate treatment of XAV-939 in vitro laminin Microtitre wells were coated with 1 μg of laminin in 50 mM sodium acetate buffer, pH 5.0, and incubated for 16 h at
4°C. Wells were washed three times with the same buffer, and laminin was treated with different sodium metaperiodate concentrations (0–100 mM) in the same buffer for 15 min at 4°C in the dark. After three washes with 50 mM sodium find more acetate buffer, wells were blocked with 200 μl of 1% BSA for 1 h at 37°C. Binding of recombinant proteins (1 μg in PBS per well) to periodate – treated laminin was evaluated as described above. Dose–response curves First, 96 – well plates were coated overnight in PBS at 4°C with 100 μl of 10 μg/ml PLG, laminin or C4bp. Plates were then blocked and increasing concentrations of the purified recombinant proteins (0–6 μM) were added (100 μl/well in PBS). The assessment of bound proteins was performed by incubation
for 1 h at 37°C with the antiserum raised against each protein at the dilution of 1:750, followed by HRP – conjugated goat anti-mouse IgG (Sigma) (1:5,000 in PBS). The reactions were detected with OPD as describe above. The ELISA data were used to calculate the dissociation constant (KD) according to the method described by tuclazepam Pathirana et al.  and Lin et al. , based on the equation: , where A is the absorbance at a given protein concentration, Amax is the maximum absorbance for the ELISA plate reader (equilibrium), [protein] is the protein concentration and KD is the dissociation equilibrium constant for a given absorbance at a given protein concentration (ELISA data point). Plasmin enzymatic activity assay 96 – well ELISA plates were coated overnight with 10 μg/ml recombinant proteins in PBS at 4°C. Lsa63, which does not bind PLG  and BSA were employed as negative control. Plates were washed once with PBS – T and blocked for 2 h at 37°C with PBS with 10% (wt/vol) non – fat dry milk. The blocking solution was discarded and 100 μl/well of 10 μg/ml human PLG was added, followed by incubation for 2 h at 37°C. Wells were washed three times with PBS – T, and then 4 ng/well of human uPA (Sigma – Aldrich) were added.
Figure 3 H. pylori grown without cholesterol fail to colonize gerbils. H. pylori strain SS1 was grown overnight in defined medium containing 0 or 50 μg/ml cholesterol. Gerbils were orally inoculated with 3.5 × 108 CFU (experiment A) or 1 × 108 CFU (experiment B). H. pylori in gastric antrum were quantitated at 11 days. Each vertical bar represents the mean of duplicate
determinations for one animal, and horizontal lines give the median for each treatment group. Where no colonies were recovered, values were recorded as 5 × 102 CFU/g tissue, the estimated limit of detection. Certain strains of H. pylori exhibited significant differences in adherence to culture vessels following passage in cholesterol, suggesting alterations in their cell ICG-001 cost surface properties (Hildebrandt & McGee, unpublished observations). For this reason, we decided to investigate Tipifarnib cell line lipopolysaccharides, which constitute the principal component of the cell envelope, and serve to present the biologically important Lewis antigens. We employed a well established whole-cell click here ELISA procedure to quantitate the predominant Lewis antigens, Lewis X and Y (Figure 4). In accordance with the literature [54, 55], primarily Lewis X was detected in strain 26695, only Lewis Y was detected
in SS1, and significant levels of both were detected in G27. In each case, absorbance readings were nonlinear with respect to sample load, an occurrence that is not unusual in ELISA assays , and that has been noted by other investigators using these same monoclonals . Thus, in order to compare antigen levels in samples of H.
pylori cultured in the absence or presence of cholesterol, we performed parallel titrations over a range of sample loadings varying from 20 to 500 ng of cell protein per well. These titrations reproducibly showed a marked increase in the amount of Lewis X and/or Lewis Y antigen detected on the cell surface when H. pylori strains Interleukin-3 receptor 26695, SS1 or G27 were cultured in the presence of cholesterol (Figure 4). In replicate independent experiments, the mean cholesterol-dependent increases were statistically significant (Table 2). Comparable results have also been obtained for Lewis X in strain 43504 (data not shown). Spiking samples with cholesterol at the end of the growth period did not alter the amount of Lewis antigen detected by ELISA (Figure 5A). In another control experiment we verified for all four of these strains that the amount of cell protein bound to the wells was unaffected by growth in cholesterol (Figure 5B). The ELISA results thus established that increased surface expression of Lewis antigens was a legitimate biological response to cholesterol that occurred in all of the strains tested. This response was specific for cholesterol, because substitution of cholesterol in the growth medium with the structural analogs β-sitosterol or sodium taurocholate had no effect on Lewis X or Y expression by G27 (Figure 4, righthand panels, and Table 3).
The most distinctive feature of these Gram-positive bacteria is the unique composition of the cell envelope, characterized by Selleck Belnacasan the presence
of long chain fatty acids, known as mycolic acids, on the surface of the cell [1, 2]. The main recognizable disease caused by C. pseudotuberculosis is caseous lymphadenitis (CLA) in sheep and goats, though this bacterium can also infect several other hosts, including humans [1, 3]. Typical manifestations of CLA in small ruminants include formation of abscesses in superficial and internal lymph nodes, and in visceral organs . Despite the important economic losses caused by this disease to sheep and goat husbandry worldwide, no Selumetinib datasheet effective treatment exists, and the efficacy of the currently available vaccines and diagnostic methods is still controversial . The search for C. pseudotuberculosis molecular determinants that contribute to CLA pathogenesis lead to the recognition of two exported proteins as the major virulence-associated factors of this bacterium known to date: a secreted phospholipase D (PLD) ; and an ABC-type transporter component of an iron uptake system (FagB) .
In fact, one might expect that the majority of the virulence determinants of C. pseudotuberculosis would be present in the exoproteome, i.e. the entire set of bacterial proteins Adriamycin found in the extracellular milieu . This is because exported proteins participate in essential steps of the host-pathogen interplay, including: (i) adhesion to host cells; (ii) invasion;
(iii) damage to host tissues; (iv) resistance to environmental stresses during infection; and (iv) subversion of the host’s immune response mechanisms [8–10]. In two previous attempts to characterize the C. pseudotuberculosis exoproteome, our group optimized a protocol of salting out of proteins using sulfate and butanol, known Cyclin-dependent kinase 3 as three-phase partitioning (TPP), for isolation of the extracellular proteins of this bacterium , and generated a library of C. pseudotuberculosis mutant strains possessing transposon insertions in genes coding for probable exported proteins . In the former study, we were able to determine the optimal conditions for obtaining the best recovery of immunoreactive extracellular proteins of C. pseudotuberculosis . The second study in turn, enabled us to identify various previously uncharacterized C. pseudotuberculosis exported proteins, being that at least two of them are apparently involved in virulence . Now, the very recent conclusion of the C.
GAS is characteristically associated with significant human morbidity and it is responsible for the clinically common superficial throat and skin infections, such as pharyngitis and impetigo, as well as invasive soft tissue and blood infections like necrotizing fasciitis and toxic shock syndrome . Although GAS biofilm has not been
associated with implanted medical devices, tissue microcolonies of GAS encased in an extracellular matrix were demonstrated in human clinical specimens . Studies reported to date support the involvement of GAS surface components in biofilm formation, including PF-02341066 purchase the M and M-like proteins, hyaluronic acid capsule, pili and lipoteichoic VRT752271 acid [11–13]. As shown by Cho and Caparon , multiple genes are upregulated during biofilm formation and development, including the streptococcal collagen-like protein-1 (Scl1).
The scl1 gene encoding the Scl1 protein has been found in every GAS strain investigated and its transcription is positively regulated by Mga [14–18], indicating that Scl1 is co-expressed with a number of proven virulence factors. Structurally, the extracellular portion of Scl1 protein extends from the GAS surface as a homotrimeric molecule composed of distinct domains that include the most outward N-terminal variable (V) region and the adjacent collagen-like (CL) region composed of repeating GlyXaaYaa (GXY) sequence. The this website linker (L) region is close to the cell surface and contains a series of conserved direct repeats. The Scl1 protein can bind selected human extracellular matrix components  and cellular integrin receptors [20–22],
as well as plasma components [23–27]. In this study, we investigated the importance of Scl1 in GAS biofilm using defined isogenic wild-type and scl1-inactivated mutant strains of GAS. We report that (i) the pathogenically diverse M41-, M28-, M3- and M1-type GAS wild-type strains have varying capacities to produce biofilm on an abiotic surface; Ribonucleotide reductase (ii) Scl1 plays an important role during the main stages of biofilm formation with Scl1-negative mutants having an abrogated capacity for adhesion, microcolony formation and biofilm maturation; and (iii) variations in surface morphology as well as in extracellular matrix associated with bacterial cells suggest two distinct but plausible mechanisms that potentially stabilize bacterial microcolonies. We additionally show that expression of Scl1 in Lactococcus lactis is sufficient to support a biofilm phenotype. Overall, this work reveals a significant role for the Scl1 protein as a cell-surface component during GAS biofilm formation among pathogenically varying strains.
The active form of Rab5 in the cell lysates was subjected by a GST-R5BD pull-down assay and was RG-7388 analyzed by Western blotting. Level of the active form of Rab5 induced by TNF-α was not affected by treatments with SB203580 and PD98059. However, treatment with SP60015 decreased the level of the active form of Rab5 induced by TNF- (Figure 8A, B). These results suggest that JNK kinase mediates activation of Rab5 by stimulation with TNF-α. Furthermore, we invastigated whether
NF-kB inhibition affects the activation of Rab5. Ca9-22 cells were transfected with an expression vector with an inserted GFP-Rab5 gene. The transfected cells were preincubated with an NF-κB inhibitor (PDTC, 5 μM) at 37°C for 1 h and were then incubated with TNF-α for 3 h. The active form of Rab5 in the cell lysates MK5108 solubility dmso was subjected to a GST-R5BD pull-down assay and was analyzed by Western blotting with anti-GFP antibodies. Treatment with PDTC also
did not affect the level of the active form of Rab5 induced by TNF- (Figure 9A, B). These results suggest that NF-κB does not mediate activation of Rab5 by stimulation with TNF-α. Figure 8 TNF-α was associated with activity of Rab5 through the JNK pathway. (A) Ca9-22 cells were transfected with an expression vector with inserted GFP-Rab5 Givinostat purchase gene. The transfected cells were preincubated with MAP kinase inhibitors, including a p38 inhibitor (SB203580, 5 μM) (indicated as “SB”), JNK inhibitor (SP600125,
1 μM) (indicated as “SP”) and ERK inhibitor (PD98059, 5 μM) (indicated as “PD”), at 37°C for 1 h and were then incubated with TNF-α for 3 h. The active form of Rab5 in the cell lysates was subjected to a GST-R5BD pull-down assay and was analyzed by Western blotting with anti-GFP antibodies as described in Methods. (B) Level of the active form of Rab5-GTP was normalized to total GFP-Rab5 and quantified by a densitometer. (Means ± deviations [SD] [n = 3]). *, P < 0.05 versus control. Figure 9 TNF-α was not PAK6 associated with activity of Rab5 through the NF-κB pathway. (A) Ca9-22 cells were transfected with an expression vector with an inserted GFP-Rab5 gene. The transfected cells were preincubated with an NF-κB inhibitor (PDTC, 5 μM) at 37°C for 1 h and were then incubated with TNF-α for 3 h. The active form of Rab5 in the cell lysates was subjected to a GST-R5BD pull-down assay and was analyzed by Western blotting with anti-GFP antibodies as described in Methods. (B) Level of the active form of Rab5-GTP was normalized to total GFP-Rab5 and quantified by a densitometer. (means ± deviations [SD] [n = 3]). TNF-α increased colocalization of P. gingivalis with ICAM-1 and Rab5 Finally, we examined the relationships among P. gingivalis, ICAM-1 and Rab5 in Ca9-22 cells.
Figure 2 MsrA/MsrB is induced upon overexpression of rpoE via transcriptional control. Protein Fosbretabulin mouse analysis of the cytoplasmic and crude membrane fraction by SDS-PAGE (A) and corresponding transcriptional analysis of msrA/mrsB by RT-PCR (B) of the wt strain (H44/76) and H44/76 transformed with pNMB2144 before (-) and after induction (+). Molecular weight markers (in kDa) indicated on SCH772984 cost the left. Arrow indicates MsrA/MsrB. MsrA/MsrB is transcriptionally controlled
by σE To ascertain that msrA/msrB is under direct control of σE, transcript levels of msrA/msrB in diverse meningococcal genetic backgrounds were analyzed by RT-PCR using RNA isolated from cells grown in the absence and presence of IPTG and primers targeting msrA/msrB. When H44/76 wt or H44/76 + pNMB2144 cells were grown in the absence of IPTG, no detectable RT-PCR products were observed. In contrast, when H44/76 + pNMB2144 cells were grown in the presence of IPTG, an RT-PCR product with a size indicative of transcription of msrA/msrB was found
(Fig. 2b). The identity of the transcript was confirmed by sequencing of the RT-PCR product. These results strongly suggest that msrA/msrB is transcriptionally controlled by σE. NMB2145 inhibits transcription of the rpoE regulon One possible explanation for low σE activity in H44/76 wt cells under the growth conditions tested is that σE is kept in an inactive selleck kinase inhibitor state through an interaction with an anti-σ factor, thereby preventing σE binding to core RNA polymerase, one of the ways to inhibit σ activity Dimethyl sulfoxide found in σ-regulator circuits in other bacteria [43–47]. Interestingly, it was
recently reported that NMB2145 contains the ZAS motif Hisx3Cysx2Cys , characteristic for a subset of group IV σ anti-σ factors, usually encoded directly downstream of rpoE and cotranscribed . Amino acid sequence comparison of orthologues of NMB2145 in genomes of three other meningococcal strains, two gonococcal strains and six commensal neisserial species (N. cinerea, N. flavescence, N. lactamica, N. mucosa, N. sicca and N. subflava) revealed that the region containing the ZAS motif, as well as the region around Cys4, are highly conserved in these neisserial orthologues of NMB2145. This in contrast with other much less well conserved parts, highlighting the importance of the conserved regions (Fig. 3). The relative positions of the Cys residue and the ZAS motif in NMB2145 (Cys4; His30, Cys34 and Cys37) correspond exactly with those of the Cys residue and the ZAS motif in RsrA (Cys11; His37, Cys41 and Cys44), the anti-σR factor of Streptomyces coelicolor, of which the Cys residues, but not His37, are essential for anti-σ activity of the protein  (Fig. 3). These observations suggest that NMB2145 codes for the meningococcal anti-σE factor.