Despite wide expression and involvement in multiple pathological conditions, the lack of OPN in mice is not embryonically lethal nor does it

causes a prominent phenotype compared to wild type mice suggesting that alternative mechanisms compensate for the lack of OPN or it may not play a key role in embryonic development [44]. One of the main challenges in characterizing role of OPN in tumor progression is the existence of two distinct families of receptors including integrins and CD44v6 OSI 906 that have the capacity to trigger downstream signaling pathways independent of each other. Therefore, inhibition of one of the two receptors/pathways may not completely suppress OPN signalling and development of therapeutic compounds to inhibit both receptors is extremely challenging if not impossible. In the tumor mass, OPN is secreted by both stroma and cancer cells [36]. It appears that there are distinct functions for tumor-derived vs. stromal-derived OPN in tumor growth and metastasis. Crawford et al developed a model of cutaneous squamous cell carcinoma in OPN null mice and showed that while the number of metastatic tumors is increased Selleckchem eFT508 in this model, the size of metastasized tumors was significantly lower

compared to corresponding wild type mice [45]. It is suggested that stromal OPN may recruit anti-tumor macrophages resulting in smaller tumor growth [45]. However, other reports in melanoma [46] and breast [47] tumors suggest that host-derived OPN is important r for tumor growth and metastasis adding to the complexity of OPN in tumor biology. Here, we developed an anti-OPN antibody capable of neutralizing human and mouse OPN, and utilized it to investigate the role of OPN in preclinical models with particular focus on lung cancer since a significant amount of data supports a role for OPN in NSCLCs [48]. All three transcripts of OPN have been identified in NSCLC patients

and gain-of-function analyses indicate that OPNa, but not OPNb or OPNc, is involved in increased proliferation, migration, and invasion of tumor cells [49]. Serum OPN has been shown to act as a biomarker in lung carcinoma [38, 50]. Conversely, reduction in serum OPN (e.g. due to resection of primary Depsipeptide research buy tumors) [51] is an indicator of better outcome in NSCLC patients treated with cytotoxic agent [52]. Despite all these reports, it remains to be clearly determined if OPN is a biomarker and/or a driver of tumor progression in NSCLC. The KrasG12D-LSLp53fl/fl mice [53] is one of the most relevant preclinical models of NSCLC since 20-30% of NSCLC patients carry Kras mutation [54] and 35-60% show genetic aberrations in p53 [55]. Capacity of tumor fragments to engraft in immuno-deficient animals provided an opportunity to test efficacy of AOM1 in NSCLC tumors. Lack of response to AOM1 in primary tumor growth indicates an overlapping mechanism between OPN and the other tumor-promoting factors.

Authors’ contributions SZR fabricated and measured the cross-point memory devices under the instruction of SM. SM arranged and finalized the manuscript. Both authors contributed to the preparation and revision of the manuscript and approved it for publication.”
“Background In the last decades, semiconductor quantum dots (QDs) have been extensively investigated because they are attractive

structures for electronic and optoelectronic advanced devices [1–3]. The characteristics of these QDs can be modified by controlling the growth parameters in order to fulfil the requirements of each device. Often, well-ordered and similar-sized QDs are required in order to take advantage of their discrete energy levels for intermediate band solar cells [4], lasers [5], and photodetectors [6]. This order can be achieved by stacking CA3 chemical structure several layers of QDs forming a QD matrix or superlattice. During the epitaxial growth, the strain fields of the buried QDs have

a large influence in the formation of the subsequent CX-5461 purchase layer as it determines the nucleation sites of the incoming stacked QDs [7, 8]. The complex strain fields around a QD can produce vertical or inclined alignments [9, 10], anti-alignments [11], or random distributions of the QDs [12], having a strong effect on the optoelectronic behaviour [13]. The simulation of the strain–stress fields in a semiconductor material in order to predict the location of stacked Ribonucleotide reductase QDs lead to a better understanding of the behaviour of these complex

nanostructures. The finite elements method (FEM) is a widespread tool to calculate the strain and stress fields in semiconductor nanostructures, and it has been used in the study of QDs [11, 14, 15], QRings [16], or QWires [17]. In order to obtain reliable predictions by FEM, the simulations should be based in experimental composition data, because of the large impact of the concentration profile of the QD systems in the strain of the structure [18]. However, because of the difficulties in obtaining three-dimensional (3D) composition data with atomic resolution, many authors use theoretical compositions [11, 19], or two-dimensional (2D) experimental composition data (obtained by electron energy loss spectroscopy [20] or extrapolating composition concentration profiles measured by the lattice fringe analysis technique [21]). This makes a direct correlation between the predictions and the experimental results unfeasible, and prevents from verifying the accuracy of FEM in predicting the nucleation sites of QDs. To solve this, 3D composition data with atomic resolution should be collected. One of the most powerful techniques to obtain 3D composition data is atom probe tomography (APT).

Epidemiol Infect 2009, 137:1217–1232.PubMedCrossRef 10. Pol M, Ruegg PL: Relationship between antimicrobial drug usage SN-38 in vivo and antimicrobial susceptibility of gram-positive mastitis pathogens. J Dairy Sci 2007, 90:262–273.PubMedCrossRef 11. LeJeune JT, Christie NP: Microbiological quality of ground

beef from conventionally-reared cattle and “”raised without antibiotics”" label claims. J Food Prot 2004, 67:1433–1437.PubMed 12. Alexander TW, Yanke LJ, Topp E, Olson ME, Read RR, Morck DW, McAllister TA: Effect of subtherapeutic administration of antibiotics on the prevalence of antibiotic-resistant Escherichia coli in feedlot cattle. Appl Environ Microbiol 2008, 74:4405–4416.PubMedCrossRef 13. Canadian Council of Animal Care: [http://​www.​ccac.​ca/​en/​CCAC_​Programs/​Guidelines_​Policies/​GUIDES/​ENGLISH/​toc_​v1.​htm] In Guide to the Care and Use of Experimental Lazertinib concentration Animals.

2nd edition. Edited by: Olfert ED, Cross BM, McWilliam AA. CCAC, Ottawa, Ontario Canada; 2003., 1: [online] 14. Diogo A, Verissimo A, Nobre M, da Costa MS: Usefulness of fatty acid composition for differentiation of Legionella species. J Clin Microbiol 1999, 37:2248–2254.PubMed 15. Clinical and Laboratory Standards Institute: Performance Standards for Antimicrobial Susceptibility Testing, 18th Informational Supplement. M100-S18, Wayne, PA; 2008. 16. National Clinical and Amine dehydrogenase Laboratory Standards Institute: Methods for Dilution Antimicrobial Susceptibility Tests for Bacteria That Grow Aerobically; Approved Standard – 6th Ed: Approved standard M7-A6. Villanova, PA, USA; 2003. 17. Canadian Integrated Program for Antimicrobial Resistance Surveillance (CIPARS): [http://​www.​phac-aspc.​gc.​ca/​cipars-picra/​pdf/​cipars-picra-2005_​e.​pdf] 2005 Annual Report. 2005. [online] 18. Mirzaagha P, Louie M, Read RR, Sharma R, Yanke LJ, Topp E, McAllister TA: Characterization of tetracycline- and ampicillin-resistant Escherichia coli isolated from

the feces of feedlot cattle over the feeding period. Can J Microbiol 2009, 55:750–761.PubMedCrossRef 19. Center for Disease Control and Prevention: PulseNet USA One-Day (24–28 h) Standardized Laboratory Protocol for Molecular Subtyping of Escherichia coli O157:H7, Non-typhoidal Salmonella Serotypes, and Shigella sonnei by Pulsed Field Gel Electrophoresis (PFGE). [http://​www.​cdc.​gov/​pulsenet/​protocols/​ecoli_​salmonella_​shigella_​protocols.​pdf] 2004. 20. Sharma R, Munns K, Alexander T, Entz T, Mirzaagha P, Yanke LJ, Mulvey M, Topp E, McAllister T: Diversity and distribution of commensal fecal Escherichia coli bacteria in beef cattle administered selected subtherapeutic antimicrobials in a feedlot setting. Appl Environ Microbiol 2008, 74:6178–6186.

Figure 3 Peptide quantitation of proteins expressed by C and S MAP strains under iron-replete conditions: Reporter ion regions (114 – 117 m/z) of peptide tandem mass spectrum from iTRAQ labeled peptides from the (A) 35-kDa major membrane protein (MAP2121c) and (B) BfrA, and the intergenic regions of MAP1508-1509 and MAP2566-2567c. Quantitation of peptides and inferred proteins are made from relative peak areas of reporter ions. Several unique peptides (>95% confidence) were mapped to each protein. However,

Cilengitide research buy only one representative peptide is shown for each protein. Peptides obtained from cattle MAP cultures grown in iron-replete and iron-limiting medium were labeled with 114 and 115 reporter ions, respectively. Peptides obtained from sheep MAP cultures grown in iron-replete and iron-limiting medium were labeled with 116 and 117 reporter ions, respectively. The peptide sequences and shown in the parenthesis and the red dashed line

illustrates the reporter ion relative peak intensities. MAP2121c alone was upregulated in the sheep MAP strain under iron-replete conditions. As expected, transcripts identified as upregulated under iron-replete conditions in C MAP strain were also upregulated in the proteome (Table 3, Additional file 1, Table S10). There was increased expression of five ribosomal proteins and a ribosome releasing factor (MAP2945c) by cattle MAP under iron-replete conditions. As previously reported, BfrA was upregulated in cattle MAP (Figure 3B). Antigen 85A and MAP0467c (mycobacterial heme, utilization and degrader) were also upregulated. However, MAP0467c and other Smad inhibitor stress response proteins were downregulated in the S MAP strain (Figure 4). Figure 4 Proteins expressed by type II MAP under iron-replete conditions: Proteins upregulated in cattle MAP strain whereas downregulated in sheep strain in the presence of iron. Fold change for each target is calculated of and represented as a ratio of iron-replete/iron-limitation.

A negative fold change represents repression and a positive fold change indicates de-repression of that particular target gene in the presence of iron. MhuD = mycobacterial heme utilization, degrader; USP = universal stress protein; CHP = conserved hypothetical protein; MIHF = mycobacterial integration host factor; CsbD = general stress response protein Identification of unannotated MAP proteins We identified two unique peptides (SSHTPDSPGQQPPKPTPAGK and TPAPAKEPAIGFTR) that originated from the unannotated MAP gene located between MAP0270 (fadE36) and MAP0271 (ABC type transporter). We also identified two peptides (DAVELPFLHK and EYALRPPK) that did not map to any of the annotated MAP proteins but to the amino acid sequence of MAV_2400. Further examination of the MAP genome revealed that the peptides map to the reversed aminoacid sequence of MAP1839. These two unique proteins were not differentially regulated in response to iron.

(C) SDS-PAGE analysis of the affinity-isolation of LacI::6 VS-4718 cell line × His. Proteins were stained with Coomassie blue. Lane 1 shows protein standards, lane 2, whole cell extract, lane 3, LacI::6 × His affinity-isolate. Conclusion We have developed a version of the two-plasmid recombineering system for generating chromosomal modifications in E. coli strains which, we have termed Gene Doctoring. This method relies on homologous recombination, mediated by the λ-Red genes, of a linear DNA fragment that is supplied in vivo by restriction of a pDOC donor plasmid by I-SceI endonuclease. The identification

of recombinants is highly efficient and reproducible, since counter-selection

using the sacB gene identifies true recombinants. This eliminates the requirement for screening large numbers of candidates by PCR, which is both costly and Cytoskeletal Signaling inhibitor time consuming. In addition, we have made a modified recombineering plasmid, pACBSCE, which carries a DNA recognition site for I-SceI in the origin of replication, meaning that recombinants are not over-exposed to the potential mutagenic side-effects of the λ-Red gene products. The gene doctoring system is principally effective for recombineering in different pathogenic E. coli strains, Phosphoglycerate kinase which as we have demonstrated, are not particularly amenable to chromosomal modification using existing

systems. This system is designed to facilitate the coupling of genes to epitope tags, though the deletion of genes can also be readily achieved. We have demonstrated the versatility of Gene Doctoring by deleting genes in both laboratory and pathogenic E. coli strains, in addition to coupling several genes to epitope tags, and we have confirmed the functionality of epitope tagged fusion proteins using biochemical methods. We believe that the gene doctoring system can be transferable to other bacteria, in which the pDOC and pACBSCE plasmids are stable and will replicate. Methods Strains The E. coli strains used in this study were MG1655 K-12 strain [21], O157:H7 Sakai EHEC strain (derivative in which the stx1 and stx2 genes were deleted by M. D. Goldberg, University of Birmingham, UK) [8], CFT073 UPEC strain [9] O42 EAEC [10] and H10407 ETEC strains [11] (from Ian R. Henderson, University of Birmingham, UK; Sequenced by the Sanger Institute: unpublished). Primers The primers used in this study are listed in table 4.

The number of micronucleated cells was counted in 2,000 reticulocytes per animal using an Olympus BH-2 microscope at 1,000× magnification [26]. The statistical analyses were made with a one-way analysis of variance (ANOVA) followed by Dunnet test. Differences were considered significant at p value of less than 0.05. Scanning and transmission electron microscopy After treatment with the IC50 (72 h) of parthenolide, axenic amastigotes

were washed in PBS and fixed in 2.5% glutaraldehyde in 0.1 M sodium cacodylate buffer at 4ºC. For scanning electron microscopy, amastigotes were placed on a specimen support with a poly-L-lysine-coated Sepantronium coverslip and washed in cacodylate buffer. The cells were dehydrated in an increasing ethanol gradient, critical-point-dried in CO2, sputter-coated with gold, and observed in a Shimadzu SS-550 SEM scanning electron microscope. For transmission electron microscopy, amastigote forms were treated with the IC50 of Linsitinib cell line parthenolide and the IC50 of amphotericin

B and fixed as described above. The cells were postfixed in a solution that contained 1% osmium tetroxide, 0.8% potassium ferrocyanide, and 10 mM calcium chloride in 0.1 M cacodylate buffer, dehydrated in an increasing acetone gradient, and embedded in Epon resin. Ultrathin sections were stained with uranyl acetate and lead citrate, and the images were examined in a Zeiss 900 transmission electron microscope. Fluorescence of monodansylcadaverine during cell death Axenic amastigotes were treated with IC50 and IC90 equivalents of parthenolide. After 72 h, the cells were washed and resuspended in PBS. To verify the induction of autophagy by parthenolide, the cells were incubated with 0.05 mM monodansylcadaverine (MDC) at 37°C for 10 min. After incubation, the cells were washed three times with PBS to remove excess MDC, immediately analyzed

by fluorescence microscopy at an excitation wavelength of 360–380 nm and emission wavelength of 525 nm, and photographed using a charge-coupled-device camera. This study was qualitative. Flow Edoxaban cytometry The antileishmanial activity of parthenolide (20 and 40 μM) on the integrity of the plasma membrane and mitochondrial membrane potential of axenic amastigotes (5 × 106 cells/ml) was determined after 3 h treatment. Amphotericin B (5.0 μM) and carbonyl cyanide m-chlorophenylhydrazone (200 μM) were used as positive controls. Untreated amastigotes were used as a negative control. Each flow-cytometric technique was evaluated by repeating each experiment three times to verify reproducibility. The integrity of the plasma membrane was assessed using L. amazonensis amastigotes at an average density of 5 × 106 cells suspended in 500 μl PBS and stained with 50 μl propidium iodide (2 μg/ml) for 5 min at room temperature. To measure mitochondrial membrane potential (ΔΨm), 1 ml of saline that contained 1 × 106 of treated amastigotes was mixed with 1 μl rhodamine 123 (5 mg/mL) for 15 min at 37°C.

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Condens Matter 2003, 15:47–53.CrossRef 37. Xin Y, Lu J, Stampe PA, Kenney RJ: Crystallographically orientated fcc Co nanocrystals in rutile TiO2 thin films. Appl Phys Lett 2006, 88:112512.CrossRef 38. Lee S, Shon Y, Kim DY, Kang TW, Yoon CS: Enhanced ferromagnetism in H2O2-treated p-(Zn0.93Mn0.07)O layer. Appl Phys Lett 2010, 96:042115.CrossRef 39. Aksu S, Bacaksiz E, Parlak M, Yılmaz S, Polat I, Altunbaş M, Türksoy M, Topkaya R, Özdoğan K: Structural, optical and magnetic properties of Mn diffusion-doped CdS thin films prepared by vacuum evaporation. Mater Chem Phys 2011, 130:340–345.CrossRef 40. Zelaya-Angel O, Lozada-Morales R: Sphalerite-wurtzite phase transformation in CdS. Phys Rev B 2000, 62:13064–13069.CrossRef 41. Madhu C, Sundaresan A, Rao CNR: Room-temperature ferromagnetism in undoped GaN and CdS semiconductor nanoparticles. Phys Rev B 2008, 77:201306.CrossRef Competing interests

The authors declare that they have no competing interests. Authors’ contributions ZY prepared all the samples, participated in all of the measurements and data analysis, and drafted the manuscript. DG and DX conceived and designed the manuscript. ZZ1 carried out the XPS measurements and data analysis. JZ participated in the SQUID and TG-DTA measurements. ZZ2 carried out the XRD measurements and data analysis. ZS participated in the data analysis and interpretation of the results. All authors have been

involved in revising the see more manuscript and read and approved the final manuscript.”
“Background Until now, lots of research have been devoted towards the development of Si-based light sources that could enable the integration of photonics with Si microelectronics [1–3]. Si-based light sources could reduce the fabrication cost because their compatibility with a conventional complementary metal-oxide semiconductor (CMOS) technology is better than any other light source such as conventional Org 27569 GaAs- and GaN-based light emitters. Despite a lot of efforts for the realization of Si-based light sources with high efficiency, luminescence efficiency from Si-based light sources is still very low due to an indirect bandgap nature of the bulk Si [4, 5]. Recently, because of this obstacle for realizing efficient Si-based light sources, Si nanocrystals (NCs) have, therefore, attracted the most attention as promising light sources for the next generation of Si-based nanophotonics [6–8]. Si NCs showed a quantum confinement effect that increased in the overlapping of electron–hole wave functions, leading to an enhancement in luminescence efficiency [9]. Another advantage for light sources using Si NCs is that the optical bandgap can be easily tuned by changing the size of NCs. This implies that Si NCs are of particular interest as a light source, covering the whole visible wavelength range.

Two representative experiments are shown. Green fluorescence, which is a measure of total biomass, is shown in absolute units. B Biofilm membrane damage, determined using the LIVE/DEAD BacLight Bacterial Viability stain. Green and red fluorescence was measured, and biofilm damage was calculated as reduction of the ratio of green/red fluorescence compared to controls without carolacton. Error values were calculated from the standard deviations of the green/red ratios of control and carolacton treated samples according to the error propagation formula of Gauss. Three representative experiments are shown. Biofilms were grown anaerobically. Mean

and standard deviation are given for triplicate samples. find more Membrane damage of the biofilm cells, determined by the LIVE/DEAD BacLight fluorescence staining method by staining with both SYTO9 (green) and propidium iodide (red), was calculated as the reduction of the green/red fluorescence ratio in biofilms grown with carolacton relative to untreated controls and is shown in Figure 5B for three independent experiments. MEK inhibitor It shows a similar pattern. Biofilm damage

was small during the first 6 h, increased rapidly until about 8.5 or 12.25 h, respectively and then remained stable or increased more slowly till the end of the experiment after 24 hours. The curves for the two concentrations of carolacton tested were very similar, as expected from the concentration range of carolacton Ribonucleotide reductase activity determined previously (Figure 4). The maximum reduction of the relative green/red fluorescence ratio was between 47%

and 69% reflecting the dynamic process of biofilm growth. The pH dropped from pH 7.8 to pH 4.3 (24 h of growth), but there was no difference in controls and carolacton treated cultures. To summarize, the data show that carolacton temporarily reduced the total amount of biofilm cells, indicated by staining with the green fluorescent dye alone, during the period of maximum biofilm growth (Figure 5A). Most importantly, carolacton strongly reduced the viability of cells within the biofilm, determined by the reduction of the relative proportion of green to red fluorescence, throughout 24 h of biofilm development but mainly during the period of maximum biofilm growth and thereafter, while little reduction of viability was observed during the initial hours of biofilm growth (Figure 5B). Investigation of the effect of carolacton on S. mutans biofilms by confocal laser scanning microscopy The effect of carolacton on the spatial distribution, architecture and viability of biofilms of wild-type S. mutans UA159 was investigated by confocal laser scanning microscopy. Figure 6A shows top-down views, flanked by pictures of vertical optical sections after 12 hours of cultivation and Figure 6B represents horizontal sections at a higher magnification.

Side Reach 45–54 93 s 0 22 55–65 0 40 The men with early OA all scored above p5, except on the dynamic bending test. One of the older men scored below p5 on the overhead working posture test. On all tests, 20–40% of the younger women and 25–65% of the older women scored below p5. Discussion This study revealed that both the 15 male and the 78 female subjects from a subsample from the CHECK cohort at baseline reported

a worse physical health status (SF-36) compared to the healthy ageing workers, whereas the women also reported a worse mental health status on 3 out of 4 scales. On the FCE, the female CHECK subjects performed significantly lower than their healthy working counterparts on all GSK1904529A cell line 6 tests. The male subjects with OA performed lower on 3 out of 6 tests. A substantial proportion of female subjects demonstrated functional capacities that would be considered insufficient to meet the lowest category of physical job demands. The worse physical health status as reported on the SF-36 can be attributed to the knee or hip complaints of the subjects, but other physical factors may also have influenced their health status. Serious comorbidity was an exclusion criterion for the CHECK cohort, but back pain and other musculoskeletal discomfort were frequently reported. Contrarily, an over representation of physically BKM120 molecular weight strong and healthy volunteers in the reference population

may have introduced bias that explains part of the observed differences. Still, the early phase of OA is clearly accompanied by self-reported limitations in physical function and physical roles for both sexes and also by mental health limitations for women. The worse self-reported health status of the subjects with early OA compared to the healthy working subjects was also reflected in a lower functional capacity as measured on the FCE. The pain and stiffness in

the hips or knees, possibly in combination with other health complaints, seem to have affected their performance in work-related physical activities. We reported earlier that in this sample the subjects with low self-reported functional status showed see more lower performances on the FCE (Bieleman et al. 2009). About half of the subjects with early OA in this study did not have a paid job. Either or not having a paid job has been reported to explain part of the performance on an FCE (Bieleman et al. 2007). For example, on ‘lifting low’ the average difference between women from this study with paid work and those without paid work was 4.7 kg (19.4 kg vs. 14.7 kg). However, after correcting for this factor, there still remains a substantial difference between the capacities of the working subjects with early OA and the reference group of healthy workers. Therefore, it was concluded that in the early phase of OA of the hips and knees a decreased functional capacity is seen, both in working people and even more in people without paid work.

: PILRalpha is a herpes simplex virus-1 entry coreceptor that associates with glycoprotein B. Cell 2008,132(6):935–944.PubMedCrossRef APR-246 Authors’ contributions AF-M participated in the design and performed all experiments and drafted the manuscript. SK and MM contributed to the interpretation of data. YH obtained funding for designed the research and critically revised the manuscript. All authors read and approved the final manuscript.”
“Background Management of meningococcal disease requires immediate treatment of patients and chemoprophylaxis of contacts. For the latter, rifampicin is the most frequently used antibiotic.

However, although it has been utilized routinely worldwide for more than 30 years, few cases of rifampicin resistant meningococci have been reported [1]. This scarce diffusion is intriguing and the reduced virulence of these strains in terms of the bacterium’s survival in the bloodstream of mice, as shown in an in vivo model, suggests a major biological cost for the microorganism [2]. The resistance phenotype is correlated with a set of mutations in the rpoB gene, encoding the β subunit of RNA polymerase, resulting in amino acid substitutions at one of the following codons: Asp542, Ser548, His552, Ser557, Gly560 [3–6]. Moreover, other mechanisms Protein Tyrosine Kinase inhibitor have been described in both Neisseria meningitidis and in Neisseria

gonorrhoeae [7, 8], i.e. resistance to diverse hydrophobic agents, including Triton X, is associated with mutations in the mtrR gene and in its promoter [7, 9, 10]. Overall, in other species, such as Mycobacterium tuberculosis, resistance was not related

to any changes in the rpoB gene in around 5% of clinical rifampicin resistant isolates [11]. Rifampicin binds to DNA-dependent RNA polymerase and inhibits initiation of RNA synthesis which is not a mechanism of action shared with other antibiotics. This effect on RNA polymerase appears to result from drug binding in the polymerase subunit deep within the DNA/RNA channel where direct blocking of the elongating RNA can occur. Little is known of the protein expression of N. meningitidis resistant to rifampicin and how this contributes to pathogenesis. In the present study, soluble proteins of two rifampicin resistant and one susceptible meningococci isolated in Italy, and previously described Parvulin [5], were analysed by two-dimensional electrophoresis (2-DE) combined with mass spectrometry (MALDI-ToF). The method has been chosen because it is a comprehensive approach to investigate the protein content of a pathogen [12], and in this context helpful to identify differential expression in specific proteins in particular in rifampicin resistance meningococci. Methods Bacterial strains and bacterial proteins extraction Two rifampicin resistant (RIFR) 870 and 901 strains and one rifampicin susceptible (RIFS) 1958 serogroup C meningococci were analysed.