(PDF 193 KB) Additional file 4: Figure showing overlap of identif

(PDF 193 KB) Additional file 4: Figure showing overlap of identified and quantified proteins by 2-DE and 2-DLC/MS with iTRAQ. Table showing relative abundance changes for 22 proteins quantified by both 2-DE and iTRAQ. (PDF 124 KB) Additional file 5: Protein sequence alignment of Flagellin (FliC/FlaA) of P. aeruginosa strains used in this

study (AES_1954, PA1092, and PA14_50290) and including an additional sequence from strain Repotrectinib price PAK with a known type A flagellin. The flagellin sequence of strain AES-1R has higher sequence similarity with the shorter A type flagellin of strain PAK (95%), while the type B flagellins of strains PA14 and PAO1 are almost identical with only a single amino acid difference. (PDF 51 KB) References 1. Stover CK, Pham XQ, Erwin AL, Mizoguchi SD, Warrener P, Hickey MJ, Brinkman FS, Hufnagle WO, Kowalik DJ, Lagrou M, et al.: Complete genome sequence of Pseudomonas aeruginosa PAO1, an SB525334 manufacturer opportunistic pathogen. Nature 2000, 406:959–964.PubMedCrossRef 2. Bleves S, Viarre V, Salacha R, Michel GP, Cyclosporin A manufacturer Filloux A, Voulhoux R: Protein secretion systems in Pseudomonas aeruginosa : a wealth of pathogenic weapons. Int J Med Microbiol 2010, 300:534–543.PubMedCrossRef 3. Lyczak JB, Cannon CL, Pier GB: Lung infections associated

with cystic fibrosis. Clin Microbiol Rev 2002, 15:194–222.PubMedCrossRef 4. Boucher RC: Airway surface dehydration in cystic fibrosis: pathogenesis and therapy. Rolziracetam Annu Rev Med 2007, 58:157–170.PubMedCrossRef 5. Hoiby N, Frederiksen B, Pressler T: Eradication of early Pseudomonas aeruginosa infection. J Cyst Fibros 2005,4(Suppl 2):49–54.PubMedCrossRef 6. Govan JR, Deretic V: Microbial pathogenesis in cystic fibrosis: mucoid Pseudomonas aeruginosa and Burkholderia cepaci . Microbiol Rev 1996, 60:539–574.PubMed 7. Armstrong DS, Nixon GM, Carzino R, Bigham A, Carlin JB, Robins-Browne RM, Grimwood K: Detection of a widespread clone of Pseudomonas aeruginosa in a pediatric cystic fibrosis clinic. Am J Respir Crit Care Med 2002, 166:983–987.PubMedCrossRef

8. O’Carroll MR, Syrmis MW, Wainwright CE, Greer RM, Mitchell P, Coulter C, Sloots TP, Nissen MD, Bell SC: Clonal strains of Pseudomonas aeruginosa in paediatric and adult cystic fibrosis units. Eur Respir J 2004, 24:101–106.PubMedCrossRef 9. Bradbury R, Champion A, Reid DW: Poor clinical outcomes associated with a multi-drug resistant clonal strain of Pseudomonas aeruginosa in the Tasmanian cystic fibrosis population. Respirology 2008, 13:886–892.PubMedCrossRef 10. Jones AM, Govan JR, Doherty CJ, Dodd ME, Isalska BJ, Stanbridge TN, Webb AK: Spread of a multiresistant strain of Pseudomonas aeruginosa in an adult cystic fibrosis clinic. Lancet 2001, 358:557–558.PubMedCrossRef 11. Cheng K, Smyth RL, Govan JR, Doherty C, Winstanley C, Denning N, Heaf DP, van Saene H, Hart CA: Spread of beta-lactam-resistant Pseudomonas aeruginosa in a cystic fibrosis clinic. Lancet 1996, 348:639–642.PubMedCrossRef 12.

g internal structure, oedema in the tumor environment, necrotic

g. internal structure, oedema in the tumor environment, necrotic areas). We observed a pronounced interior structuring of an s.c. HT29 tumor after i.v. injection of the contrast agent Gd-BOPTA. Histological analyses revealed

that a large central necrotic/fibrotic area was associated with contrast enhancement. Such an effect can also be observed in patient tumors. After the characteristic initial tumor rim enhancement a centripetal progression of the signal can occur depending on the tumor structure, e.g. determined by different vascular architecture [12, 15, 21]. Early peripheral enhancement with centripetal progression was seen in invasive carcinomas with a high peripheral and a low central microvessel density, which was associated with fibrosis and/or necrosis [12, 21]. This demonstrates that depending on the tumor and used contrast agent the BT-MRI system is suitable for observation of intratumoral PF477736 structures and that characteristic features of patient tumors can be reproduced in the model system. It offers the opportunity to follow intratumoral processes under therapy. Further work will be done particularly with regard to imaging of

different orthotopic installed tumors and their progression as well as the development of metastatic disease. Other contrast agents will also be examined in order to find Selleck Eltanexor better enhancement of (small) tumor sites and metastases. Moreover, other contrast enhancer could lead to better results for imaging of interior tumor structures. Conclusions The results of the current study show that BT-MRI is, despite its limitations with respect to the magnetic field strength and magnet homogeneity, clearly capable of providing satisfactory image slice quality to visualize organs and tumors and to monitor tumor progression in mouse models. Acknowledgements We would like to thank Dr. Ian Nicholson and his colleagues from Oxford Instruments for the development, manufacture and installation of the BT-MRI prototype apparatus. Ponatinib mw The study was supported in part by grants from the Federal State of Saxonia-Anhalt (FKZ 3646A/0907). References 1. Malaterre V, Metz H, Ogorka J, Gurny R, Loggia N, Mader K:

Benchtop-magnetic resonance imaging (BT-MRI) characterization of push-pull osmotic controlled release systems. J CDK inhibitor Control Release 2009, 133:31–36.PubMedCrossRef 2. Metz H, Mader K: Benchtop-NMR and MRI – a new analytical tool in drug delivery research. Int J Pharm 2008, 364:170–175.PubMedCrossRef 3. Strubing S, Abboud T, Contri RV, Metz H, Mader K: New insights on poly(vinyl acetate)-based coated floating tablets: characterisation of hydration and CO2 generation by benchtop MRI and its relation to drug release and floating strength. Eur J Pharm Biopharm 2008, 69:708–717.PubMedCrossRef 4. Strubing S, Metz H, Mader K: Characterization of poly(vinyl acetate) based floating matrix tablets. J Control Release 2008, 126:149–155.PubMedCrossRef 5.

The same geometry is used to measure the profile of the incident

The same geometry is used to measure the profile of the incident GF120918 manufacturer field by scanning it across the probe. Results and discussion The initial optimization of the parameters was performed by looking for optimal plasmon coupling by the corrugations. The starting point for grating period was chosen by matching the real part of the propagation constant k sp of the surface plasmon at a smooth metal dielectric interface with a normally exiting plane wave, which gives (2) for diffraction orders ±1 of the grating. In our case (Al/NOA interface, λ = 632.8 nm) k sp ≈ (15.9 + 0.12i) μm-1, which gives d ≈ 400 nm. Since the effective

surface plasmon propagation distance along a non-corrugated surface is only 1/Ik sp ≈ 21.5d, the number of grooves on each side of the slit was set to 9, which should ensure efficient outcoupling of the surface plasmon field. Leaving some space (≈ 4 μm) between the corrugated region and the PMLs as indicated in Figure 2 lead us to GSK2118436 cell line choose a superperiod D = 20 μm in the FMM design. It is conceivable that the radiant intensity in the direction normal to the interface (which in the FMM analysis corresponds to the zero-order diffraction efficiency η 0 of the superperiodic grating) may be used as the criterion to optimize the performance of the transmission side corrugations in the

present application. Alternatively, one might consider using the integrated radiant intensity in the positive half-space, i.e., the sum η of the efficiencies of all transmitted Chloroambucil propagating orders in the FMM analysis. The best criterion would in principle be the integrated radiant intensity within the NA 4SC-202 mw of the collection optics, but this would depend on the type of detection scheme used. We therefore compare the first two methods in Figure 5 by plotting in Figure 5a the zeroth-order efficiency η 0 and in Figure 5b the total transmission efficiency η for different values of groove depth h m  and grating period d, assuming

a fill factor f/d = 0.5. The optimum values of the parameters differ somewhat, with zeroth-order criterion giving a somewhat larger period and a considerably smaller groove depth than the criterion based on total transmission. Although high-numerical-aperture collection optics was used in our experiments, we chose the former criterion, which would allow the use of a detector without any collection optics provided that it covers a reasonable solid angle in the far field. Thus, the grating parameters d = 370 and h m  = 30 nm were chosen for further design. Figure 5 Corrugation design. Transmission side corrugation optimization using as the criterion either (a) the zeroth-order efficiency or (b) the total transmission efficiency, which are plotted here as functions of the corrugation height h m  and period d. The final step in the design of the field probe is to choose the optimum thickness h of the Al layer.

monocytogenes is only slightly impaired when it lacks the activit

monocytogenes is only slightly impaired when it lacks the activities of Lmo2812 or both Lmo2812 and PBP5 [11, 12]. Reduced growth rates

have also been reported for a S. pneumoniae mutant lacking functional PBP3 [24] and for a double N. gonorrhoeae mutant lacking both PBP3 and PBP4 [28]. On the other hand, no changes in growth rate were observed for E. coli or B. subtilis mutants lacking most or all of their DD-carboxypeptidase activity [27, 29]. However, the loss of Lmo2812 did result in significant changes in morphology. The mutant cells were significantly longer, slightly curved and had bent ends. These CHIR-99021 molecular weight changes were even more pronounced in the double mutant AD07 lacking both Lmo2812 and PBP5. This finding is interesting because we

did not notice any alterations selleckchem in cell shape in a L. monocytogenes mutant lacking PBP5 alone, although the cell wall of the mutant was much thicker than that of the parental strain [11, 12], even though Guinane et al. [15] did describe such changes. The differences between our observations may be due to variation in the strain (EGD versus EGDe) or growth conditions employed [15]. The reason for the prominent morphological changes in strain KD2812 is difficult to pinpoint since there do not seem to be any remarkable changes in the muropeptide structure of the peptidoglycan of this mutant. However, the observed changes in cell morphology implicate the protein in the late stages of peptidoglycan synthesis, presumably in the determination of the availability of pentapeptide substrates. Our finding that Lmo2812 preferentially degrades low-molecular-weight substrates may point to the a role for this protein triclocarban in cell wall turnover. Further Entospletinib price studies are required to

clarify the function of Lmo2812, although, as in the case of extensive studies on the D-alanine carboxypeptidases of E. coli [30] and other bacteria, they may not yield conclusive results. Conclusions The results of this study conclusively show that nine of the ten previously identified putative PBP genes of L. monocytogenes code for proteins that bind β-lactam antibiotics and their labeled or fluorescent derivatives. Eight of these proteins were identified in whole cell extracts, whereas the ninth protein, Lmo2812, was only shown to bind β-lactams following expression in E. coli and subsequent purification by affinity chromatography. The inability to detect Lmo2812 activity in the L. monocytogenes cell may be explained by the low abundance of this protein, whose expression is regulated by the two-component system CesRK [21]. We have also demonstrated that the LMM PBP Lmo2812 is a DD-carboxypeptidase and has no discernible β-lactamase activity. Mutants lacking the protein grow normally, although their cells are often longer and slightly curved. Similar morphological changes were observed in the case of a double mutant lacking two LMM carboxypeptidases: Lmo2812 and Lmo2754.

5 times larger than the toddlers in this study After normalizing

5 times larger than the toddlers in this study. After normalizing shedding numbers by the body surface factor of 3.5, the numbers of S. aureus shed by adults were 4 times more than toddlers on average (21 times on median). Pexidartinib nmr Therefore, in this investigation, toddlers in diapers shed fewer organisms than the adults; however, additional studies need to be done under the same conditions to confirm these findings. Conclusions The results of this study showed that both MSSA and MRSA were shed by human populations into marine waters. The amount of shedding varied, was likely dependent upon the level of colonization of

the host, and colonization was not limited Selleck FK228 to the anterior nares. In this study, the shedding of MRSA was directly dependent upon its colonization of the human host. MRSA shedding was observed intermittently, only among Group II adults and water, with the apparent lower number of humans colonized by MRSA relative to MSSA. No MRSA was observed in the sand samples as the pediatric populations evaluated in this study were apparently not colonized with MRSA. However, it is highly likely that similar studies with additional pediatric participants would result in the isolation of MRSA [29]. Future studies should focus on the collection

of additional samples from human participants as the current study was limited by the restricted numbers of carriers identified. These future studies should collect samples from the skin and from other areas where S. aureus check details resides, in addition to samples from the anterior nares. Once S. aureus is released from bathers, its potential for transmission is highly dependent on its persistence in the environment. Gregg and LaCroix [30] inoculated saltwater pool water with MRSA, and found very low levels after 1 hour exposure. They concluded

that swimming pool water would not likely put children at risk for acquiring MRSA. However, we argue here that more research is needed to evaluate the risk of illness associated with water exposures and the potential else for transmission through sand, including the residency time of these human pathogens in both recreational marine waters and beach sand [12]. Future research should be conducted with S. aureus species from actively colonized individuals, as the current study found large amounts released from individuals, and the actively growing clinical strains may survive differently in comparison to laboratory grown strains used for inoculation experiments. Experimentation should closely control environmental factors as some studies have documented growth of S. aureus under optimal environmental conditions [31]. Overall, the results from this study confirmed that both adults and toddlers can be sources of potentially pathogenic MSSA and MRSA in recreational marine waters, and support the potential for exposure and transmission of these organisms through the use of recreational beaches.

DCs play a key role in antigen presentation, which

DCs play a key role in antigen presentation, which Entinostat results in activation of T cell populations that can lead to efficient phagocyte killing of the intracellular bacillus, via granulysin-induced phagocyte death, or by cytokine release (e.g. IFN-γ) that supports the mycobactericidal capacity of phagocytes [38–41]. Although outside the scope of this current article, it is possible that dying DCs share some properties of dying macrophages, and contribute to this T cell response. In the present study we found that both the attenuated H37Ra and virulent H37Rv strains cause death of human DCs. The caspase-independent cell death we report in H37Ra-infected DCs appears to be neither apoptosis

nor pyroptosis (both of which require caspase activity) [22, 42]. There are various modes of

non-apoptotic cell death, such as pyronecrosis and necroptosis, which can occur without caspase activation. The way in which cells die shapes the response of the immune system; death can be immunogenic, tolerogenic or silent [43, 44]. Therefore, the type of cell death undergone by Mtb-infected DCs is of interest, as it may either support or inhibit cytotoxic and helper T cell responses. Macrophage apoptosis appears to be Selleck PFT�� beneficial for the host response to tuberculosis by having direct bactericidal effects on intracellular mycobacteria and also in the stimulation of protective immunity. The genome of M. tuberculosis contains genes that actively inhibit macrophage apoptosis and enhance buy Savolitinib its intracellular survival, including nuoG, pknE and secA2 [45]. It is likely that the products of these genes would also inhibit apoptosis of DCs, possibly steering the cells towards the non-apoptotic mode of cell death seen in the present study. Interestingly, foamy macrophages (which are positive for DC markers) in granulomas Celecoxib in the lungs of mice infected with M. tuberculosis have been found to express high levels of TNFR-associated factors (TRAFs) 1-3 which are associated with resistance to apoptosis [46]. Although H37Ra and H37Rv are highly related, being derived from the same parental H37 strain, they differ in important respects at the

genetic [47], transcriptional [48] and post transcriptional [49] levels. As a result H37Ra displays several characteristics that are different from H37Rv (e.g. variations in PE/PPE/PE-PGRS proteins [47], decreased survival inside human macrophages [50, 51], differences in the composition of mannose caps on lipoarabinomannin [52] and impaired ability to secrete ESAT 6 [49]) each of which could have an impact on the mode of cell death [53, 54]. Indeed, similar to our previous finding in human macrophages [10], H37Rv infection killed DCs at a significantly faster rate than H37Ra. Further work will be needed to determine whether infection of DCs with H37Rv causes a similar caspase-independent mode of cell death. Caspases can have variable effects on the immunogenic potential of dying cells.


To troubleshoot this issue, we accounted for this heterogeneity during the establishment of the RMS library (MSL). We hypothesized that MS identification effectiveness could be enhanced by increasing both the number of reference meta spectra (RMS) of a given strain included in the Stattic cell line reference library and the number of deposits used to generate each RMS. The primary objective of this study was to test the effectiveness of distinct reference spectra library architectures for the MALDI-TOF MS-based identification of filamentous fungi. More

precisely, we assessed the influence on identification effectiveness of the following: i) the number of technical replicates, i.e., the number of analyzed deposits (spots) from one culture used to generate an RMS; ii) the number of biological Vactosertib ic50 replicates, i.e., the number of RMS derived from distinct subcultures for each strain; and iii) the number of distinct strains of one species used to

construct the library. Figure 1 Comparison of mass spectra obtained from four subcultures of a strain of Aspergillus flavus. The Aspergillus flavus 1027804 strain was find more subcultured on four different agar plates. Spectra A, B, C, and D display the

mTOR inhibitor first spectrum acquired from the subcultures 1, 2, 3 and 4, respectively. Spectra A to D display many common peaks; however, a few varying peaks are also clearly visible and characteristic of one of the subcultures. Results Phenotypic and genotypic identification of clinical isolates The results of the classical and DNA sequence-based identification of 200 clinical isolates (Table 1) were applied to classify the isolates into two groups: isolates included and isolates excluded from the MSL. The MS results of both groups are summarized in Table 2. The isolates belonged to 28 different genera and 38 different species. Moreover, 174 isolates corresponded to 18 species, which were represented among those used to construct the eight libraries, whereas the 26 remaining isolates belonged to 20 species that were not represented in the libraries. Table 1 Identification of the 200 clinical isolates included in the study Species Number of Isolates Corresponding RMS in the MSLs Acremonium sp.

agalactiae PG2 T liposoluble proteins The results of 2D DIGE wit

agalactiae PG2 T liposoluble proteins. The results of 2D DIGE with the two field strains Nurri and Bortigali are also reported (TPH, total peptide hits; NA, not applicable). (DOC 258 KB) Additional file 8: Proteins identified in the M. agalactiae proteome potentially resulting from Horizontal Gene Transfer events with M. mycoides subsp. mycoides and M. capricolum subsp. capricolum. (DOC 49 KB) Additional file 9: Proteins identified in the M. agalactiae proteome potentially resulting from Horizontal Gene Transfer events with other bacteria. (DOC 30

KB) References 1. Razin S, Yogev D, Naot Y: Molecular biology and pathogenicity of mycoplasmas. Mol Biol Rev 1998, 62:1094–1156. 2. Rottem S: Interaction #Selleck 4EGI-1 randurls[1|1|,|CHEM1|]# of mycoplasmas with host cells. Physiol Rev 2003, 83:417–432.PubMed 3. You XX, Zeng YH, Wu YM: Interactions between mycoplasma lipid-associated membrane proteins and the host cells. J Zhejiang Univ Sci B 2006, 7:342–350.PubMedCrossRef 4. Kühner S, van Noort V, Betts MJ, Leo-Macias A, Batisse C, Rode M, Yamada T, Maier T, Bader S, Beltran-Alvarez P, Castaño-Diez D, Chen WH, Devos D, Güell M, Norambuena T, Racke I, Rybin V, Schmidt A, Yus E, Aebersold R, Herrmann R,

Böttcher B, Frangakis AS, Russell RB, Serrano L, Bork P, Gavin AC: Proteome organization in a genome-reduced bacterium. Science 2009, 27:1235–1240.CrossRef selleck 5. Lambert M: Contagious agalactia of sheep and goats. Rev Sci Tech OIE 1987, 6:699–711. Mycoplasmoses of ruminants 6. Corrales JC, Esnal A, De la Fe C, Sánchez A, Assunçao P, Poveda JB, Contreras A: Contagious agalactia in small ruminants. Small Rum Res 2007, 68:154–166.CrossRef 7. Bergonier D, Berthelot X, Poumarat F: Contagious agalactia of small ruminants: current knowledge concerning epidemiology, 4��8C diagnosis and control. Rev Sci Tech Off Int Epizoot 1997, 16:848–873. 8. Chessa B, Pittau M, Puricelli M, Zobba R, Coradduzza E, Dall’ara P, Rosati S, Poli

G, Alberti A: Genetic immunization with the immunodominant antigen P48 of Mycoplasma agalactiae stimulates a mixed adaptive immune response in BALBc mice. Res Vet Sci 2009, 86:414–420.PubMedCrossRef 9. Fusco M, Corona L, Onni T, Marras E, Longheu C, Idini G, Tola S: Development of a sensitive and specific enzyme-linked immunoadsorbent assay based on recombinant antigens for rapid detection of antibodies against Mycoplasma agalactiae in sheep. Clin Vaccine Immunol 2007, 14:420–425.PubMedCrossRef 10. Greco G, Corrente M, Buonavoglia D, Aliberti A, Fasanella A: Inactivated vaccine induces protection against Mycoplasma agalactiae infection in sheep. New Microbiol 2002, 25:17–20.PubMed 11. Nicholas RAJ: Contagious agalactia and other mycoplasmal mastitides of small ruminants. In The Merck Veterinary Manual. 9th edition. Edited by: Kahn CM, Line S. Merck & Co. Inc., Whitehouse Station, NJ; 2005:1114–1116. 12.

Patients and methods Patients This prospective study involved 37

Patients and methods Patients This prospective study involved 37 consecutive patients with a median age of 28 years (range: 19-58 years) who underwent an allogeneic hematopoietic stem cell transplantation (HSCT) from June 2009 to February 2011 at the Transplantation Centre of Hematology Department selleck screening library at University Hospital Bratislava. There were 24 males and 13 females. Their diagnosis included acute find more myeloid leukemia (AML) in 13 patients,

acute lymphoblastic leukemia (ALL) in 14 patients, chronic myeloid leukemia (CML) in 2 patients, Hodgkin’s lymhoma in one patient, myelodysplastic syndrome (MDS) in 3 patients, osteomyelofibrosis in one patient and severe aplastic anemia in 3 patients. Twenty-seven patients were conditioned with myeloablative regimens including cyclophosphamide (CY) 60 mg/kg body weight intravenously on 2 consecutive days in combination with fractionated total

body irradiation (TBI) 12 Gy in six fractions of 2 Gy over 3 days in 12 patiens or in combination with peroral busulphan 4 mg/kg body weight daily for 4 days in 15 patients. The remaining 10 patients were conditioned Cobimetinib clinical trial with nonmyeloablative learn more regimens (cyclophosphamide, busulphan, fludarabine, etoposide, cytosine arabinoside, melphalan, idarubicin, carmustine or with combination of antithymocyte globulin). Fifteen patients received hematopoietic

stem cells from an HLA-matched related donor and 22 patients from an HLA-matched unrelated donor. Cyclosporine A and short-term methotrexate were administered for the prophylaxis of graft-versus-host disease (GVHD). Two patients had arterial hypertension, 2 patients had diabetes mellitus and 14 patients had dyslipidemia before transplantation. One patient had a prior history of a cardiac disease because of leukemic infiltration of the heart (at the time of diagnosis of acute leukemia). The cumulative dose of anthracyclines (ANT) (idarubicin, daunorubicin and mitoxantrone) was calculated as the equivalent dose of doxorubicin. Twenty-nine patients were previously treated with ANT (median 250 mg/m2, range: 100-470). Characteristics of patients are summarized in Table 1.

Author´s contributions DC did the bacterial cultures, harvested t

Author´s contributions DC did the bacterial cultures, harvested the supernatants, performed the EIA, established and performed the cytotoxicity assays. RW did the bacterial cultures, harvested the supernatants, and quantified the transcriptional response of bacteria. MW established conditions for the bacterial cultures, harvested the supernatants. GP genotyped the bacteria and quantified the transcriptional response of bacteria. OU coordinated the study, established the cytotoxicity

assay, analysed data and wrote the manuscript. MK designed the study, analysed data and wrote the manuscript. All authors read and approved the final manuscript.”
“Background learn more Enterovirus 71 (EV71), an RNA virus of the Picornaviridae family, is first recognized from the patients with neurological abnormalities click here in California in 1969 [1]. It is known to be a causative agent of hand-foot-and-mouth disease (HFMD), and occasionally its infection would

lead to severe complications including encephalitis, aseptic meningitis, pulmonary edema or hemorrhage, and acute flaccid paralysis [2]. Outbreaks of EV71 had been reported worldwide during the last decade [2–7]. In Taiwan, there was a large epidemic of HFMD in 1998. More than 120,000 cases were reported and the outbreak resulted in 78 deaths [2]. Two years later, there was another outbreak of HFMD with 80,677 reports and 41 deaths (data from

CDC, Taiwan). 2-hydroxyphytanoyl-CoA lyase EV71 can induce the apoptosis of human glioblastoma cells [8], human microvascular endothelial cells [9], and Jurkat cells [10]. Although it has been demonstrated that the spinal cord and brain stem were the target of EV71 infections [6, 11], the infection mechanism, tissue tropism, and the neurovirulence of EV71 remain unclear. In 2009, two receptors for EV71 were discovered [12, 13]. Nishimura et al. found that human P-selectin glycoprotein ligand-1 (PSGL-1) was a functional receptor for EV71 [12]. Yamayoshi et al. reported that scavenger receptor class B2 (SCARB2) was cellular receptor for EV71 [13]. PSGL-1 is glycosylated with sialyl Lewisx epitope, and SCARB2 is also a highly glycosylated protein. According to these results, cell surface glycans histone deacetylase activity should participate in the infection of EV71. Hence, the glycomic factors which contribute to the epidemics of EV71 infection have attracted our attention. Carbohydrates expressed on cell surface involve in many physiological and pathological communications by interacting with their corresponding proteins or receptors [14, 15]. Among these events, cell surface glycan receptors which mediate viral binding and infection were well documented. For instance, Jackson et al. indicated that the entry of food-and-mouse disease virus (FMDV) into cell was initiated by the contact with cell surface heparin sulfate [16].