All tests were two-sided and P < 0 05 was considered statisticall

All tests were two-sided and P < 0.05 was considered statistically significant. Results Patient characteristics The baseline characteristics of the study population are given in Table 1. All patients were female, with a mean ± standard deviation (SD) age of 51.6 ± 12.5 years Staurosporine purchase (range, 13.5 to 80.7 years) and a mean ± SD tumor size of 3.1 ± 1.8 cm (range, 0.4 to 9.5 cm). Lymph node involvement was positive in 115 patients (78.2%). According to TNM classification, 14 patients (9.5%) were stage I, 56 (38.1%) were stage II, 76 (51.7%) were stage III, and 1 (0.7%) was stage

IV. Of the 147 patients, 57 (38.8%) were positive for ER expression, 64 (43.5%) were positive for PR, 70 (47.6%) were positive for Her2, and 39 (26.5%) were positive for basal-like

features (defined as immunohistochemically negative for both SR and Her2). Of the 147 patients, 87 (59.2%) were received adjuvant chemotherapy and 95 (64.6%) were received agents targeted against estrogen receptor. Median follow-up time was 23.0 months (range, 2 to 91 months), during which 40 patients (27.2%) experienced tumor recurrence and 51 (34.7%) developed metastases. Presence of CD44+/CD24- phenotype in invasive ductal carcinoma tissue The presence of CD44 and CD24 antigens on invasive ductal carcinoma JAK inhibitor tissues was analyzed using double-staining immunohistochemistry. Figure 1 displays representative staining patterns of CD44 and CD24. CD44 was visible primarily as membranous permanent red staining, with only eight tumors displaying cytoplasmic and membranous staining. CD24 was visible mainly as cytoplasmic diaminobenzidine staining, with only six tumors displaying membrane diaminobenzidine staining. To determine the proportion of tumorigenic CD44+/CD24- cells within each tumor, we scanned for the presence of permanent red staining without any diaminobenzidine interference. CD44+/CD24- tumor cells were present in 103 of the 147 (70.1%) tumors, but absent from the other 44 (29.9%), with the proportion of tumor cells expressing this phenotype

ranging from a few to 70%, with a median proportion of 5.8%, next and this median proportion was selected to categorize patients as CD44+/CD24- tumor cells high group and CD44+/CD24- tumor cells low group according to cutoff definition. The frequency of tumors with different proportions of CD44+/CD24- tumor cells is presented in Table 2. The proportions of CD44+/CD24- tumor cells in clinical specimens correlated significantly with lymph node involvement (P = 0.026) and PR expression (P = 0.038). Higher proportions of CD44+/CD24- tumor cells were observed in specimens from patients with (19.20%) than without (8.66%) lymph node involvement and with (21.06%) than without (13.09%) PR expression.

It was speculated

that different subcelluar distribution

It was speculated

that different subcelluar distribution of phospho-p70S6K might have distinct biological function in the malignant transformation of gastric epithelial cells. The 70-kDa S6 kinase (p70S6K) is a cytoplasmic Ser/Thr kinase that is mainly known to regulate protein translation through phosphorylation of the 40S ribosomal protein S6. Activation of p70S6K is achieved through phosphorylation on multiple Ser/Thr residues by stimulation with growth factors such as epidermal growth factor (EGF), thrombin, and lysophosphatidic acid (LPA)[23, 24]. To the role of phopsho-p0S6K protein in the progression of gastric carcinoma, its expression was compared with the aggressive behaviors of carcinoma and for the first time found that nuclear phosphor-P70S6K expression was inversely linked to tumor size, depth of invasion, lymph node metastasis and UICC staging. It was suggested that down-regulated AZD1480 expression of nuclear phospho-P70S6K was involved in the growth, invasion and metastasis of gastric carcinoma and might be employed to indicate the biological behaviors of gastric carcinoma in clinicopathological practice. Although gastric cancer is malignant tumor originating from the same gastric epithelium, its morphological features vary substantially with the individual patients [13]. According to Lauren’s classification,

intestinal-type carcinomas are characterized by cohesive carcinoma cells forming gland-like tubular structures with expanding or infiltrative growth pattern. The cell cohesion is less apparent or absent in diffuse-type carcinoma and cancer cells diffusely spread in the gastric wall lesions. Tumors that contain approximately equal quantities of intestinal and diffuse components are called mixed carcinoma [13, 14]. These three markers were preferably expressed in the older patients with gastric cancer and intestinal-type carcinoma. Here, it was noted that mTOR, cytoplasmic and nuclear P70SK6 expression was higher in intestinal-than diffuse-type carcinomas, indicating that these three markers might play an important role in intestinal-type carcinogenesis, Montelukast Sodium but less in de novo carcinogenic pathway and underlie the molecular basis for differentiation

of both carcinomas. To clarify the prognostic significance of mTOR, cytoplasmic or nuclear P70S6K expression, we here analyzed their relation with the survival of 412 patients with gastric carcinoma and found a close relationship link between the positivity of mTOR and nuclear phospho-P70S6K expression and favorable survival. Multivariate analysis demonstrated six independent prognostic factors such as age, depth of invasion, lymphatic invasion, lymph node metastasis, Lauren’s classification and mTOR expression were independent prognostic factors for overall gastric carcinomas. However, several evidences indicated that phosphor-mTOR expression was closely linked to the poor prognosis of the patients with cervical adenocarcioma or hepatocellular carcinoma [18, 25].

The production of p-nitroaniline (pNA) was monitored at 405 nm D

The production of p-nitroaniline (pNA) was monitored at 405 nm. Detection GDC 941 of PaAP antibodies in sera from CF patients Outer membranes were purified as described [46, 47]. Briefly, cells were harvested in stationary phase, resuspended (20% sucrose in 30 mM Tris, pH 8), treated with

DNase I and RNaseA and broken by French Press. Membranes were separated using a sucrose gradient. Purified S470 outer membrane and vesicles (2 μg) were separated by SDS-PAGE and SYPRO Ruby protein stained or transferred to PVDF, immunoblotted using sera (1:10 dilution) from anonymous CF patients or anti-PaAP antibodies, and developed with SuperSignal (Pierce). Acknowledgements We thank J. R. Wright (Duke University) for P. aeruginosa strain S470, C.R.H. Raetz

for strain MT616 and plasmid pJQ200SK, Erich Lanka for plasmid pMMB66EH, and M. Knowles (Adult CF Genetic Modifier Study, UNC-Chapel Hill, NC) for providing CF patient sera, Andy Ghio for providing HBE cells (EPA, NC), Chris Nicchitta (Duke Univeristy Medical Center) for TRAPα and β-tubulin antibodies, and David FitzGerald (NCI, Bethesda, MD) for monoclonal anti-PaAP antibody. We also thank J. Rudolph and T. Hsieh for equipment use, and J.L. Plank for troubleshooting. This work was supported by a Burroughs Wellcome Investigator in Pathogenesis of Infectious Disease Award (to M.J.K.), an American Lung Association research LY3023414 nmr grant, the Cystic Fibrosis Foundation, the Thomas H. Davis Research Award of the ALA of NC, and the N.I.H. Electronic supplementary material Additional file 1: Vesicles primarily colocalize with CT and transferrin in peri-nuclear regions. The data show fluorescently labeled S470 vesicles colocalize with CT and transferrin in perinuclear regions of A549 cells. (PDF 757 KB) Additional file 2: PaAP contributes to the cell association of vesicles in a dose-dependent manner. The data show the amount of PaAP on vesicles correlates with the amount of vesicle association with A549 cells. (PDF 215 KB) Additional file 3: Vesicle expression and click here activity of S470APKO5 complemented with

plasmid-expressed PaAP. The data show the lack of PaAP activity in the APKO5 strain, the correlation between secreted aminopeptidase activity of the complemented strain with the amount of PaAP secreted, and that induced, plasmid-expressed PaAP in APKO5 is secreted to the same extent as S470 but is not vesicle-associated. (PDF 171 KB) References 1. Yoon SS, Hennigan RF, Hilliard GM, Ochsner UA, Parvatiyar K, Kamani MC, Allen HL, DeKievit TR, Gardner PR, Schwab U, Rowe JJ, Iglewski BH, McDermott TR, Mason RP, Wozniak DJ, Hancock RE, Parsek MR, Noah TL, Boucher RC, Hassett DJ: Pseudomonas aeruginosa anaerobic respiration in biofilms: relationships to cystic fibrosis pathogenesis. Developmental cell 2002,3(4):593–603.CrossRefPubMed 2.

Rawson and colleagues [7] supplemented male subjects with Cr for

Rawson and colleagues [7] supplemented male subjects with Cr for 5 days prior to 50 maximal eccentric contractions. The study showed that maximal isometric force of the elbow flexors, and serum creatine kinase (CK) and lactate dehydrogenase (LDH) activity, in response to eccentric exercise were not significantly different between the Cr-supplemented and control groups during the 5 days following exercise.

Therefore, it was suggested that Cr supplementation does not reduce indirect markers of muscle damage or enhance recovery from high-force eccentric exercise. Similarly, Warren et al. [8] demonstrated that recovery of mouse anterior crural muscle strength after damage (induced Selleckchem LY333531 by 150 eccentric contractions) was unaffected RXDX-101 following 2-weeks of

Cr supplementation. Following 3 minutes recovery, there was no effect on isometric strength or on torque loss at any eccentric or concentric angular velocity. However, a number of limitations exist with this study. Firstly, researchers were only interested in how increased muscle Cr influenced peak strength loss and not the recovery of strength per se after injury. Therefore, the 3 min recovery period may not be long enough to see any beneficial effect of Cr supplementation on muscle strength loss. Secondly, Cr supplementation may have attenuated other markers of muscle damage such as blood concentrations of myocellular proteins. However, since injury assessment was only muscle function based, these were not measured. The effect of Cr supplementation upon inflammatory and muscle soreness markers has also been examined following prolonged running [5]. Experienced marathon runners were supplemented (4 doses of 5 g of Cr) for 5 days prior to a 30 km race. Blood samples were collected pre-race, and 24 hours following the end of the test, to measure for CK, LDH, prostaglandin

E2 (PGE2) and TNFalpha (TNF-α). Farnesyltransferase Athletes from the control group presented an increase in all muscle soreness markers, indicating a high level of cell injury and inflammation, while Cr supplementation significantly attenuated these increases, with the exception of CK. However, while this Cr supplementation protocol may be an effective strategy in maintaining muscle integrity during and after intense prolonged aerobic exercise, it may not be sufficient to protect muscle fibres from more damaging exercises, such as those shown by Rawson et al. [7]. Therefore, the purpose of this investigation was to supplement a group of healthy participants with either Cr or a placebo prior to, and in the days after a single bout of eccentric exercise. The extent of, and recovery from, damage was evaluated by the following established, indirect markers of exercise-induced muscle damage; knee extension/flexion force development (MVC), and plasma CK and LDH activity [9, 10].

Electronic supplementary material Additional file 1: Comparison o

Electronic supplementary material Additional file 1: Comparison of HmuY homologues. BIRB 796 cell line Comparison of homologous HmuY amino-acid sequences identified in human pathogens (A) and bacteria identified in oral tissues (B). Amino-acid sequences lacking signal peptides are shown. Positions with identical amino acids in more than 30% of the sequences are shown in black boxes and partial homology is indicated in grey boxes. Phylogenetic relationship between homologous HmuY amino-acid sequences (C). Bacteria infecting the oral cavity are shown in bold. The phylogenetic tree was determined with the Neighbor-Joining method. Bootstrap values are included. Pgi, Porphyromonas gingivalis; Pen, P. endodontalis;

Pue, P. uenonis; Bfr, Bacteroides fragilis; Bfi, B. finegoldii; Bco, B. coprocola;

Bst, B. stercoris; Bdo, B. dorei; Bvu, B. vulgatus; Bov, B. ovatus; Bca, B. caccae; Bth, B. thetaiotaomicron; Bcp, B. coprophilus; Bsp, Bacteroides sp.; Coc, Capnocytophaga ochracea; Cgi, C. gingivalis; Csp, C. sputigena; Lbo, Leptospira borgpetersenii; Lin, L. interrogans; Ssp, Sphingobacterium spiritivorum; Pbi, Prevotella bivia; Por, P. oris; Pbe, P. bergensis; Pti, P. timonensis; Pme, P. melaninogenica; Pve, P. veroralis; Psp, Prevotella sp.; Pta, P. tannerae. Selleck CUDC-907 (DOC 318 KB) Additional file 2: Analysis of surface exposure of HmuY. Analysis of surface exposure of P. gingivalis HmuY analyzed by whole-cell ELISA. P. gingivalis wild-type (A7436, W83) and hmuY deletion mutant (TO4) strains were grown in basal medium supplemented with hemin (Hm) or dipyridyl (DIP). The cells were washed and diluted with PBS (starting at OD660 = 1.0). Varying dilutions of P. gingivalis cells were adsorbed on the wells of the microtiter plate and reacted with pre-immune serum (A) or purified pre-immune IgGs (pre) (B) and immune anti-HmuY Nitroxoline serum (A) or purified immune anti-HmuY IgGs (im) (B). Representative data are shown. (DOC 74 KB) Additional file 3: P. gingivalis growth in broth cultures and biofilms, and biofilm accumulation. P. gingivalis growth was analyzed by measuring the OD at 660 nm, cell viability by plating cells on ABA

plates and colony forming unit (CFU) calculation, and biofilm accumulation by microtiter plate assay. (DOC 36 KB) References 1. Pihlstrom BL, Michalowicz BS, Johnson NW: Periodontal diseases. Lancet 2005, 366:1809–1820.PubMedCrossRef 2. Schenkein HA: Host responses in maintaining periodontal health and determining periodontal disease. Periodontol 2000, 200640:77–93. 3. Mayrand D, Holt SC: Biology of asaccharolytic black-pigmented Bacteroides species. Microbiol Rev 1988, 52:134–152.PubMed 4. Lamont RJ, Chan A, Belton CM, Izutsu KT, Vasel D, Weinberg A: Porphyromonas gingivalis invasion of gingival epithelial cells. Infect Immun 1995, 63:3878–3885.PubMed 5. Belton CM, Izutsu KT, Goodwin PC, Park Y, Lamont RJ: Fluorescence image analysis of the association between Porphyromonas gingivalis and gingival epithelial cells.

Phys Chem Chem Phys 2008, 10:303–310 CrossRef 14 Krueger A, Steg

Phys Chem Chem Phys 2008, 10:303–310.CrossRef 14. Krueger A, Stegk J, Liang Y, Lu L, Jarre G: Biotinylated nanodiamond: simple and efficient functionalization of detonation diamond. Langmuir 2008, 24:4200–4204.CrossRef 15. O’brien RW, Ward DN: Electrophoresis

of a spheroid with a thin double layer. J Colloid Interface Sci 1988, 121:402–413.CrossRef 16. Cheng XK, Kan AT, Tomson MB: Naphthalene adsorption and desorption from aqueous C60 fullerene. J Chem Eng Data 2004, 49:675–683.CrossRef 17. Brooks PC, Montgomery AM, Cheresh DA: Use of the 10-day-old chick embryo model for studying angiogenesis. Methods Mol Biol 1999, 129:257–269. 18. Blacher S, Devy L, Hlushchuk R, Larger E, Lamandé N, Burri P, Corvol P, Djonov V, Foidart JM, Noël A: Quantification of angiogenesis in the chicken chorioallantoic membrane (CAM). Image Analysis selleckchem & Stereology 2005, 24:169–180.CrossRef 19. Ribatti D, Vacca A, Roncali L, Dammacco F: The chick embryo chorioallantoic membrane as a model for in vivo research on angiogenesis. Int J Dev Biol 1996, 40:1189–1197. 20. Flamme I: Is extraembryonic angiogenesis FK228 in the chick

embryo controlled by the endoderm? A morphology study. Anat Embryol (Berl) 1989, 180:259–272.CrossRef 21. Javerzat S, Franco M, Herbert J, Platonova N, Peille AL, Pantesco V, De Vos J, Assou S, Bicknell R, Bikfalvi A, Hagedorn M: Correlating global gene regulation to angiogenesis in the developing chick extra-embryonic vascular system. PLoS One 2009, 4:e7856.CrossRef 22. Bakowicz-Mitura K, Bartosz G, Mitura S: Influence

of diamond powder particles on human gene expression. Surf Coatings Technol 2007, 201:6131–6135.CrossRef 23. Bhattacharya E, Mukherjee P, Xiong Z, Atala A, Soker S, Mukhopadhyay D: Gold nanoparticles inhibit VEGF165-induced proliferation of HUVEC cells. Idoxuridine Nano Lett 2004, 4:2479–2481.CrossRef 24. Mukherjee P, Bhattacharya R, Wang P, Wang L, Basu S, Nagy JA, Atala A, Mukhopadhyay D, Soker S: Antiangiogenic properties of gold nanoparticles. Clin Cancer Res 2005, 11:3530–3534.CrossRef 25. Wang K, Ruan J, Song H, Zhang J, Wo Y, Guo S, Cui D: Biocompatibility of graphene oxide. Nanoscale Res Lett 2011, 6:8. 26. Liao KH, Lin Y, Macosko CW, Haynes CL: Cytotoxicity of graphene oxide and graphene in human erythrocytes and skin fibroblasts. ACS Appl Mater Interfaces 2011, 3:2607–2615.CrossRef 27. Jiang Q, Li JC, Wilde G: The size dependence of the diamond-graphite transition. J Phys Condens Matter 2000, 12:5623.CrossRef 28. Wang J, Morita I, Onodera M, Murota SI: Induction of KDR expression in bovine arterial endothelial cells by thrombin: involvement of nitric oxide. J Cell Physiol 2002, 190:238–250.CrossRef 29. Duval M, Bédard-Goulet S, Delisle C, Gratton JP: Vascular endothelial growth factor-dependent down-regulation of Flk-1/KDR involves Cbl-mediated ubiquitination. Consequences on nitric oxide production from endothelial cells. J Biol Chem 2003, 278:20091–20097.

Bold italic bases indicate the HindIII restriction sites Underli

Bold italic bases indicate the HindIII restriction sites. Underlined bases are the overlapping learn more sequences recognized by the in-fusion enzyme. In CaNik1p (1081 aa), all the HAMP domains (63–485 aa) were deleted using

the in-fusion HD cloning kit (Clontech). Briefly, the in-fusion enzyme is able to fuse up to four DNA fragments with a linearized vector upon recognizing 15 bp overlapping sequences at their ends. To allow this fusion, the 15 bp overlaps were introduced to the primers which were used to amplify the target fragments. The pYES2 vector was linearized using the restriction enzyme HindIII and the pYES-CaNIK1-TAG vector was used as a template for amplification of the gene fragments. The sequence of CaNIK1 upstream of the fragment encoding the HAMP domains (1–186 bp) was amplified using the HMPF1 and HMPR1 primers (Table 2). HMPF1 included homologous 15 bp with the end of the linearized vector downstream of the galactose promoter. The CaNIK1 fragment located downstream the sequence encoding the HAMP domains and extended by the His-FLAG tag (1454–3243 bp) NVP-BGJ398 mw was amplified using the HMPF2 and HMPR2 primers

(Table 2). HMPF2 and HMPR2 shared 15 bp homologous stretches with the 172–186 bp fragment of CaNIK1 and with the other end of the HindIII-linearized pYES2 vector, respectively. HindIII restriction

sites were introduced into the sequences of the HMPF1 and HMPR2 primers. After separation of the PCR amplified fragments Phosphatidylinositol diacylglycerol-lyase by electrophoresis on 1.2% agarose gels, the gel pieces carrying the amplification products were excised and the DNA was purified using a gel extraction kit (Qiagen). The purified fragments were ligated into the digested pYES2 vector using the in-fusion enzyme according to the manufacturer’s instructions. The existence of the introduced mutations was further confirmed by sequencing the generated constructs (Dept. GNA, HZI, Braunschweig) using primers spanning the target fragments. The mutated constructs were used to transform S. cerevisiae using the lithium acetate method [40]. Transformants (Table 1) were selected on SD-ura agar plates. Susceptibility assays In 96 well microtiter plates, working cultures of the transformants were incubated in 180 μl SG-ura supplemented with the appropriate concentrations of the antifungals in triplicates for 24 h. The starting OD at 620 nm was 0.

Jpn J Appl Phys 2009, 48:04C187 CrossRef 18 Huang CH, Igarashi M

Jpn J Appl Phys 2009, 48:04C187.CrossRef 18. Huang CH, Igarashi M, Horita S, Takeguchi CP-868596 manufacturer M, Uraoka Y, Fuyuki T, Yamashita I, Samukawa S: Novel Si nanodisk fabricated by biotemplate and defect-free neutral beam etching for solar cell application. Jpn J Appl Phys 2010, 49:04DL16.CrossRef 19. Huang CH, Wang XY, Igarashi M, Murayama A, Okada Y, Yamashita I, Samukawa S: Optical absorption characteristic

of highly ordered and dense two-dimensional array of silicon nanodiscs. Nanotechnol 2011, 22:105301.CrossRef 20. Hirano R, Miyamoto S, Yonemoto M, Samukawa S, Sawano K, Shiraki Y, Itoh KM: Room-temperature observation of size effects in photoluminescence of Si 0.8 Ge 0.2 /Si nanocolumns prepared by neutral beam etching. Appl Phys Express 2012, 5:082004.CrossRef 21. Budiman MF, Hu W, Igarashi M, Tsukamoto R, Isoda T, Itoh KM, Yamashita I, Murayama A, Okada Y, Samukawa S: Control of optical bandgap energy and optical absorption coefficient by geometric parameters in sub-10 nm silicon-nanodisc array structure. Nanotechnol 2012, 23:065302.CrossRef 22. Igarashi M, Budiman MF, Pan W, Hu W, Tamura Y, Syazwan ME, Usami N, Samukawa S: Effects of formation of mini-bands in two-dimensional array of silicon nanodisks with SiC interlayer

for quantum dot solar cells. Nanotechnol 2013, 24:015301.CrossRef 23. Kuo DMT, Guo GY, Chang YC: Tunneling current through a quantum dot array. Appl Phys Lett 2001, 79:3851.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions

MI and SS conceived NSC 683864 nmr and designed the experiment, fabricated the silicon nanodisk samples, performed electrical and optical measurements, analyzed these data, and wrote the paper. MMR and NU fabricated the solar cell structures and analyzed the I-V data. WH performed the theoretical calculations. All authors discussed the results, commented on the manuscript, and read and approved the final version.”
“Background Dye-sensitized solar cells (DSSCs) have attracted considerable attention as a viable alternative to conventional silicon-based photovoltaic cells [1] because of their Suplatast tosilate low-production cost, high conversion efficiency, environmental friendliness, and easy fabrication procedure [2–5]. A typical DSSC is comprised of a nanocrystalline semiconductor (TiO2), an electrolyte with redox couple (I3 −/I−), and a counter electrode (CE) to collect the electrons and catalyze the redox couple regeneration [6]. Extensive researches have been conducted in order for each component to achieve highly efficient DSSCs with a modified TiO2[7], alternative materials [8, 9], and various structures [10–12]. Usually, Pt-coated fluorine-doped tin oxide (FTO) is used as a counter electrode owing to its superior catalytic activity [13]. However, there are researches reporting that Pt corrodes in an electrolyte containing iodide to generate PtI4[14, 15].

The B-C17 profile was predominant in Scotland in this cohort of i

The B-C17 profile was predominant in Scotland in this cohort of isolates, specifically in learn more the regions of Aberdeenshire, Angus, Borders and Perth and Kinross (Table 1 and see supplementary dataset in Additional file 1 and Additional file 2: Table S1). The C1 profile was more widely spread across

Europe and was found in the Czech Republic, Greece, Finland, The Netherlands, Norway and Spain, (Table 1 and see supplementary dataset in Additional file 1 and Additional file 2: Table S1). Table 1 Combined PFGE, MIRU-VNTR and IS900-RFLP profiles by Map origin Profile     No of isolates Country1-Host2 PFGE 3 MIRU-VNTR 4 IS900-RFLP 5   CZ ES FL GR NL NO SCO [1-1] 1 C1 2 RD       G     [1-1] 2 C1 7 C, RD C C(2)   C, RD     this website [1-1] 2 C18 1     C         [1-1] 2 C5 1         C     [1-1] 6 C1 2         C(2)     [2-1] 1 C1

13 C(4), FD, M C C(2)     G(3), S   [2-1] 1 C9 1 H             [2-1] 1 C17 39           C, S B, C(6), CR, F(2), H, R(13), RK, S(7), ST(3), W, WM [2-1] 2 C17 2             C(2) [2-1] 2 C1 9 C FD     C(2), G, S(4)     [2-1] 2 C5 1         C     [2-1] 2 C36 1         C     [2-1] 5 C10 1 C             [2-1] 19 C17 1             S [2-1] 24 C1 1         S     [2-1] 22 C38 1         G     [2-1] 25 C17 1             R [2-10] 1 C1 1           G   [2-17] 2 C22 1         S     [2-19] 2 C5 2       G, S       [2-30] 1 C16 1         RD     [2-30] 25 C16 1             W [3-2] 1 C17 3             F, G, J [5-2] 1 C17 1             S [9-7] 21 S4 1             S [15-16] 38 C1 1   G           [15-25] 26 C1 7   G(7)           [16-11] 20 I5 1   G           [18-1] 13 C1 1   G           [20-1] 1 C1 1 C             [26-1] 35 C1 1 C             [27-18] 2 C27 1   C           [29-15] 36 C1 1       G       [29-15] 37 C1 3       G(3)       [30-21] 2 C1 1         G     [31-17] 69 C39 1   G           [32-29] 1 C17 1             ST [34-22] 2 C1 2         RD(2)     [34-22] 8 C1 1         RD     [36-27] 1 C1 1 M             [37-23] 29 I4 1 FD             [40-28] 26 C1 1   G           [41-1] 1 C9 1 C             [58-64] 35 C1 1 M

            1. Amino acid Country: CZ Czech Republic, ES Spain, FL Finland, GR Greece, NL The Netherlands, NO Norway, SCO Scotland 2. Host: B badger (Meles meles), C cow (Bos taurus), CR crow (Corvus corone), F fox (Vulpes vulpes), FD fallow deer (Dama dama), G goat (Capra hircus), H hare (Lepus europaeus), J jackdaw (Corvus monedula), M moufflon (Ovis musimon), R rabbit (Oryctolagus cuniculus), RD red deer (Cervus elaphus), RK rook (Corvus frugilegus), S sheep (Ovis aries), ST stoat (Mustela erminea), W weasel (Mustela nivalis), WM wood mouse (Apodemus sylvaticus). The number of isolates obtained from each host species within a country is given in parenthesis. 3. Nomenclature as defined by Stevenson et al. 2002 [11] 4. Nomenclature as defined by Thibault et al. 2007 [56] 5. Nomenclature as defined by Pavlik et al.

Histochem Cell Biol 2006, 126:159–164 CrossRefPubMed 23 Nilsson

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