With respect to the reference genome, β1 strains had between 688 and 9,828 SNPs and β2 strains had between 17,355 and 21,071 SNPs (Figure  2). In the β1 strains the number of SNP-dense

regions was low, whereas there were many more SNPs in the β2 strains due to their greater phylogenetic difference from the reference. The single ψ strain had 32,828 SNPs (not shown in Figure  2). Although the β2 strains and the ψ strain had a broadly similar number of SNPs, they were clustered in patterns that were distinct between the groups, a finding consistent with regions of high SNP density likely representing distinct recombination events. We hypothesised that “blocks” of NVP-LDE225 DNA sequence with a high frequency of SNPs, separated by regions of the genome with low SNP density, could each represent an individual transformation event (Figure  2). To investigate this, we analysed two strains (RM7578 and RM7122) that have the same multi-locus sequence type. RM7578, the strain most closely related to the reference strain 10810, has five blocks of SNPs. For this analysis, blocks were defined as contiguous regions containing at least 30 SNPs, with each SNP separated by mTOR inhibitor no more than 300 bp. 91%

of 694 SNPs between strains RM7578 and 10810 were found within these five blocks, amounting in total to 23.5 kbp of DNA, or 1.2% of the genome. Strain RM7122 had 15 blocks of SNPs when compared to strain 10810, equivalent to 2.4% of the genome. In the β1 strains, the size of these blocks ranged from less than 0.5 to more than 25 kbp, with a median size of 4.8 kbp (Figure  3), findings within the range recently reported experimentally for H. influenzae strains [17]. We concluded that the blocks of SNPs identified between the closely related Hib strains represented recombination events, click here resulting in allelic exchanges that could delete or insert novel DNA, including whole genes. Figure 3 Size of SNP blocks found in the β1 group of Hib

strains. This histogram represents the frequency of different sizes of SNP blocks (as defined in the text) in the genomes of β1 H. influenzae type b strains. Inserted or deleted regions of DNA in Hib strains, relative to the genome sequence of reference strain 10810, were identified by BLASTN searches and the ACT genome browser. For a closely related strain, DC800, an example of insertion of a novel block of SNPs, mediated through transfer of DNA from an unknown donor, was identified. This inserted DNA included a putative gene flanked by regions of significant similarity. As a further example, comparison between two more divergent genomes (RM7060 and 10810) revealed at least 16 regions of DNA, each over 500 bp in length, that were present in one strain but not the other (Table  2). These regions constitute over 17.

Mice were euthanised selleck products after 3 days of infection,

and then the catheters were removed carefully and washed briefly with phosphate-buffered saline (PBS). Catheters were placed in 1 ml of sterile PBS and sonicated for 30 s to remove the adherent bacteria. The number of bacteria was determined by plating on tryptic soy agar (TSA). Anaerobic conditions Biofilm formation was also monitored under anaerobic conditions. The Forma Anaerobic System (Thermo, Waltham, USA) was used to provide strictly anaerobic conditions for bacterial growth and related operations. Overnight cultures were adjusted to OD600 of 6.5, and then the bacterial cultures were carried into the anaerobic system for 1:100 dilution and inoculated into 24-well

plates. Resazurin, which is used as an indicator for anaerobic conditions, was added to final concentration of 0.0002% (w/v). The plates were incubated at 37°C for 4 h and OD560 was determined after crystal violet staining. A standard anaerobic jar of 120 ml volume was used to monitor the biofilm formation of the WT strain and the mutants under anaerobic conditions. Medium and containers with thorough scavenging were prepared as follows. Water was boiled using a three-necked bottle to degas the water while nitrogen AZD8055 ic50 was bubbled into the bottle to keep the contents anaerobic. TSBg medium was prepared with this degassed water. Then each anaerobic jar was dispensed Metalloexopeptidase with 50 ml TSBg while nitrogen was gassed into the jar to drive out the oxygen. The rubber plug was quickly stuffed up following by an aluminium cap added, and then the jar containing TSBg was autoclaved at 121°C, 15 m. After preparation of the medium, biofilm formation under anaerobic conditions was examined and the operations

were carried out in the anaerobic system. Scanning electron microscopy (SEM) Biofilm bacteria were grown on coverslips for five days, and then the coverslips were cut from the flow-cell settings and immediately fixed with 2.5% (vol/vol) glutaraldehyde in Dulbecco PBS (pH 7.2) overnight. According to the methods described previously [50], the coverslips were rinsed with PBS three times and dehydrated through an ethanol series (30%, 50%, 75%, 85% and 95%). Samples were dried and gold-palladium coated prior to SEM examination and micrographs were made with a XL-30 SEM at × 1500 to × 5000 magnification (FEI, Hillsboro, USA). RNA isolation and real-time RT-PCR All the bacteria used for RNA isolation to investigate the expression of genes that affect biofilm formation were those that grew statically in the 24-well plate. Bacteria in the wells of biofilm formation at different time courses (4 h, 8 h, 12 h) were collected and re-suspended in TE (Tris-EDTA) buffer (pH 8.0) containing 10 g/l lysozyme and 40 mg/l lysostaphin. After incubation at 37°C for 8 m, S.

A vector with constitutively active Renilla luciferase (pRL-CMV, Promega) was chosen as internal control. One day prior to transfection, approximately 0.5 × 105 cells per well were seeded in a 24-well format. Transfection was performed for 6 h using 1.5 μl/well of Lipofectamine 2000 (Invitrogen), 0.54 μg/well of pNFκB-Luc and 0.06 μg/well of pRL-CMV. Lipofectamine 2000 and plasmids were diluted in serum-free Opti-MEM (Invitrogen) during preparation of DNA-liposome complexes. All plasmids were isolated by an endofree plasmid isolation kit (Macherey-Nagel)

according to the manufacturer’s instructions. Luciferase was detected Selleckchem ITF2357 using the dual-luciferase reporter assay system (Promega) and a Turner TD20/20 luminometer (Turner biosystems) set to 10s measurement with an initial 2s delay. Transcription factor activation was expressed as relative NF-κB activation, defined as the ratio between firefly luciferase and Renilla luciferase activity. Ratios were normalized against either non-stimulated control cells or cells stimulated with E. coli. The difference between means was tested statistically by using Student’s t-test, with the limit for statistical Anti-infection Compound high throughput screening significance set to p-values < 0.05. Epithelial cell line challenge T24 bladder cells transfected with luciferase vectors (pNFκB-Luc

and pRL-CMV) were challenged for 24 h in a 24-well plate format with 2 × 107 cfu/ml of viable or the equivalent number of heat-killed lactobacilli (L. rhamnosus GR-1 or GG). For activation of NF-κB, as well as cytokine and chemokine release, epithelial cells were stimulated with heat-killed E. coli (108 cfu/ml). Cell culture supernatants for ELISA were collected from Carnitine palmitoyltransferase II challenge experiments using non-transfected cells and stored at -20°C until use. For qPCR, cells were stimulated

in the same way although all experiments were done in 6-well plates (with proportional increase in number of cells and bacteria) for increased amounts of RNA. Cell viability was determined by staining dead cells using propidium iodide followed by flow cytometry (Cytomics FC500, Beckman Coulter). To inhibit agonist activation of TLR4 in T24 cells, transfected cells were exposed to Polymyxin B (Invivogen), which effectively binds to LPS and thereby inhibits TLR4 activation, at a concentration of 50 μg/ml for 1 h prior to the experiment and subsequently challenged with bacteria, as previously described. Enzyme-linked immunosorbent assays TNF, IL-6 and CXCL8 levels were determined by BD ELISA sets (BD Biosciences) according to the manufacturer’s instructions. A volume of 100 μl of capture antibody (diluted 1:250 coating buffer) was added to each well of a 96-well ELISA microplate (Nunc) and allowed to bind overnight at 4°C. Wells were washed three times with PBST (PBS pH 7.0 with 0.05% Tween-20) and blocked with PBS supplemented with 10% heat-inactivated FBS (HyClone) for 1 h in room temperature after which the wells were washed three times with PBST.

Because of the higher prevalence of TB and emerging availability of anticoagulation services in this setting, there exists a growing population of patients who are facing this drug interaction [18, 19]. Even though anticoagulation clinics have been shown to improve patient outcomes when compared to individual physician care, the limited data concerning this drug–drug interaction in this population presents an enormous challenge to clinicians providing care to patients on concomitant rifampicin

and warfarin therapy [2]. Without https://www.selleckchem.com/products/chir-99021-ct99021-hcl.html data from patients receiving care in developing countries, clinicians have to rely primarily on the previously published case reports conducted only in developed countries, some of which suggest the need to increase warfarin doses by greater than 100–200 % [5, 9, 10]. The objective of this case series is to provide insight to practicing clinicians on the unique dynamics of the drug interaction between rifampicin and warfarin therapy in a resource-constrained setting in western Kenya. The case series will provide details on commonly encountered scenarios in these settings and the adjustments made to maintain a therapeutic INR. With the high numbers of TB infected patients within this setting, this represents one of the largest case series on this often encountered drug interaction and the first which considers the unique characteristics

of patients within a rural resource-constrained setting. 2 Methods The study is a retrospective chart review of patients receiving concurrent anti-TB medications containing rifampicin and oral anticoagulation therapy with warfarin. This study Fulvestrant was conducted in a pharmacist-managed anticoagulation clinic

within the Moi Teaching and Referral Hospital (MTRH) in Eldoret, Kenya. The anticoagulation clinic was established through a partnership formed by the Purdue University College of Pharmacy, the Academic Model Providing Access to Healthcare (AMPATH), MTRH and Moi University School of Medicine [20]. The clinic was developed as AMPATH expanded its Aprepitant scope of practice from the human immunodeficiency virus (HIV) pandemic to chronic disease management and primary health care. Since the clinic’s inception in December 2008, it has served over 700 patients and currently has more than 350 active patients. The majority of patients are enrolled into the anticoagulation clinic through referrals from MTRH clinicians providing health services in the public inpatient and outpatient clinics. Most patients are referred from the cardiology, obstetrics/gynecology, internal medicine and hematology/oncology departments. The most common indications for anticoagulation in the clinic include VTE, valvular damage secondary to rheumatic heart disease (RHD) and atrial fibrillation. Patients with mechanical heart valves and other cardiomyopathies also receive anticoagulation therapy within the clinic [18].

Analysis of CYPs expressional Fulvestrant levels in tumor cells may allow prognosis decisions and therapy predictions. In this study, only the expression level of CYP2C40 increased at all stages of hepatocarcinogenesis in rat models, while the remaining CYPs decreased (Figure 6C). Clearly, further investigation is needed to determine the role(s) of CYPs in hepatocarcinogenesis. In addition to the deregulated expression of metabolism associated genes, we noticed that among the DEGs in the hepatocarcinogenesis

of rat models, some known tumor-associated genes, such as Rb1 and Myc, showed deregulated expression occurring at all the stages of hepatocarcinogenesis. Their persisting activation or deactivation could induce the tumor phenotype, as well as play roles at the later stage of progression and metastasis. Meanwhile, some known metastasis-associated genes are found deregulated at the promotion stage of tumor development. For example, the expression level of Ndrg2 and Hrasls3 (HRAS like suppressor 3) decreased at all stages compared to the normal livers, while the expression level of Nme1 (expressed in non-metastatic cells 1) increased. Generally, it was thought that genes involved in the development of

carcinoma activation participated at the early stage, while genes participating in the metastasis were activated at the latter stage of tumor progression[42]. In opposition to the traditional model, Bernards and Weinberg proposed that the metastatic ability of tumor cells occurred at the early stage of tumor development[43]. Some oncogenes such as Ras and DMXAA concentration Src assigned the tumor cells with the metastatic phenotype [44–46]. As we known, the important characteristic of malignant tumor cells is the capability of invading the vicinity, forming metastasis foci at the remote organ,

overcoming the host’s control over the microenvironment[47, Resminostat 48]. The malignant transformation of liver cells occurred on the basis of chronic injury, regeneration and cirrhosis. The liver cancer cells could synthesize ECM components and the ECM surrounding liver cancer cells was found to be different from that of stroma in the normal organ [49–51]. Integrin and laminin are the major components of ECM. The interaction between integrin and laminin is closely related to the signal transduction, providing survival signals for the cells, mediating the liver cancer cells formation of pseudopodia, and adherence with laminin, which are imperative if a liver cancer cell is to migrate and invade [52–55]. In the process of hepatocarcinogenesis in this rat model, the deregulated expression of many ECM associated genes plays important roles in the hepatocarcinogenesis, e.g. Itga6, Lamc1, Col1a1 and Spp1, etc. (Table 2, 3 and additonal file 2). The differential expression profile of ECM associated genes in time course and space is very important to cellular proliferation and migration.

Assessment of response to radiotherapy We monitored patients during daily radiotherapy sessions and also during post-radiotherapy follow up. Response assessment to radiotherapy was assessed by means of computed tomography and endoscopies. In addition, WHO performance

status, bowel overall function and daily movements, blood pressure and body weight were also monitored. Evaluation of toxicity During radiotherapy and on a weekly basis, clinical examination and signs of toxicity were recorded according to Common Toxicity Criteria (CTC, version 2.0). Amifostine toxicity was also assessed by the CTC criteria. After the DAPT mouse end of radiotherapy and every three months for the first two years and then every six months for the next years, clinical examination and evaluation of toxicity were also planned. Histopathological study Bowel mucosa biopsies were fixed in 4% buffered formalin, embedded in paraffin and cut in 5 μm sections. For histological evaluation the sections were stained with the standard haematoxylin-eosin (H&E) stain. Furthermore, immunostaining was performed by the labeled straptavidin-avidin-biotin method (LSAB Kit, Dako SA, Glostrup, Denmark) using the monoclonal antibody directed against active Ferroptosis inhibitor caspase

3 (dilution 1:500; clone C92-605, Pharmigen, San Diego, CA), as previously described [12]. Evaluation of Haematoxylin-eosin (H&E) staining Since there www.selleck.co.jp/products/BAY-73-4506.html are no general and precisely defined criteria for histologic diagnosis and grading of radiation colitis our histologic reports were based on relevant studies and textbooks

[13, 14]. According to these colitis lesions were graded as absent (-), mild (+) and moderate to severe (++/+++). Histologic features of colitis included presence of increased inflammatory infiltration of the lamina propria (estimation of proportion of neutrophils, eosinophils, lymphocytes and plasma cells, as well as the presence of muciphages-foamy cells), presence of erosions or ulcers, absence of viable crypts and presence of cryptitis (inflammatory cells permeating the crypt epithelium and destroying crypts) and crypt abscesses (cellular cell irregularities, cytoplasmic vacuolation, nuclear abnormalities, increased apoptotic bodies), architectural crypt distortion (crypt branching and shortening, crypt disarray-slight distortion with widening, atrophy) presence of fibrosis of the lamina propria, vascular changes (telangiectasia, endothelial degeneration, platelet thrombi formation). Evaluation of immunostaining The number of active caspase 3 positive epithelial cells, within the surface epithelium as well as within the crypts, was recorded by using the ×40 objective lens. Since the tissue contained in the biopsies was limited, the whole biopsy area was evaluated in all cases.

Int J Radiat Oncol Biol Phys 2000, 47:895–904.PubMedCrossRef Sorafenib in vitro 11. Pedersen AN, Korreman S, Nyström H, Specht L: Breathing adapted radiotherapy of breast cancer: reduction of cardiac and pulmonary doses using voluntary inspiration breath-hold. Radiother Oncol 2004, 72:53–60.PubMedCrossRef

12. Sixel KE, Aznar MC, Ung YC: Deep inspiration breath hold to reduce irradiated heart volume in breast cancer patients. Int J Radiat Oncol Biol Phys 2001, 49:199–204.PubMedCrossRef 13. Remouchamps VM, Vicini FA, Sharpe MB, Kestin LL, Martinez AA, Wong JW: Significant reductions in heart and lung doses using deep inspiration breath hold with active breathing control and intensity-modulated radiation therapy for patients

treated with locoregional breast irradiation. Int J Radiat Oncol Biol Phys 2003, 55:392–406.PubMedCrossRef 14. Korreman SS, Pedersen AN, Nottrup TJ, Specht L, Nystrom H: Breathing adapted radiotherapy for breast cancer: Comparison of free breathing gating with the breath-hold technique. Radiother Oncol 2005, 76:311–318.PubMedCrossRef 15. Kini VR, Vedam SS, Keall PJ, Patil S, Chen C, Mohan R: Patient training in respiratory-gated radiotherapy. Med Dosim 2003, 28:7–11.PubMedCrossRef 16. Stranzl BAY 80-6946 ic50 H, Zurl B: Postoperative irradiation of left-sided breast cancer patients and cardiac toxicity. Strahl Onkol 2008, 184:354–358.CrossRef 17. Pinnarò P, Soriani A, Landoni V, Giordano C, Papale M, Marsella A, Marucci L, Arcangeli G, Strigari L: Accelerated hypofractionated radiotherapy as adjuvant regimen after conserving surgery for early breast cancer: interim report of toxicity after a minimum follow up of 3 years. J Exp Clin Cancer Res 2010, 29:9.PubMedCrossRef 18. Kong FM, Klein EE, Bradley JD, Mansur DB, Taylor ME, Perez CA, Myerson RJ, Harms WB: The Impact of central lung distance,

maximal hearth distance, and radiation technique on the volumetric dose of the lung and heart for intact breast radiation. Int J Radiat Oncol Biol Phys 2002, 54:963–971.PubMedCrossRef 19. Lyman JT: Complication probability as assessed from dose volume histograms. Radiat Res 1985,104(8):13–9.CrossRef Edoxaban 20. Bruzzaniti V, Abate A, Pedrini M, Benassi M, Strigari L: IsoBED: a tool for automatic calculation of biologically equivalent fractionation schedules in radiotherapy using IMRT with a simultaneous integrated boost (SIB) technique. J Exp Clin Cancer Res 2011, 30:52.PubMedCrossRef 21. Martel MK, Sahijdak WM, Ten Haken RK, Kessler ML, Turrisi AT: Fraction size and dose parameters related to the incidence of pericardia effusion. Int J Radiat Oncol Biol Phys 1998, 40:155–161.PubMedCrossRef 22. Gagliardi G, Constine LS, Moiseenko V, Correa C, Pierce LJ, Allen AM, Marks LB: Radiation Dose-Volume effects in the heart. Int J Radiat Oncol Biol Phys 2010,76(3):77–85.CrossRef 23.

2002), static light scattering (Chen and Szostak, 2004) and merocyanine-540 HDAC phosphorylation assays (Dixit and Mackay 1983). As an alternative, we used conductimetric titration (Briz and Velásquez 2002) to determine the CVC of fatty acid vesicles. When the conductance of a micellar solution of a fatty acid is measured as fatty acid concentration increases, all of the fatty acid anions and counterions are available to carry ionic current. However, when the concentration of fatty acid exceeds the CVC, half of the fatty acid anions and counterions become unavailable because they are incorporated in the inner leaflet of the vesicle bilayer membranes. When concentration is plotted against conductivity the slope decreases above the CVC, and

the intersect of the two linear fits gives the value of CVC (Williams et al. 1955). The CVC was determined by conductimetric titration. The sample temperature was kept at 25.0 ± 0.1 °C with a thermal circulating water bath. An analogue electrical conductivity meter and an electrode with cell constant of 0.55 cm−1 were used to measure 5-Fluoracil mouse electrical conductivity. The cell constant was determined by calibration

with KCl samples of known concentration. Titration was performed by successive dilution of the sample with 10 mM Tris buffer (pH 7.4), lowering the decanoic acid concentration of the sample 3 mM at a time. Solutions were allowed to equilibrate a few minutes after dilution until a stable conductivity measurement was obtained. CVC values were calculated using the Williams method. The linear fits of data points at high concentration (above CVC) and low concentration (below CVC) had an R2 > 0.99. The permeability

of the mixed membranes to small solutes was studied using a turbidity assay (Monnard and Deamer 2003; Cohen and Bangham 1972). When solutes are added to vesicles in solution, osmotic pressure causes the vesicles to shrink, resulting in increased light scattering (measured as absorbance). If the membranes Tangeritin are permeable, solute molecules diffuse through the membrane and the vesicles swell, lowering the absorbance. The initial rate at which absorbance decreases is a measure of the relative permeability of the membrane to that solute (Apel et al. 2002). Permeability measurements were performed according to Apel et al. (2002). An aliquot of each vesicle preparation (0.9 ml) was added to a 1 ml quartz cuvette. Absorbance was measured at 600 nm with a VarianCary50 UV/Vis Spectrophotometer. After 20 s, 100 μl solute was added and mixed thoroughly for a final 0.1 M solute concentration. Measurements were performed every 10 s, and data points were fitted to exponential decay using Origin Pro 8.0. The initial rate of permeation in Abs/s was determined by extrapolating to zero (point of solute injection) and calculating the first derivative. Fitting the curve to an exponential decay function provided a mean lifetime used to calculate permeability coefficients.

In our study too, despite the homogenous population, several species were site-specific, while others were subject-specific and undergo succession from health to disease. Hence, even a slight distinction in bacterial community at non-tumor and tumor sites has significance as the samples were from two adjoining sites of same OSCC subject. The underlying species-specific shift implicates alterations in bacterial colonization at tumor sites. The translocation of bacteria from oral cavity to cervical lymph nodes and more in metastatic than in uninvolved nodes in oral cancer patients has

been reported by Sakamoto et al. [35]. Conclusions Together, the results indicate that certain bacterial species/phylotypes detected in this study may play a role in triggering chronic inflammation in oral cavity and possibly be associated at different stages selleck chemical of cancer [95]. This may be due to disrupted oral mucosal surface allowing bacterial invasion and perhaps serve as point of entry to the regional lymph nodes [33, 35]. This indicates that though the bacterial biota were commensals of oral cavity and may become pathogenic when their balance is disturbed.

Microbial shift or dysbiosis has been implicated in some diseases due to unequal ratio of beneficial symbionts to pathogens [96]. This study recognized association of some new bacterial species, like J. ignava not detected earlier in tumor samples by culture- dependent

or independent methods. However, these studies were performed with limited sample XL765 nmr size. Therefore, further investigation with larger sample size using high throughput sequencing would validate these findings and broaden our perspective on bacterial association and oral cancer. Acknowledgements This work was supported by NIDCR Grants DE019178 and DE020891. Electronic supplementary material Additional file 1: Figure S1. Distribution of pentoxifylline relative abundance of classes detected by HOMD and RDP in tissue samples from non-tumor and tumor sites of OSCC subjects. (DOC 79 KB) Additional file 2: Figure S2. Distribution of relative abundance of order detected by HOMD and RDP in tissue samples from non-tumor and tumor sites of OSCC subjects. (DOC 100 KB) Additional file 3: Figure S3. Distribution of relative abundance of families detected by HOMD and RDP in tissue samples from non-tumor and tumor sites of OSCC subjects. (DOC 124 KB) Additional file 4: Figure S4. (a) Individual-based rarefaction; and (b) Rank abundance curves for bacterial species associated with non-tumor tissue and tumor tissue libraries. (DOC 80 KB) References 1. Bagan J, Sarrion G, Jimenez Y: Oral cancer: clinical features. Oral Oncol 2010,46(6):414–417.PubMedCrossRef 2. Rosenquist K: Risk factors in oral and oropharyngeal squamous cell carcinoma: a population-based case-control study in southern Sweden. Swed Dent J Suppl 2005, 179:1–66.PubMed 3.

Among 13 serovars, S. Albany, S. Blockley, S. Havana,

and S. Redba as well as few isolates of S. Choleraesuis, S. Enteritidis, and S. Typhimurium lacked plasmid. All other serovars harbored at least one plasmid and differed in plasmid profile. Serovar association between chicken and human isolates S. Albany, S. Anatum, S. Choleraesuis, S. Derby, S. Enteritidis, and S. Typhimurium were in common for 13 chicken serovars and 66 human serovars and other 7 serovars of chicken isolates were not or barely observed in human (Table 2, 4 and 5). Total serovar number of each serogroup Decitabine decreased from serogroup C1, B, C2, E to D for human isolates (Table 4). Despite of the presence of 66 serovars, there were only presence of 11 H1 antigens including b, c, d, j, k, r, y, eh, g-complex, and z-complex and 5 H2 antigens including -, z6, lw, 1-complex, and en-complex (Table 4). Common antigens in all serogroups were “”i”" for H1 antigen: and “”-”" for H2 antigen. In compared the chicken and human isolates from Taiwan, United Kingdom and United States, the common serovars were S. Typhimurium, S. Enteritidis, S. Anatum, and S. Derby with

common antigens of . “”g complex; i; z4,z24; and e,h”" for H1 antigen and “”- and 1 complex”" for H2 antigen selleckchem (Table 5). Table 4 The H1 and H2 antigens of 66 Salmonella serovars of human isolates collected from 2003 to 2005   Serogroup B C1 C2 D E Others H antigen   11 19 9 7 8 12 H1 b ±a – - – + –   c – + – - – -   d + – + + – +   i + + + + + +   k + + + – - –   r – +

– - + –   y – + – - – -   e,h – - – - + –   g complex               f,g/f,g,s/[f],g,m, [p]/g,p +/+/-/-b -/-/-/- -/-/-/- -/-/+/+ -/-/-/- -/-/-/-   g,m, [s]/g,m, [p],s/g,s,t -/-/- -/+/- +/-/- -/-/+ -/-/+ -/-/-      l complex               l,v/l,w/l,z13 -/-/- -/-/- -/-/- +/+/- -/-/+ +/-/-      z complex               z/z4/z10/z29/z38 +/-/+/-/- +/-/+/+/- -/+/+/-/- -/-/-/-/- -/-/-/-/- -/+/-/-/+   Total antigens 6 7 5 4 5 4   – + + + + + +   l,w – - – - + +   z6 – + + – - – H2    1 complex               1,2/1.5/1,7/[1, 2, 7] +/+/+/- +/+/+/+ +/+/±/- -/+/-/- +/+/-/- -/-/-/-      en complex               e,n,x/e,n,z15 -/- +/+ STK38 +/- -/+ -/- -/-   Total antigens 2 4 4 3 3 2 a ± means presence (+) or absence (-) of b antigen. b +/+/-/- indicates presence (+) of antigens f,g/f,g,s and absence (-) of antigens [f],g,m, [p]/g, Table 5 Serovars of chicken isolates associated with those of human isolates collected from 2003 to 2005       Prevalence (%) of serovar of chicken and human isolates from different area   H antigen 2003 2004 2005 Serovars of chicken isolates in this study     Chicken Human Chicken Human Chicken Human   1 2 USA a UK b USA T c USA UK USA T USA UK USA T Serogroup B                             Derby f,g [1, 2] 0.2 0.3 0.3 2.4 0 0 3.8 2.7 0.03 0.2 0.34 2.3 Kubacha l,z13,z28 1,7 0 0 0 0 0 0 0 0 0 0 0 0 Mons d l,w 0 0 0 0 0 0 0 0 0 0 0 0 Typhimurinum i 1,2,[7] 4.7 2.8 15.8 25.