Microbiol Mol Biol Rev

2007, 71:36–47 PubMedCrossRef 21

Microbiol Mol Biol Rev

2007, 71:36–47.PubMedCrossRef 21. Hynes MF, McGregor NF: Two plasmids other than the nodulation plasmid are necessary for formation SCH772984 price of nitrogen-fixing nodules by Rhizobium leguminosarum . Mol Microbiol 1990, 4:567–574.PubMedCrossRef 22. Dehal PS, Joachimiak MP, Price MN, Bates JT, Baumohl JK, Chivian D, Friedland GD, Huang KH, Keller K, Novichkov PS, Dubchak IL, Alm EJ, Adam PA: MicrobesOnline: an integrated portal for comparative and functional genomics. Nucleic Acids Res 2010, 38:396–400.CrossRef 23. Williams KP, Sobral BW, Dickerman AW: A robust species tree for the Alphaproteobacteria . J Bacteriol 2007, 189:4578–4586.PubMedCrossRef 24. Guo X, Flores M, Mavingui P, Fuentes SI, Hernández G, Dávila G, Palacios R: Natural genomic design in Sinorhizobium meliloti : novel genomic architectures. Genome Res 2003,

13:1810–1817.PubMed 25. García-de los Santos A, Brom S: Characterization of two plasmid-borne lpsβ loci of Rhizobium etli required for lipopolysaccharide synthesis and for optimal interactions with plants. Mol Plant Microbe Interact 1997, 10:891–902.PubMedCrossRef 26. Noel KD, Sánchez A, Fernández L, Leemans J, Cevallos MA: Rhizobium phaseoli symbiotic mutants with transposon Tn 5 insertions. J Bacteriol 1984, 158:148–155.PubMed 27. Encarnación Tyrosine Kinase Inhibitor Library S, Willms K, Mora J: Fermentative and aerobic metabolism in Rhizobium etli . J Bacteriol 1995, 177:3058–3066.PubMed 28. Sambrook J, Fitsch EF, Maniatis T: Molecular Cloning: A Laboratory Manual. Cold Spring Harbor, Cold Spring Harbor Press; 1989. 29. Schafer A, Tauch A, Jager W, Kalinowski J, Thierbach G, Puhler A: Small mobilizable multi-purpose cloning vectors derived from the Escherichia coli plasmids pK18 and pK19:

selection of defined deletions in the chromosome of Corynebacterium glutamicum . Gene 1994, 145:69–73.PubMedCrossRef 30. García-de los Santos A, López E, Cubillas CA, Noel KD, Brom S, Romero D: Requirement of a plasmid-encoded catalase for survival of Rhizobium etli CFN42 in a polyphenol-rich environment. Appl Environ Microbiol 2008, 74:2398–2403.PubMedCrossRef 31. Flores M, González V, Brom S, Martinez E, Piñero D, Romero D, Dávila G, Palacios R: Reiterated DNA sequences in Rhizobium and Agrobacterium spp. J Bacteriol 1987, 169:5782–5788.PubMed 32. Altschul S, Madden T, Schaffer Glycogen branching enzyme A, Zhang J, Zhang Z, Millar W, Lipman D: Gapped BLAST and PSI-BLAST: a new generation of protein database search programs. Nucleic Acids Res 1997, 25:3389–3402.PubMedCrossRef 33. Poggio S, Abreu-Goodger C, Fabela S, Osorio A, Dreyfus G, Vinuesa P, Camarena L: A complete set of flagellar genes acquired by horizontal transfer coexists with the endogenous flagellar system in Rhodobacter sphaeroides . J Bacteriol 2007, 189:3208–3216.PubMedCrossRef 34. Edgar RC: MUSCLE: a multiple sequence alignment method with reduced time and space complexity.

Figure 1 Percentage change of fasting salivary and serum immunolo

Figure 1 Percentage change of fasting salivary and serum immunological indices 0 vs. 14 days. Ig denotes immunoglobulin, NKC natural killer cells, and WBC white blood cells. * Indicates Selleck SRT1720 significance (P < 0.05) for the interaction effect (treatment × time).

Figure 2 Post-exercise changes in salivary immunological indices at baseline and after the intervention. Ig denotes immunoglobulin, PLA placebo group, and NUC nucleotides group. * Indicates significance (P < 0.05) for the pre vs. post administration. Discussion The oral application of nucleotides is not a new concept yet only a few human studies evaluated modulation of the immune response mediated by dietary nucleotides. Exogenous nucleotides have been reported beneficial, especially in infants when the nutrition supply was inadequate, since they positively affect NKC activity and production of interleukin-2 [6], plasma levels of immunoglobulin Ferroptosis inhibitor M [7], and antibody response [8]. In two studies by Mc Naughton and co-workers [3, 4] the authors reported an increase in the level of salivary immunoglobulin A in a group of physically active males supplemented with nucleotides for 60 days. In the present study, sublingual administration of nucleotides formulation for 14 days increased serum immunoglobulin A, NKC count and cytotoxic

activity, and offset the post-exercise drop of salivary immunoglobulins M and A in healthy volunteers, with no adverse effects reported. This implies that nucleotides are absorbed from the mucous membrane under the tongue, enter the circulation and are available for lymphocyte subpopulation activation and proliferation, and modulation of immunoglobulin production. The precise mechanism of the effects of oral nucleotides on cellular immunity is not clear. Gill [1] suggested that the exogenous nucleotides may either

affect initial phase of the antigen processing and lymphocyte proliferation, modulate T-helper cell-mediated antibody production, or mediate signal membrane transduction and expression of a number of genes, some of which can directly affect the levels of cell-signaling protein molecules. Further studies are needed to explicate the mechanism of Oxalosuccinic acid immunostimulatory effects of the sublingual nucleotides, with longer administration protocol and a higher dosage of the formulation, along with proven bioavailability coupled with monitoring of the other indicators of immunity. Our study suggests that the immunostimulatory potential of sublingual nucleotides in healthy subjects is superior as compared to oral intervention, since oral nucleotides significantly raised salivary immunoglobulin A by up to 5% and attenuate the drop in post-exercise IgA by up to 3% [3], while bioavailability after oral nucleotides administration was less than 10% [5, 9].

The lipolytic agent methyl tetradecylthioacetic acid is also incl

The lipolytic agent methyl tetradecylthioacetic acid is also included. It is known to stimulate Daporinad beta oxidation [28] and is clearly involved in lipid transport and utilization [29]. Finally, the satiety hormone cholecystokinin (CCK-8) may have an influence on food intake if provided over a prolonged period of time. Collectively, the above ingredients

appear to represent a substantial list of potentially effective lipolytic agents. While it is possible that these additional ingredients may have contributed to the overall effectiveness of the dietary supplement in regards to our findings of increased lipolysis and metabolic rate, based on the relatively low dosages provided (in comparison to those used in prior investigations where these ingredients have been studied in isolation),

it is difficult to state with certainty that their contribution was significant. It is important to note that our findings for all blood variables following intake of the dietary supplement were highest at the 90 minute post ingestion mark. It is indeed possible that further increases may have been observed at times distant KU-60019 supplier to this. Further study to determine the time course of increased lipolysis is warranted. Based on the work of Hoffman et al. [16] who noted an increase in metabolic rate during hours one, two, and three following ingestion of this dietary supplement, it is likely that the corresponding blood variables would also remain elevated during this time. If so, the potential for increased fat mobilization is apparent. More importantly, if coupled with acute bouts of exercise, fat “”burning”" may be increased significantly during this period of time, potentially resulting in decreased body weight/body fat. Of course, PD-1 inhibitor longer term intervention studies are needed to test this hypothesis. Conclusion In conclusion, we report that the finished product Meltdown®, ingested at the exact

dosage as recommended by the manufacturer, results in an acute increase in plasma NE, glycerol, and FFA (measured using AUC), EPI (measured using ANOVA), as well as metabolic rate. This occurs despite a minimal increase in heart rate and systolic blood pressure. Our findings are specific to a sample of young, healthy, and lean resistance trained men. Further study is needed to determine if similar or more pronounced findings are observed in a sample of overweight/sedentary men and women, who often respond to a greater extent to such treatment. Longer term studies are also needed to determine if the lipolytic effects of this supplement extend beyond 90 minutes post ingestion. Finally, intervention studies are warranted to determine the impact of this dietary supplement on weight/fat loss. Acknowledgements Funding for this work was provided in part by Vital Pharmaceuticals, Inc. and the University of Memphis. References 1. Consitt LA, Bell JA, Houmard JA: Intramuscular lipid metabolism, insulin action, and obesity. IUBMB Life 2009,61(1):47–55.CrossRefPubMed 2.

With the help of the reposition-reexamination process, the correc

With the help of the reposition-reexamination process, the correctness of all three simulated cases for AF nanowires was validated. Figure 6a, b, c shows the results from the same nanowire. As shown in panels a and b, the projected preferred growth directions labeled as yellow lines are perpendicular to the lines tying the 010 and diffraction spots. These experimental results agree with the simulated ‘AF case 1’ and ‘AF case 2’ shown in Figure 4 and Table 1, indicating that this nanowire is an AF nanowire. After reposition, the characteristic selleck inhibitor features of planar defects are clearly revealed in Figure 6c to confirm that

this nanowire is an AF one. Figure 6d, e shows the experimental results of another nanowire, which confirm the correctness of ‘AF case 3’. Figure 6 Experimental validation of the three simulated AF cases. TEM results of a nanowire whose planar defects are invisible from both (a) [001] and (b) zone axes. The analyzed diffraction Crizotinib clinical trial patterns agree with the simulated ‘AF case 1’ and ‘AF case 2’, indicating that the nanowire is an AF one. (c) After the reposition-reexamination process, planar defects are revealed and the nanowire is confirmed to have axial faults. TEM results of another nanowire (d, e), which confirm the correctness of ‘AF case 3’. Summary In brief, an approach to identify the fault

orientation of a nanowire based on TEM results from the off-zone condition was developed. The key of this approach is to analyze the geometrical relation between the projected preferred growth direction of a nanowire and certain diffraction spots from its diffraction patterns recorded along the off-zone directions. Comparison with experimental data shows that this approach correctly identifies

the fault orientation in a boron carbide nanowire without going through the tedious reposition-reexamination buy Verteporfin process. Knowing the fault orientation of each nanowire could help us to establish reliable structure–property relations of boron carbide nanowires. Conclusions In summary, a thorough discussion on the observation of planar defects in boron carbide nanowires is presented. There are two major findings. (1) Planar defects can easily become invisible during TEM examination, in which case, observation along different zone axes is a must when studying the nature of planar defects. A roadmap based on simulated diffraction patterns along several low index zone axes parallel to planar defects is constructed to facilitate the practical TEM examination. (2) An approach has been developed to determine the fault orientation (i.e., transverse faults or axial faults) within a nanowire even if the planar defects are not revealed by TEM, which could facilitate further examination of the nanowire and help to establish the structure–property relations.

Characterization of resistivity behavior Gorrasi et al [5] and L

Characterization of resistivity behavior Gorrasi et al. [5] and Liu et al. [16] showed that the resistivity of carbon nanotube-based nanocomposites as a function of the electric power P = V × I can be described by an exponential expression: (4) where α is an index which generally varies between −1 and 0. The value of α is indicative of the nonlinearity of the current-voltage relationship, i.e., α = 0 corresponds to ohmic behavior, and CP-690550 manufacturer α decreases with increasing nonlinearity of the current-voltage curve; r is a parameter relating to the resistivity

of the nanocomposite when the electrical power passing through the sample is 1 W [16]. Computed nanocomposite resistivities are displayed as a function of the electric power in the graph in Figure 9. Data obeying Equation 4 appear in the form of straight lines owing to the graph’s logarithmic scale. As shown in Figure 9, the slope of the lines decreases as the nonlinearity is decreasing with increasing filler loading. The values of α as a function of filler volume fraction are provided in Figure 10. It is shown that α values are increasing with rising filler volume fraction. A discontinuity in α values can be observed in this graph for filler

volume fractions of about 5%, which is associated with the percolation volume fraction. The behavior of data simulated herein is qualitatively congruent with results reported in [5] for carbon GW-572016 purchase nanotube nanocomposites. Figure 9 Resistivity of nanocomposites with 100-nm circular nanoplatelets as a function of electric power. Figure 10 Value of α as a function of filler volume fraction for nanocomposites with 100-nm learn more circular nanoplatelets. Conclusions In this study, the current-voltage behavior of conductive nanoplatelet-based nanocomposites was investigated. To this end, a numerical modeling approach was developed. The simulations predicted the resistivity of nanoplatelet-based nanocomposites to be strongly affected by the applied electric field. The nanocomposites exhibit nonohmic behavior, that is, resistivity is a nonlinear function of the applied electric field. Further, nanocomposite resistivity

was ascertained to decrease with increasing voltage, while the degree of nonlinear behavior was found to decline with rising filler volume fraction. A good qualitative agreement was observed between simulations and experimental data, the latter of which was obtained employing measurements on nanographene/epoxy nanocomposites. The qualitative agreement between numerical and experimental studies encourages conducting a more comprehensive study to establish a quantitative agreement. The analysis further revealed that nanocomposite resistivity as a function of electrical power can be described by an exponential relation, where the exponent is a measure of the deviation from nonohmic behavior of the conductive nanocomposite.

Principle findings: We utilized structure prediction server (http

Principle findings: We utilized structure prediction server (http://​www.​robetta.​org) to predict the three dimensional structure of active heparanase. The structure obtained clearly delineates a TIM-barrel fold previously anticipated for the enzyme. Interestingly, the model also revealed the existence of a C-terminal domain (C-domain) apparently not being an integral part of the TIM-barrel fold. We provide evidence that the C-domain is critical for heparanase enzymatic activity and secretion. Moreover, the C-domain Omipalisib concentration was found to mediate non-enzymatic functions of

heparanase, facilitating Akt phosphorylation, cell proliferation, and tumor xenografts progression. Binding experiments indicate the existence of high affinity, low abundant cell surface receptor, and cross-linking experiments revealed the existence of two major cell surface binding protein(s)/receptor(s) complexes, exhibiting molecular weights of ~ 130 and ~ 170 kDa that interact with heparanase

C-domain. Conclusions: These findings support the notion that heparanase exert enzymatic activity-independent function, selleck inhibitor and identifies, for the first time, protein domains responsible for heparanase-mediated signaling. Inhibitors directed against the C-domain, combined with inhibitors of heparanase enzymatic activity, are expected to neutralize heparanase function and to profoundly affect tumor progression and metastasis. Poster No. 74 Polarization of Macrophages in Lung Metastasis Formation Annamaria Gal 1 , Thomas Tapmeier1, Ruth J. Muschel1 1 Gray Institute for Radiation Oncology & Biology, University of Oxford, Oxford, UK Tumor associated macrophages have been described in primary tumors. They polarize towards the alternatively activated phenotype (M2) with a distinct receptor and cytokine pattern and support tumor

growth. Less is known however about macrophage polarization and the pro-tumoral macrophages in metastasis formation. In a mouse model of experimental metastasis, we i.v. injected B16F10 melanoma cells into Y-27632 2HCl C57BL/6 syngeneic mice and monitored lung colony formation. In a time course of tumor cell challenge, we analysed immune cell infiltration and cytokine expression in order to characterize the metastatic lung environment. Shortly after tumor cell injection (30 min), we found an inflammatory response, involving Gr-1+, CD11b+, Ly6C+neutrophil and monocyte infiltration that ceased within 24 h. After 24 h, we observed CD68+, CD11b+monocyte/macrophage recruitment that lasted no longer than up to 48 h of tumor cell challenge. The recruited macrophages displayed a cytokine pattern resembling the M1 macrophage subpopulation predominantly with IL-12 expression.

ANZ J Surg 77(10):889–891CrossRefPubMed

ANZ J Surg 77(10):889–891CrossRefPubMed Enzalutamide molecular weight 3. Weller I, Wai EK, Jaglal S, Kreder HJ (2005) The effect of hospital type and surgical delay on mortality after surgery for hip fracture. J Bone Joint Surg Br 87(3):361–366CrossRefPubMed 4. Rogers FB, Shackford SR, Keller MS (1995) Early fixation reduces morbidity and mortality in elderly patients with hip fractures from low-impact falls. J Trauma 39(2):261–265CrossRefPubMed 5. Dorotka R, Schoechtner H, Buchinger W (2003) The influence of immediate surgical treatment of proximal femoral fractures on mortality and quality of life. Operation within six hours of the

fracture versus later than six hours. J Bone Joint Surg Br 85(8):1107–1113CrossRefPubMed 6. Hoerer D, Volpin G, Stein H (1993) Results of early and delayed surgical fixation of hip fractures in the elderly: a comparative retrospective study. Bull Hosp Jt Dis 53(1):29–33PubMed 7. Bottle A, Aylin P (2006) Mortality associated with delay in operation after hip fracture: observational study. BMJ 332(7547):947–951CrossRefPubMed 8. McGuire KJ, Bernstein J, Polsky D, Silber JH (2004) The 2004 Marshall Urist award: delays until surgery after hip fracture increases mortality. Clin Orthop Relat Res 428:294–301CrossRefPubMed 9. Radcliff

TA, Henderson WG, Stoner TJ, Khuri SF, Dohm M, Hutt E (2008) Patient risk factors, operative care, and outcomes among older community-dwelling male veterans with hip fracture. J Bone Joint Surg Am 90(1):34–42CrossRefPubMed 10. Parker MJ, Pryor GA (1992) The timing of surgery for proximal femoral fractures. J Bone Joint Surg Br 74(2):203–205PubMed NVP-LDE225 price 11. Majumdar SR, Beaupre LA, Johnston DW, Dick DA, Cinats JG, Jiang HX (2006) Lack of association between mortality and timing of surgical isometheptene fixation in elderly patients with hip fracture: results of a retrospective population-based cohort study. Med Care 44(6):552–559CrossRefPubMed 12. Sund R, Liski A (2005) Quality effects of operative delay on mortality in hip fracture treatment. Qual Saf Health

Care 14(5):371–377CrossRefPubMed 13. Lefaivre KA, Macadam SA, Davidson DJ, Gandhi R, Chan H, Broekhuyse HM (2009) Length of stay, mortality, morbidity and delay to surgery in hip fractures. J Bone Joint Surg Br 91(7):922–927CrossRefPubMed 14. Holt G, Smith R, Duncan K, Finlayson DF, Gregori A (2008) Early mortality after surgical fixation of hip fractures in the elderly: an analysis of data from the Scottish hip fracture audit. J Bone Joint Surg Br 90(10):1357–1363CrossRefPubMed 15. Kenzora JE, McCarthy RE, Lowell JD, Sledge CB (1984) Hip fracture mortality. Relation to age, treatment, preoperative illness, time of surgery, and complications. Clin Orthop Relat Res 186:45–56PubMed 16. Mullen JO, Mullen NL (1992) Hip fracture mortality. A prospective, multifactorial study to predict and minimize death risk. Clin Orthop Relat Res 280:214–222PubMed 17. Novack V, Jotkowitz A, Etzion O, Porath A (2007) Does delay in surgery after hip fracture lead to worse outcomes? A multicenter survey.

Furthermore, the usage of GNP for diagnosis and even destruction

Furthermore, the usage of GNP for diagnosis and even destruction of microorganisms [6] or AuNP for biological applications [7–9] should be mentioned. Although GNPs are believed to be biologically inert, they can be engineered to possess

chemical and biological functionality. GNP exhibits a plasmon resonance (PR) at wavelengths from 510 to 580 nm [10] leading to enhanced absorption and scattering in this part of the optical spectrum. The PR is affected by the size and shape of the GNP, the type of selleck inhibitor the supporting substrate (mainly its refractive index) and/or the surrounding material of the gold nanoparticles. The distance between the nanoparticles is also relevant, especially if it is small enough to enable electromagnetic coupling [11]. GNPs are usually prepared by precipitation from aqueous solutions [12, 13] on various materials, e.g., on etched www.selleckchem.com/products/Rapamycin.html glass surfaces [13, 14]. Thermal annealing of thin gold films produced by evaporation or sputtering [15] can also lead to a gold aggregation into GNP [16]. The formation of GNP from continuous gold layers is driven by the minimization of the surface energy and is denoted as

solid state dewetting [17]. However, all the described methods suffer from the poor adhesion of GNP to the substrate surface [18]. It is known that the biocompatibility of a substrate is affected, besides of several other factors, by their electrical conductivity, chemical structure, surface morphology, roughness, and wettability (polarity) [19]. In this work, we studied the surface morphology, sheet electrical resistance, contact angle, ultraviolet–visible (UV–vis) spectra, adhesion, and proliferation of living muscle cells

on gold structure sputtered on glass surface. Methods Materials and modification The gold layers were sputtered on 1.8 × 1.8 cm2 microscopic glass, supplied by Glassbel Ltd., Prague, Czech Republic. The surface roughness of glass, measured over the area of 1×1 μm2 and calculated as an average value from five different measuring positions, was R a = DOK2 0.34 ± 0.03 nm [16]. The gold sputtering was accomplished on Balzers SCD 050 device from gold target (supplied by Goodfellow Ltd., Huntingdon, England). The deposition conditions were DC Ar plasma, gas purity of 99.995%, sputtering time of 10 to 400 s, current of 10 to 40 mA (discharge power 3 to 15 W), total Ar pressure about 5 Pa, and the electrode distance of 50 mm. The power density of Ar plasma in our case was 0.13 W·cm−2, and the average deposition rate was 0.15 nm s−1. The glass substrate was cleaned with methanol (p.a.) and dried in a stream of N2. The prepared samples were stored at laboratory conditions. Measurement techniques The mean thickness of gold films was measured by gravimetry using Mettler Toledo UMX2 microbalance (Columbus, OH, USA). The thickness was calculated from the sample weights before and after sputtering using gold bulk density.

OVK, PDM, RCD, and DS aided in sample processing for proteomic an

OVK, PDM, RCD, and DS aided in sample processing for proteomic analysis. PE and OVK performed MS runs. VS performed statistical analysis on MS data. All authors read and approved the final manuscript.”
“Background Pseudomonas aeruginosa is a versatile Gram-negative bacterium, able to metabolise multiple carbon sources and exploit diverse ecological niches, e.g. soil, water, plants and animal hosts [1, 2]. This opportunistic pathogen causes a range of human infections, including acute infections

of severe wounds [3] and burns [4, 5] and chronic lung infections in cystic fibrosis (CF) patients [6]. P. aeruginosa forms biofilms in the CF lung that are highly resistant to antibiotics and clearance by the immune system [7]. Once established, such biofilms cannot be eradicated and are associated with greatly increased morbidity and mortality [8]. Several CF-associated transmissible Selleck LEE011 strains of P. aeruginosa, capable of between patient transmission, have been identified in the UK, Europe, Australia and North America [9]. The Liverpool Epidemic Strain (LES), a UK transmissible strain, was first isolated in 1996 at Alder Hey Children’s Hospital (AHCH), Liverpool [10]. This strain is capable of super-infection, supplanting pre-existing P. aeruginosa populations in the CF lung [11]. Chronic infection with LES is associated with increased morbidity and

mortality compared to other P. aeruginosa strains [12]. The LES is highly prevalent within individual hospital CF units [13] and is the most abundant MK-2206 research buy P. aeruginosa strain amongst CF patients in the UK [14]. It was also recently isolated from the sputa of CF patients in North America [15]. Sequencing of the earliest LES isolate, LESB58, demonstrated that the genome shares 95% similarity

with the lab strain PAO1. However, its core genome is punctuated by multiple norfloxacin-inducible prophages [16]. Specifically, there are five inducible prophage genomes (LESφ2; LESφ3 LESφ4 LESφ5 and LESφ6) that are mosaic in nature. The gene organisation of LESφ2 and LESφ3 resembles that of lambdoid phages. These two phage genomes share 82.2% Oxymatrine identity across a 13.6-kb region at their 3’ ends that makes up 32% of the phage genomes. The closest known relative to both these phages is the Pseudomonas phage F10 [17]. LESφ3 also contains a 7.5 kb region that shares 99.8% homology with LESφ5, which exhibits a considerable sequence similarity to the O-antigen converting phage D3 [18]. LESφ4 is a transposable Mu-like phage that closely resembles phage D3112 [19]. The LESφ6 sequence resembles a pf1-like filamentous phage [16]. Temperate phages have been shown to confer selective, beneficial traits to a range of P. aeruginosa hosts [20]. For example, phage D3 orchestrates O antigen conversion from O5 to O16 in PAO1, which may aid evasion of the immune system and resistance to phage superinfection [18, 21].

Microbiologica 1986, 9:39–45 PubMed 11 Krízová J, Spanová A, Rit

Microbiologica 1986, 9:39–45.PubMed 11. Krízová J, Spanová A, Rittich B: Evaluation of amplified ribosomal DNA restriction analysis (ARDRA) and species-specific PCR for identification of Bifidobacterium species. Syst Appl Microbiol 2006, 29:36–44.PubMedCrossRef 12. Ventura M, Elli M, Reniero R, Zink R: Molecular microbial analysis of Bifidobacterium isolates from different environments by the species-specific amplified ribosomal AZD1208 solubility dmso DNA restriction analysis (ARDRA). FEMS Microbiol Ecol 2001, 36:113–121.PubMedCrossRef 13. Temmerman R, Masco L, Vanhoutte T, Huys G, Swings J: Development and validation of a nested-PCR-denaturing gradient gel electrophoresis method for taxonomic characterization

of bifidobacterial communities. Appl Environ Microbiol 2003, 69:6380–6385.PubMedCrossRef 14. Matsuki T, Watanabe K, Tanaka R, Oyaizu H: Rapid identification of human intestinal bifidobacteria by 16S rRNA-targeted species- and group-specific primers. FEMS Microbiol Lett 1998, 167:113–121.PubMedCrossRef 15. Matsuki T, Watanabe K, Tanaka R, Fukuda M, Oyaizu H: Distribution of bifidobacterial species in human intestinal microflora examined with 16S rRNA-gene-targeted species-specific primers. Appl Environ Microbiol 1999, 65:4506–4512.PubMed 16. Matsuki T, Watanabe K, Fujimoto J, Kado Y, Takada T, Matsumoto K, Tanaka R: Quantitative PCR with 16S rRNA-gene-targeted Daporinad supplier species-specific primers for analysis

of human intestinal bifidobacteria. Appl Environ Microbiol 2004, 70:167–173.PubMedCrossRef 17. Matsuki T, Watanabe K, Tanaka R: Genus- and species-specific PCR primers for the detection and identification of bifidobacteria. Curr Issues Intest Microbiol 2003, 4:61–69.PubMed 18. Ventura M, Canchaya C, Del Casale A, Dellaglio F, Neviani E, Fitzgerald GF, van Sinderen D: Analysis of bifidobacterial evolution using

a multilocus approach. Int J Syst Evol Microbiol 2006, 56:2783–2792.PubMedCrossRef 19. Shuhaimi M, Ali AM, Saleh NM, Yazid AM: Utilisation of enterobacterial repetitive intergenic consensus (ERIC) sequence-based PCR to fingerprint the genomes of Bifidobacterium isolates and Loperamide other probiotic bacteria. Biotech Lett 2001, 23:731–736.CrossRef 20. Ventura M, Meylan V, Zink R: Identification and tracing of Bifidobacterium species by use of enterobacterial repetitive intergenic consensus sequences. Appl Environ Microbiol 2003, 69:4296–4301.PubMedCrossRef 21. Gómez Zavaglia A, de Urraza P, De Antoni G: Characterization of Bifdobacterium strains using Box primers. Anaerobe 2000, 6:169–177.CrossRef 22. Masco L, Huys G, Gevers D, Verbrugghen L, Swings J: Identification of Bifidobacterium species using rep-PCR fingerprinting. Syst Appl Microbiol 2003, 26:557–563.PubMedCrossRef 23. Vincent D, Roy D, Mondou F, Déry C: Characterization of bifidobacteria by random DNA amplification. Int J Food Microbiol 1998, 43:185–193.PubMedCrossRef 24.