Pediatr Res 48:218–226. doi:10.​1203/​00006450-200008000-00016 www.selleckchem.com/products/LY2603618-IC-83.html PubMedCrossRef Takken T (2006) Physical Activity Readiness Questionnaire. In: Inspanningstests

Elsevier gezondheidszorg. Maarssen, The Netherlands, p 129 Tarkiainen TH, Timonen KL, Tiittanen P, Hartikainen JE, Pekkanen J, Hoek G, Ibald-Mulli A, Vanninen EJ (2005) Stability over time of Y-27632 short-term heart rate variability. Clin Auton Res 15:394–399. doi:10.​1007/​s10286-005-0302-7 PubMedCrossRef Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (1996) Heart rate variability. Standards of measurement, physiological interpretation, and clinical use. Eur Heart J 17:354–381 Theorell T, Blomkvist V, Lindh G, Evengard B (1999) Critical life events, infections, ML323 manufacturer and symptoms during the year preceding chronic fatigue syndrome (CFS): an examination of CFS patients and subjects with a nonspecific life crisis. Psychosom Med

61:304–310PubMed van Houdenhoven B, Neerinckx E, Lysens R, Vertommen H, van Houdenhoven L, Onghena P, Westhovens R, D’Hooghe MB (2001) Victimization in chronic fatigue syndrome and fibromyalgia in tertiary care: a controlled study on prevalence and characteristics. Psychosomatics 42:21–28. doi:10.​1176/​appi.​psy.​42.​1.​21 CrossRef Vercoulen JH, Swanink CM, Fennis JF, Galama JM, van der Meer JW, Bleijenberg G (1994) Dimensional assessment of chronic fatigue syndrome. J Psychosom Res 38:383–392. doi:10.​1016/​0022-3999(94)90099-X

PubMedCrossRef Vercoulen JH, Alberts M, Bleijenberg G (1999) De Checklist Individual Strength (CIS). Gedragstherapie 32:131–136 Ware NC, Kleinman A (1992) Culture and somatic experience: the social course of illness in neurasthenia and chronic fatigue syndrome. Psychosom Med 54:546–560PubMed Ware JE Jr, Sherbourne CD (1992) The MOS 36-item short-form health survey (SF-36) I. Conceptual framework and item selection. Med Care 30:473–483. doi:10.​1097/​00005650-199206000-00002 PubMedCrossRef Ware JE Jr, Snow KK, Kosinski M, Gandek B (1993) SF-36 Health Survey Manual and Interpretation Guide. New England Medical Center, The Health Institute, stiripentol Boston Ware JE Jr, Kosinski M, Keller SD (1994) SF-36 Physical and Mental Health Summary Scales: a user’s manual. The Health Institute, New England Medical Center, Boston Wientjes CJ (1992) Respiration in psychophysiology: methods and applications. Biol Psychol 34:179–203. doi:10.​1016/​0301-0511(92)90015-M PubMedCrossRef”
“Introduction Sickness absence is an important measure for general health in the population. Long-term sickness absence is a predictor of disability and mortality (Gjesdal and Bratberg 2002; Kivimäki et al. 2003) and imposes considerable costs to both the employer and society as a whole (Henderson et al.

The time of administration of each condition was similar to the recommended time of intake provided on the product label, while a recent study using GlycoCarn® for performance improvement had GSK2118436 supplier subjects consume this condition

90 minutes prior to exercise [12]. www.selleckchem.com/products/pf-03084014-pf-3084014.html Our rationale for the change to 60 minutes prior to exercise was based on our inclusion of maltodextrin to the GlycoCarn® in the current design and the fact that the added carbohydrate may have enhanced uptake of the GlycoCarn®, as well as the fact that we wanted to maintain as much similarity in the treatment protocol as possible. Prior to using any of the above five conditions, all subjects underwent an identical test protocol using water only. This was to serve as a baseline familiarization trial to the protocol, as

we have previously noted that even in well trained men, such a protocol as used in the present design requires one session in order to fully familiarize subjects to the exercise movements and the volume of exercise (unpublished findings). Hence, a total of six sessions of the exercise protocol were performed by all subjects. It should be noted that the baseline condition, although presented within the Stattic results section for comparison purposes, was not used in the statistical analysis. Figure 1 Supplement 1 ingredients (per one serving). Figure 2 Supplement 2 ingredients (per one serving). Figure 3 Supplement 3 ingredients (per one serving). All conditions were provided in powder form and were fruit punch flavor. The placebo and GlycoCarn® Dapagliflozin conditions were produced and then packaged into

individual servings by Tishcon Corporation (Westbury, NY). The three supplements used for comparison were purchased from a local General Nutrition Center store in containers. To ensure precision of dosing, each of these three conditions was weighed on a laboratory grade balance prior to mixing in water. Again, two servings of each condition were used in this design. Our rationale for this was based on the fact that the majority of users of such supplements use 2-3 servings rather than one. In fact, the label instructions for use of these products indicate a serving size between 1 and 3 servings. Unlike GlycoCarn®, which is obviously a single ingredient (mixed with maltodextrin in the present design), the supplements contained numerous ingredients (as can be seen in Figures 1, 2, and 3), some of which are stimulants. Exercise Test Protocol For all six test days, subjects reported to the lab following a minimum of an eight hour overnight fast. After arrival to the lab, a blood sample was obtained following a 10 minute period of rest. Subjects then rated their perceived and subjective level of muscle “”pump”" in the upper body using a visual analog scale (0 = no pump; 10 = the most intense pump ever experienced).

Scand J Pub Health Epacadostat molecular weight 36(6):564–572CrossRef Westman M, Etzion D, Gurtler E (2004) The work–family interface and burnout.

Int J Stress Manag 11(1):413–428CrossRef Winslow S (2005) Work–family conflict, gender, and parenthood 1977–97. J Family Issues 26(6):727–755CrossRef”
“Skin diseases are very frequent, and although they are rarely life-threatening, they might not only limit the quality of life, but as well affect the ability to work and to be employed. In accordance with the German “Occupational Preventive Medical Care Ordinance” (ArbMedVV), the company physician has to examine the skin in order to prevent occupationally induced skin diseases. During this examination, he might come across skin disorders which have to be medically assessed. In case of skin diseases totally or partially induced by occupation, it has to be decided whether the preventive measures within the company (substitution of working this website material, changes in working processes, www.selleckchem.com/products/emricasan-idn-6556-pf-03491390.html consequent implementation of protective measures, skin cleansing, and skin care) can easily be realized and whether they are sufficient for healing. During the medical assessment,

the company physician sometimes has to give his opinion on existing, non-occupational induced skin diseases as well. If a patient is already under medical treatment with regard to a rare skin disease, the company physician generally has to take this diagnosis into consideration during the preventive occupational examination. For the evaluation of such cases, it is extremely helpful to be up to date with the knowledge of classification, diagnosis, and therapy in dermatology. “Dermatologie und Venerologie”

by Braun-Falco, Plewig, and Wolff has been a German standard work of dermatology for decades. This standard work has now been updated, revised, and extended and is published as 6th edition. This PRKD3 edition (or previous one) is likely to be found in most German dermatological practices and clinics and is therefore a good basis for the communication between company physicians and dermatologists. In English, the 3rd edition (“Braun-Falco’s Dermatology” by Burgdorf, Plewig, Wolff, and Landthaler) has, along with the 1st and 2nd edition, gone through various stages of translation and adaptation of the German edition. The book imparts knowledge of the fundamental principles of examination and diagnostic procedures as well as the pathogenesis of skin diseases on a high standard. The topics are clearly structured and allow a quick classification of dermatological disease patterns and important differential diagnoses. In this connection, 1,200 color images are of essential value. One chapter addresses occupational dermatoses and their assessment, whereas the book clearly focuses on the presentation of dermatology as a whole and not on occupational dermatology in depth.

These observations led us to wonder how Wolbachia is detected AZD5363 nmr within the cell, how Wolbachia evades the host immune system, and what are the consequences of these manipulations on host cell physiology. In the present study, most of the canonical immune PGRP receptors were differentially-regulated in the presence of Wolbachia, probably through lipoprotein or polysaccharide binding, and the outcome of the interaction tended towards under-expression of immune effectors of the Toll, Imd and JAK-STAT pathways. Even when the regulation

cascade was too complex to analyze, the expression patterns of most immune genes were modified in response to symbiosis, suggesting that Wolbachia may adopt an active strategy of immune evasion in A. tabida. However, as few immune genes from the see more Toll signaling pathway are also known to play a role in development, expression data have to be interpreted with caution with respect to the important development defect of ovaries in aposymbiotic females. The regulation appeared to be tissue or sex-specific, immune genes being expressed to a greater extent

in males than in ovarian tissues. Wolbachia is mainly concentrated in the ovaries of females, whereas they are spread more widely throughout the male body [61]. Hence, modulation of immune pathways could be both gene- and tissue-specific, as shown in the differential immune regulation of bacteriocytes vs. whole body in Sitophilus zeamais [62]. The immune response to Wolbachia also seems to be host strain-specific, with the Pi3 strain generally exhibiting a more pronounced pattern than the NA strain. Finally, the immune response to Wolbachia seems to be host-specific, as Drosophila simulans did

not repress or induce antimicrobial peptides production [63], whereas the D. melanogaster cell line over-expressed antimicrobial peptides in response to Wolbachia infection [23]. Similarly, the presence of Wolbachia tends to increase immune gene expression in the mosquito hosts when stably introduced [20, 21, 50]. By comparing aposymbiotic and symbiotic tissues of A. tabida, we also highlighted the influence of Wolbachia click here on host immunity in its broad sense, and especially on the regulation of cell homeostasis and the oxidative environment, which are known to play a key role in physiological responses to invasion by pathogens. Indeed, processes involved in the control of the oxidative environment were highlighted both in in silico and in vitro subtractions, and confirmed by qRT-PCR. Given these observations, we further demonstrated the influence of Wolbachia on iron homeostasis and oxidative stress regulation in A. tabida [8, 14]. We confirmed the differential expression of Fosbretabulin ic50 Ferritin, a protein involved in iron storage and transport, in males, females and ovaries from the Pi strain [14].

Data analysis was performed using manufacturer’s program and is based on the ddCt method, with normalization of the raw data to the panel of housekeeping genes provided in the array. The genes showing modulation find more by 1.5 fold up or down were only www.selleckchem.com/products/U0126.html selected for further analysis. Functional annotations of the selected genes were carried out by the

bioinformatics software David for Bioinformatics. Three independent experiments with a pool of 2 donors each were analyzed. Statistical analysis Statistical evaluation of the data was done using GraphPad Prism 5 software. Student t-test was performed for simple comparison between 2 means. For multiple comparisons, the results were analysed by two-way ANOVA followed by Bonferoni’s post-test. p < 0.05 was considered statistically significant. All shown data are representative for at

least 3 independent experiments. Results Chlamydia trachomatis infect monocytes and monocyte-derived DCs in a comparable manner Monocytes isolated from human peripheral blood mononuclear cells (PBMCs) and monocyte-derived DCs were infected with C. trachomatis serovars Ba, D and L2 (Figure 1). Results show that all the three serovars were capable of infecting both the monocytes and DCs and form Tariquidar clinical trial inclusions as detected by immunofluorescence microscopy 2 days post infection (p.i.). However, the inclusions were smaller in size compared to typical inclusions that have been reported in

HeLa cells (Additional file 2: Figure S2). The inclusion morphology and staining intensity varied between the infected monocytes and DCs. Figure 1 Immunofluorescence microscopy of infected monocytes and monocyte-derived Dendritic cells (DCs). Monocytes (upper panel) and monocyte-derived DCs (lower panel) were infected with C. trachomatis serovars Ba, D and Clostridium perfringens alpha toxin L2 (MOI-3) for 2 days. Chlamydial inclusions (green) were stained with FITC conjugated anti-chlamydia LPS antibody and counterstained with Evans Blue. Pictures were taken at 63X magnification with Leica DMLB. The figures are representative of 3 independent experiments. In monocytes, the percentage of infected cells were comparable among the three serovars and did not seem to change even when the infection duration was extended to 3 days (Table 1). For DCs, the percentage of infected cells were similar for serovars Ba and D but serovar L2 showed a higher infection rate as compared to the other two (Table 1). However, the infection rate declined remarkably for all the three serovars when infected for 3 days. The infection rate was nevertheless much lower in both monocytes and DCs than in HeLa. Mock controls were prepared for each round of experiments which showed absence of chlamydial antigens in the donors (Additional file 3: Figure S3). Table 1 Comparison of infection rate in monocytes and monocyte-derived DCs infected with C.

Conclusions In the present study, we report

the existence of a new pathway for arresting cell growth that involves the interaction of troglitazone-induced VEGF and NRP-1 in selleck chemical NSCLC cells. This suggests that TZDs may be effective anti-cancer agents, and it may be possible to develop a new anti-cancer therapy if the mechanisms underlying these anti-cancer effects are better understood. Acknowledgements This work was supported by a Grant-in-Aid for Young Scientists (B) (20790562) to ST from the Ministry of Education, Science, Sports and Culture, Japan. References 1. Spiegelman BM: PPAR-gamma: Adipogenic regulator and thiazolidinedione receptor. Tariquidar nmr Diabetes 1998, 47:507–514.PubMedCrossRef 2. Elstner E, Muller C, Koshizuka K, Williamson EA, Park D, Asou H, Shintaku P, Said JW, Heber D, Koeffler HP: Ligands for peroxisome proliferator-activated receptor gamma and retinoic acid receptor inhibit growth and induce apoptosis of human breast cancer cells in vitro and in BNX mice. Proceedings of the National

Academy of Sciences of the United States of America 1998, 95:8806–8811.PubMedCrossRef 3. Lambe KG, Tugwood JD: A human peroxisome-proliferator-activated receptor-gamma is activated by inducers of adipogenesis, including thiazolidinedione drugs. European Journal of Biochemistry 1996, 239:1–7.PubMedCrossRef 4. Mueller E, Sarraf P, Tontonoz P, Evans RM, Martin KJ, Zhang M, Fletcher C, Singer S, Spiegelman BM: Terminal differentiation Methocarbamol of human breast cancer through PPAR gamma. Molecular Cell 1998, 1:465–470.PubMedCrossRef check details 5. Takahashi N, Okumura T, Motomura L, Fujimoto Y, Kawabata I, Kohgo Y: Activation of PPAR gamma inhibits cell growth and induces apoptosis in human gastric cancer cells. Febs Letters 1999, 455:135–139.PubMedCrossRef 6. Heaney AP, Fernando M, Yong WH, Melmed S: Functional PPAR-gamma receptor is a novel therapeutic target for ACTH-secreting

pituitary adenomas. Nature Medicine 2002, 8:1281–1287.PubMedCrossRef 7. Keshamouni VG, Reddy RC, Arenberg DA, Joel B, Thannickal VJ, Kalemkerian GP, Standiford TJ: Peroxisome proliferator-activated receptor-gamma activation inhibits tumor progression in non-small-cell lung cancer. Oncogene 2004, 23:100–108.PubMedCrossRef 8. Kubota T, Koshizuka K, Williamson EA, Asou H, Said JW, Holden S, Miyoshi I, Koeffler HP: Ligand for peroxisome proliferator-activated receptor gamma (troglitazone) has potent antitumor effect against human prostate cancer both in vitro and in vivo. Cancer Research 1998, 58:3344–3352.PubMed 9. Motomura W, Okumura T, Takahashi N, Obara T, Kohgo Y: Activation of peroxisome proliferator-activated receptor gamma by troglitazone inhibits cell growth through the increase of p27(Kip1) in human pancreatic carcinoma cells. Cancer Research 2000, 60:5558–5564.PubMed 10.

difficile infection is invariably associated with the disruption of the normal intestinal microflora by the administration of broad spectrum antibiotics. Thus there is a pressing need to develop therapies that selectively target C. difficile while leaving the intestinal microflora intact. The C. difficile reference strain 630 encodes a single predicted sortase, CD630_27180, which has strong amino acid similarity with SrtB of S. aureus PP2 nmr and B. anthracis

[24]. Sortase substrates frequently contribute toward pathogenesis via their involvement in attachment to specific tissues during infection [17,41–44], as well as the bacteria’s ability to evade the immune response of the host [32,36]. Sortases, although not essential for growth or viability of the organism, are often essential for virulence in Gram-positive organisms; inactivation of sortases reduces colonization in mice [8,13,44,45], and decreases adhesion and invasion in vitro [8,10,14,46,47]. Sortases and their substrates are considered promising targets

for the development of new anti-infective compounds [10,14,48]. Unusually for Gram-positive bacteria, C. difficile appears to possess a single sortase enzyme that is likely to be important for the viability of the pathogen as we have been unable to construct a C. difficile strain 630 SrtB defined mutant (unpublished data). Inhibiting the C. difficile sortase could prove to be a strategy to specifically target C. difficile. In this study, we cloned, expressed and characterized the sortase encoded by CD630_27180 learn more of C. difficile 630, a predicted class B sortase (SrtB). Sortase nomenclature is based on sequence similarity to the known classes of sortase, A-F [7]. Sortases of class B typically are involved in heme-iron uptake and tend to be expressed in operons with their substrates [17,18]. Genes encoding class A sortases are not found in proximity to their substrates, which consist of a variety of surface proteins with diverse biological MK 8931 solubility dmso functions. Several selleck chemicals exceptions to these rules have already

been described, notably a class B sortase that polymerizes pilin subunits in S. pyogenes [49], and a class E sortase from C. diphtheriae that serves a housekeeping function [50]. The potential C. difficile sortase substrates identified in this paper comprise a diverse range of surface proteins, suggesting that SrtB may serve as a housekeeping sortase in C. difficile, a function usually reserved for class A sortases. These potential sortase substrates in C. difficile strain 630 comprise of seven proteins, all containing an (S/P)PXTG motif, that are predicted to be surface localized and are conserved across C. difficile strains. Recently it was proposed that a C. difficile collagen binding protein, CbpA, may be sorted to the cell surface by sortase recognizing an NVQTG motif [30]. In this study, we developed a FRET-based assay to demonstrate that SrtB of C.

Formation of structure defects on martensite PRI-724 molecular weight transformations results in azimuthal tailing of diffraction reflections of single-crystalline samples. From the magnitude of tailing and from the increase of the misorientation angle of crystal lattice regions after multiple martensitic transformations, one can deduce the capability of fragmentation and grain refinement of an austenite phase [4, 6]. In Fe-based alloys, three types of martensitic transformations are realized: γ-α-γ in Fe-Ni-based alloys with face-centered cubic (f.c.c.)-body-centered cubic (b.c.c.)-f.c.c. structure rebuilding, γ-ϵ-γ in Fe-Mn-based alloys with f.c.c.-hexagonal mTOR signaling pathway close-packed (h.c.p.)-f.c.c. transformation [7], and

γ-ϵ′-γ in Fe-Mn-based alloys with f.c.c.-18-layer rhombic (18R)-f.c.c. transformation [8, 9]. It is shown experimentally that the SRT1720 manufacturer restoration of the initial austenite structure after cyclic γ-ϵ-γ and γ-ϵ′-γ transformations turned out to be superior against that of alloys with γ-α-γ transformations. This regularity is based on the fact that the density of dislocations increases by more than 103 after cyclic γ-α-γ transformations connected with a high volume change – up to 3% to 4%, while it increases only by 10 after cyclic γ-ϵ-γ transformations (with a smaller volume change – up to approximately 0.75%) and practically does not change after γ-ϵ′-γ transformations (volume change – up

to approximately 0.5%) [4, 7]. In the austenitic phase,

additional subgrain boundaries can form under conditions of dislocation generation by direct and reverse martensite transformations, for example, by means of wall formation by one-sign dislocations. On account of these processes, the fragmented structure of reverted austenite is received. The process of structure fragmentation can be essentially different for alloys with different types of martensitic transformations. In the present article, the effect of multiple martensitic transformations of different types is studied in Fe-Ni- and Fe-Mn-type alloys. The development of austenitic structure fragmentation and the capability of particular alloys to form highly dispersive structures due to the accumulation of structure defects are elucidated. Methods The following PFKL alloys: Fe – 24.8 wt.%, Ni – 0.50 wt.%, C (alloy 1); Fe – 19.5 wt.%, Mn – 2 wt.%, Si (alloy 2); Fe – 16.7 wt.%, Mn – 0.45 wt.%, C (alloy 3), and Fe – 15.2 wt.%, Mn – 0.32 wt.%, C (alloy 4), were chosen for the investigation. All the alloys were melted in a furnace in purified argon. Single-crystalline samples (∅ 0.8 mm, L = 5 to 10 mm in size) for X-ray investigations in an RKV-86 (Moscow, USSR) rotational camera were cut out from large grains of the bar. All the alloys display an austenitic structure at room temperature after quenching from 1,000°C to 1,050°C in cold water.

Table 1 summarizes the hydrodynamic Selleckchem PCI-34051 (shear) forces associated with displacement of the biofilm from the tubing at various stages of growth. (The approximate dimensions of the 3 h biofilm with respect to the tubing were indicated in Figure 2b). The yeast inoculum was not rinsed from the surface by the relatively low shear force (0.016 dyn cm-1) of the medium flow which is an indication that

this hydrodynamic force is quite gentle. However, it was completely displaced from the surface by selleck inhibitor draining the tubing (data not shown). In contrast biofilms cultured for between 30 min and 1 h have established a sufficiently firm adhesion so that the biofilm can withstand application of a substantial shear force (17.3 dynes/cm2). Table 1 Hydrodynamics of biofilm displacement from the surface   Shear Force (dynes/cm 2 ) 1   0.016 17.3 Yeast inoculum2 + – 30 min-1 h Biofilm + + 2–6 h Biofilm + – > 8 h Biofilm – - 1Computed as indicated in the Methods section 2 At the end of the 1 h inoculation period + biofilm remains buy LY3023414 attached – biofilm is removed Initial

biofilm adhesion is dependent on expression of BCR1 and ALS3 but not on HWP1 A simple hypothesis is that the loss of adhesion described above involves a temporal shift in expression of two adhesins (ALS3 and HWP1), regulated by the BCR1 transcription factor, that were shown play a prominent role in C. albicans biofilm development [11, 19, 35]. In order to pursue this idea we first determined if these genes were involved in establishment of the initial strong adhesive bond to the surface. Figure 5 shows that at 40 min the reference (wild type) strain has established adhesion to the tubing surface while the bcr1/bcr1 and als3/als3 mutant biofilms are almost completely displaced

from the surface by draining the tubing. BCR1 is a positive regulator of morphogenesis. However, the lack of establishment of adhesion of bcr1/bcr1 and als3/als3 strains was not entirely coupled to filamentation in a simple manner since a substantial proportion of the bcr1/bcr1 and als3/als3 mutant cells germinated (20 and 70%) during the 40 min time interval. (The mean germ tube length of these cells was 14 +/- 12 and 10 +/- 7 μm, respectively). The results for the hwp1/hwp1 mutant indicated selleck products that expression of this gene was not essential for establishment of firm adhesion, i.e., under our conditions and at this early stage in biofilm development. At 40 min the biofilm was multilayered and clearly attached. These results led us to characterize the detachment phenotype of a strain that overexpressed ALS3 which is described below. Figure 5 Influence of deletion of HWP1, BCR1 and ALS3 and on establishment of early firm adhesion. Biofilms formed from the strains indicated at the top of each column were harvested at 40 min and the tubing was drained.

[http://​www.​repeatmasker.​org] 53. House CH, Runnegar B, Fitz-Gibbon ST: Geobiological analysis using whole genome-based tree building applied to the bacteria, archaea, and eukarya. Geobiology 2003, 1:15–26.CrossRef 54. Huse SM, Huber JA, Morrison HG, Sogin ML, Welch DM: Accuracy and quality of massively parallel DNA pyrosequencing. Genome see more Biol 2007,8(7):R143.PubMedCrossRef 55. Kunin V, Engelbrektson A, Ochman H, Hugenholtz P: Wrinkles in the rare biosphere: pyrosequencing

errors can lead to artificial inflation of diversity estimates. www.selleckchem.com/products/sbe-b-cd.html Environ Microbiol 2010,12(1):118–123.PubMedCrossRef 56. Niu B, Fu L, Sun S, Li W: Artificial and natural duplicates in pyrosequencing reads of metagenomic data. BMC Bioinforma 2010,11(1):187.CrossRef 57. Gilbert MTP, Binladen J, Miller W, Wiuf C, Willerslev E, Poinar H, Carlson JE, Leebens-Mack JH, Schuster SC: Recharacterization of ancient DNA miscoding lesions: insights in the era of sequencing-by-synthesis. Nucleic Acids www.selleckchem.com/products/wh-4-023.html Res 2007,35(1):1–10.PubMedCrossRef 58. Quince C, Lanzen A, Davenport RJ, Turnbaugh PJ: Removing noise from pyrosequenced amplicons. BMC Bioinforma 2011, 12:38.CrossRef 59. Kitts CL: Terminal restriction fragment patterns: a tool for comparing microbial communities and assessing community dynamics. Curr Issues Intest Microbiol 2001,2(1):17–25.PubMed 60. Bukovska P, Jelinkova M, Hrselova H, Sykorova Z, Gryndler M: Terminal restriction fragment length measurement errors are affected mainly

by fragment length, G plus C nucleotide content and secondary structure melting point. J Microbiol Methods 2010,82(3):223–228.PubMedCrossRef 61. Kaplan CW, Kitts CL: Variation between observed and true terminal restriction fragment length is dependent on true TRF

length and purine content. J Microbiol Methods 2003,54(1):121–125.PubMedCrossRef 62. Osborn AM, Moore ERB, Timmis KN: An evaluation of terminal-restriction fragment length polymorphism (T-RFLP) analysis for the study of microbial community structure and dynamics. Environ Microbiol 2000,2(1):39–50.PubMedCrossRef 63. Clement BG, Kehl LE, DeBord KL, Kitts CL: Terminal restriction fragment patterns (TRFPs), a rapid, PCR-based method for the comparison of complex bacterial communities. J Microbiol Methods 1998,31(3):135–142.CrossRef 64. Egert M, Friedrich MW: Formation of pseudo-terminal Grape seed extract restriction fragments, a PCR-related bias affecting terminal restriction fragment length polymorphism analysis of microbial community structure. Appl Environ Microbiol 2003,69(5):2555–2562.PubMedCrossRef 65. Pilloni G, von Netzer F, Engel M, Lueders T: Electron acceptor-dependent identification of key anaerobic toluene degraders at a tar-oil-contaminated aquifer by pyro-SIP. FEMS Microbiol Ecol 2011,78(1):165–175.PubMedCrossRef 66. Meyer F, Paarmann D, D′Souza M, Olson R, Glass EM, Kubal M, Paczian T, Rodriguez A, Stevens R, Wilke A, et al.: The metagenomics RAST server – a public resource for the automatic phylogenetic and functional analysis of metagenomes.