Similar risks were also found when analyses were performed on the subset of patients followed up for

at least 1 year, and in those who had their last visit <2 years before the date of analysis (data not shown). Of note, in the latter set of patients, the RR associated with calendar year was even higher (RR=0.59, 95% CI 0.57–0.62; P<0.0001). We formally tested the interactions between calendar year and both mode of HIV transmission and ART status, using the whole study population. The inclusion of interactions between year and mode of transmission led to a significant improvement in the fit (log-likelihood P=0.00012). In detail, the effect of year in the various subgroups was as follows: RR=0.843 (95% CI 0.81–0.876) CHIR-99021 cell line for heterosexual contact, RR=0.780 (95% CI 0.764–0.842) for other routes of infection, RR=0.89 (95% CI 0.87–0.92) for IDU, and RR=0.853 (95% CI 0.8179–0.886) for homosexual LY294002 purchase contact (P=0.01), suggesting that the immunological

benefit conferred by ART in IDU was significantly smaller than that observed for people who acquired HIV infection via sexual contact. The interaction between year and ART status also yielded a significant improvement in the log-likelihood (P=0.0007). The effect of year in the ART status strata was as follows: RR=0.84 (95% CI 0.81–0.86) for people on ART for ≥6 months; RH=0.89 (95% CI 0.86–0.92) for those on ART for <6 months; RH=0.89 (95% CI 0.85–0.94) for those on

an ART interruption; and RH=0.89 (95% CI 0.85–0.92) for ART-naïve patients. In the subset of patients previously on ART for ≥6 months (Table 2b), the decrease in the risk of having a CD4 count ≤200 cells/μL per more recent year appeared to be as rapid as in the main analysis. The RRs associated with the other covariates were consistent with those of acetylcholine the main analysis. The evidence for an interaction between calendar year and mode of HIV transmission was confirmed in this subset of patients (P<0.0001). In a univariable Poisson regression, calendar year was again significantly associated with the probability of having a VL >50 copies/mL (this probability decreased from 66 to 40% from 1998 to 2008; RR=0.94, 95% CI 0.94–0.95; P<0.0001). Figure 1 (right panel) depicts annual trends overall and after stratifying for mode of transmission and ART status. When we stratified by mode of transmission, overall, the highest prevalence of poor virological prognosis was found in IDU (58%), followed by those infected via heterosexual contact (53%), those infected via homo/bisexual contact (51%) and those infected by other routes (46%). χ2 comparisons showed a significant difference among all groups (P<0.0001); however, this difference was no longer significant in the multivariable analysis.

PCR products were digested with appropriate enzymes and inserted into pDM4-lacZ. Transconjugation was performed in WT and ΔsraG to obtain crossed single-copy lacZ fusion strains. All strains carrying the single copy of lacZ fusions were cultured to mid-exponential Selleck SP600125 phase (OD600 nm of ~0.6) at 28 °C. β-Galactosidase assays were performed as described by Miller (1992). Results are expressed as the averages of more than three independent assays, and all tests were done in triplicate. Overnight cultures of WT and ΔsraG were grown to exponential phase (OD600 nm of ~0.6) and centrifuged at 5000 g for 5 min at 4 °C. Preparation of protein samples, gel

electrophoresis and spot quantification were performed as described elsewhere (Hu et al., 2009). Each sample was prepared and analysed in triplicate. Proteins with densities which increased or decreased ≥ 1.5-fold in WT compared Enzalutamide mw with that in ΔsraG in all three experiments were excised, digested with trypsin and identified by MALDI-TOF (matrix-assisted laser desorption ionization time-of-flight) MS. The coding region of YPK_1205 was amplified using primers p1205eBF and p1205eHR (Table S1), digested with BamHI and HindIII and inserted into pET28a (Novagen). Protein was induced and purified

as described previously (Hu et al., 2009). The purified protein was used to immunize rabbits to obtain serum which was used as a polyclonal anti-YPK_1205 antibody. Overnight cultures were diluted 1/100 in fresh YLB medium and grown to an OD600 nm of 0.6. Protein samples were prepared and Western blotting was performed as described by Sittka et al. (2007). Samples were transferred to a polyvinylidene Olopatadine difluoride membrane, hybridized by specific antiserum, and followed by alkaline phosphatase-labelled anti-rabbit IgG (Sigma). NBT/BCIP substrate (BBI) was used to develop the colour. Overnight cultures of WT, ΔsraG and the complemented ΔsraG strain were diluted 1 : 100 into fresh YLB medium and cultured to the indicated

growth phases. Total RNA was extracted with TRIzol reagent (Invitrogen) according to the manufacturer’s protocol. After treatment with RNase-free DNase I (Promega), 4 μg of each RNA sample was used in reverse transcription to obtain the cDNA template. Random 9 mers (TaKaRa) or specific sraG gene primer (pairing with 81–106 of the sraG gene) were used in reverse transcription. The nested PCR was performed to detect SraG RNA transcript. Genomic DNA and DNase I-treated RNA were used as positive and negative controls. Potential interactions of SraG with YPK_1205 and YPK_1206 were predicted with the RNAhybrid software based on hybridization free energy and interaction site accessibility (Rehmsmeier et al., 2004). The region of SraG excluding the terminator (1–150) was used as a search seed. The intergenic region between YPK_1207 and YPK_1206 and +1 to +63 according to the translation start site (A of ATG) of YPK_1206 was used as the seed search region.

5. Genes involved in carbohydrate metabolism are regulated by a transcription factor named Cra for ‘catabolite repressor/activator’ (Saier & Ramseier, 1996); this information led us to speculate on the involvement of Cra in the regulation of this acid

survival process. In this report, the role of Cra in acid survival regulation is characterized. Overnight culture (100 mL) of Y. pseudotuberculosis YpIII strain grown in Yersinia–Luria–Bertani (YLB) broth (1% tryptone, 0.5% yeast extract and 0.5% NaCl) at pH 7.0 at 28 °C was shifted to 37 °C for 2 h or diluted into YLB at pH 4.5 (adjusted with hydrochloric acid) for acid challenge assay and then incubated at 37 °C for 2 h. Protein sample preparation and 2D gel running were performed as described previously (Hu et al., 2009). Gels were stained with colloidal CBB G-250 and then scanned with

a PowerLook 1000 (UMAX Technologies). Spot densities selleck products were quantified and analyzed with the pd quest software package (version 7.3.0, Bio-Rad). Each sample was prepared and analyzed in triplicate. Proteins with densities which increased or decreased ≥2-fold in all three experiments (P<0.01 in Student's t-test) were excised and digested with trypsin and Antidiabetic Compound Library concentration identified by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) MS. To construct plasmids containing the translational gene∷lacZ fusions, two primers were designed for each gene in which the reverse primer was designed at the 3′-end (missing the stop codon), and the forward primer of each gene

was designed around 600 bp upstream of the stop codon. The primers were listed in Supporting Information, Table S1. Each PCR product was inserted between the SalI and SpeI sites of pDM4-lacZ (Hu et al., 2009) to generate a series of plasmids named pDM4-2762Z, pDM4-2764Z and pDM4-3529Z, which was transformed into Escherichia coli S17-1. Homologous click here recombination and subsequent selection were carried out as described (Hu et al., 2009). YpIII strains carrying the gene∷lacZ fusions were cultured overnight at 28 °C in YLB broth and diluted into fresh YLB (pH 4.5) to ∼108 CFU mL−1. After incubation at 37 °C for 0 and 2 h, cells were collected and washed with phosphate-buffered saline (PBS; pH 7.0). β-Galactosidase activity was determined and calculated as described previously (Hu et al., 2010). Data were analyzed by Student’s t-test. For Δcra construction, two DNA fragments (493 and 500 bp) up- and downstream of the cra gene, which omitted the entire cra gene were amplified using two pairs of primers, P3529-u-F/R and P3529-d-F/R (Table S1). These two PCR products were digested with the appropriate restriction enzymes and inserted into the similarly digested pDM4 to obtain pDM4-cram, which was subsequently transformed into E. coli S17-1. Transconjugation was performed to obtain Δcra strain.

Consistent with ITS and β-tubulin phylogenies, molecular clustering based on lac3-1 sequence analysis grouped the P. cinnabarinus and P. puniceus strains into two highly supported specific lineages. The P. sanguineus and P. coccineus strains were distributed through four distinct, well supported clades

and sub-clades. A neotropical sub-clade grouped the P. sanguineus strains from French Guiana and Venezuela – and the reference strain CIRM-BRFM 902 – corresponding to P. sanguineus sensu stricto. A paleotropical sub-clade clustered the strains from Madagascar, Vietnam and New Caledonia, and could be defined as Pycnoporus cf. sanguineus. The Australian clade of P. coccineus, including the reference strain MUCL 39523, corresponded to P. coccineus sensu stricto. This clade also included

LY2109761 purchase the Malesian strain from the Solomon Islands, positioned separately, consistent with the high level of endemic species in that country (Udvardy, 1975). this website The fourth group was the Eastern Asian region clade, clustering the strains from China, including CIRM-BRFM 542 of unknown origin and the strain MUCL 38527 from Japan. The strains of this last clade shared polymorphism in ITS and β-tubulin sequences with P. coccineus sensu stricto strains, as well as intron length in β-tubulin gene sequences, known to be characteristic of a lineage in basidiomycetes (Begerow et al., 2004). This suggests a misidentification of Chinese specimens, very recently confirmed by macroscopic observation of basidiocarps. The high degree of similarity of the morphological characters between Interleukin-3 receptor P. sanguineus and P. coccineus and the high variability of specimens across the season and the geographical area could explain this field misidentification (Nobles & Frew, 1962). Accordingly, the

Eastern Asian region strains of Pycnoporus (from China and Japan), together with the related strain CIRM-BRFM 542 (suspected to be of East Asian descent), formed a P. coccineus-like group defined as Pycnoporus cf. coccineus (Fig. 3). Biogeographic phylogenetic structure was related in polyporoid fungi such as Grifola frondosa, separating Eastern North American strains from Asian strains, and no morphological distinction was detected between them (Shen et al., 2002). In the Ganoderma applanatum/australe species complex, eight distinct clades were strongly correlated with the geographic origin of the strains, and corresponded to mating groups (Moncalvo & Buchanan, 2008). Interestingly, the East Asian clade in our study corresponded to the functional group of Pycnoporus strains previously reported for their high level of laccase production (Lomascolo et al., 2002).

It is difficult to compare our results to those obtained in earlier studies. Weber et al.5 focused solely on business travelers without providing information on size and type of employer and Van Herck et al.6 provided little to no specific information about the subgroup of business travelers. This study demonstrates that company employees will largely make use of internally provided travel health resources when available. This supports the need for ensuring constant review

and audit of travel clinic service delivery and may provide a cautionary tale for other companies PLX-4720 clinical trial against overprescribing of malaria prophylaxis. Because experienced travelers tend not to seek advice, this requires systems to be put in place to ensure compliance. Finally, among FBT’s, there is still an ongoing educational need to improve knowledge of the incubation period and range of malaria symptoms. We are indebted to the frequent business traveler population of SIEP (Shell Exploration and Production), based in Rijswijk, The Netherlands for their participation. We also relied on the goodwill of C. Bollin, MD, and www.selleckchem.com/products/epacadostat-incb024360.html D.N. Twilhaar, respectively the occupational health physician and HSE manager at the time. We also would like to thank S. Cannegieter, MD, PhD and S. Kuipers, MD, PhD of the University of Leiden, Department of Clinical Epidemiology for their initial advice and support. The authors state they have no conflicts

of interest to declare. “
“International travelers were at risk of acquiring influenza A(H1N1)pdm09 (H1N1pdm09) virus infection during travel and importing the virus to their home or other countries. Characteristics of travelers reported to the GeoSentinel Surveillance Network who carried H1N1pdm09 influenza virus across international

borders into a receiving country from April 1, 2009, through October 24, 2009, are described. The relationship between the detection of H1N1pdm09 in travelers and the level of H1N1pdm09 transmission in the exposure country as defined by pandemic intervals was examined using analysis of variance (anova). Among the 203 (189 confirmed; 14 probable) H1N1pdm09 case-travelers identified, 56% were male; a majority, 60%, traveled for tourism; (-)-p-Bromotetramisole Oxalate and 20% traveled for business. Paralleling age profiles in population-based studies only 13% of H1N1pdm09 case-travelers were older than 45 years. H1N1pdm09 case-travelers sought pre-travel medical advice less often (8%) than travelers with non-H1N1pdm09 unspecified respiratory illnesses (24%), and less often than travelers with nonrespiratory illnesses (43%; p < 0.0001). The number of days from first official H1N1pdm09 case reported by a country to WHO and the first GeoSentinel site report of a H1N1pdm09-exported case in a traveler originated from that country was inversely associated with each country’s assigned pandemic interval, or local level of transmission intensity.

AT-rich codons are much more abundant, reflecting the high AT content of the P. solitum mitochondrial genome. Codons for amino acids with nonpolar side chains (Phe, Leu and Ile) are very frequent, which is not surprising given the hydrophobic nature of encoded proteins of respiratory membrane complexes. Among

the 27 tRNA genes, there are several isoacceptor tRNAs for glycine, arginine, leucine, serine and isoleucine. The abundant ATA codons for isoleucine are probably read by one of the three predicted tRNA-M following the Tofacitinib research buy cytosine to lysidine modification of the CAU anticodon, like in fungal, protist and fission yeast mitochondrial genomes (Bullerwell et al., 2003; Grayburn et al., 2004). Phylogenetic relationships Palbociclib among Eurotiales based on multigene comparison of nuclear-encoded genes are well established (Spatafora et al., 2006). Our

phylogenetic analysis based on concatenated mitochondrial protein sequences confirmed the monophletic origin of Eurotiomycetidae and the current view of the taxonomic position of Aspergilli and Penicilli within Onygenales and related taxa (Geyser, 2006). Phylogenetic trees constructed using both ML and Bayesian approaches were essentially congruent (Fig. 2 and Fig. S4). Aspergillus and Penicillium species were divided into two well-resolved clades with high support. Interestingly, the determined phylogenetic position of the pathogenic dimorphic fungus P. marneffei suggests that this species is more distantly related to the studied members of Trichocomaceae. The higher degree of divergence of mitochondrial protein sequences SPTLC1 between P. marneffei and other members of Trichocomaceae correlates with the difference of gene order in P. marneffei mitochondrial genome relative to the mitochondrial genomes of A. nidulans and other Aspergillus and Penicillium mtDNAs described here. Altogether, these observations question the current taxonomic position of P. marneffei and suggest that this fungus may represent a separate genus within Trichocomaceae, as suggested earlier during nuclear genome comparisons (van den Berg et al., 2008). The extensive similarity of Aspergillus and Penicillium mitochondrial genomes

in terms of gene size, content and sequence homology (Table 1) was also reflected in the almost perfect conservation of mitochondrial gene order in compared species. The genus-specific syntenic regions cover whole genomes, include all main protein- and RNA-encoding genes and are only interrupted by insertions of several ORFs with unknown functionality. The very high degree of colinearity of Aspergillus and Penicillium genomes is also evident from the intergenera gene order comparison (Fig. S2). The main architectural features, such as the presence of two clusters of tRNA genes flanking the rnL gene and clusters of atp and nad genes characteristic of syntenic patterns and specific to Pezizomycotina mitochondrial genomes, are present (Ghikas et al., 2006).

[13] Further, vitamin D has been reported to attenuate inflammation in periodontal tissue induced by Porphyromonus gingivalis, again a strong triggering event for development of RA.[14] Such associations of low vitamin D state with many other systemic autoimmune diseases, including lupus, are also well known and readers will have no difficulty in finding Forskolin in vitro enough, and convincing, publications in this regard.[15, 16] Apart from its osteoimmunological implications, vitamin D deficiency and the renin angiotensin system (RAS) activity may represent two sides of the same

coin which is responsible for metabolic syndrome and high cardiovascular mortality, as hypothesized and reported by some.[17] This is all the more relevant as vitamin D is also reported to have a protective role against metabolic syndrome in RA.[18] An inverse relationship between vitamin D levels and C-reactive protein is yet another factor in imparting cardiovascular protection in RA.[19] In contrast, there is a query if vitamin D levels should be tested indiscriminately for every ache and pain in rheumatology and this was addressed in a study from Kuwait published in this issue of IJRD. While the authors report otherwise in this study, there are some elements of truth in the other school of thought too. Most of these studies have methodological flaws, heterogeneous cohort, smaller sample

size and are underpowered to address this issue. However, the majority of the reports from different populations have documented lower vitamin D levels in vague aches and pain than reference populations.[20-22] Correlation between low back pain in people selleck products with modic changes and vitamin D insufficiency also

do exist in the literature.[23] A randomized controlled trial conducted among non-Western immigrants with nonspecific musculoskeletal pain in the Netherlands suggests modest benefit of vitamin D.[24] Low D-malate dehydrogenase vitamin D state in a cohort of fibromyalgia patients and good response to corrective treatment have been documented both in veiled, conservatively dressed, as well as in non-veiled subsets alike.[25] Even in the elderly, post-menopausal, as well as in mixed cohorts of patients with different rheumatic diseases, vitamin D showed clear improvement in musculoskeletal pain[26-28] and negative studies have been reported only occasionally.[29] To add further, vitamin D deficiency leading to hypersensitivity to pain in muscles via nerve endings has been described.[30] And finally, what is non-specific musculoskeletal pain (NSMP)? Is it a harbinger of evolving early inflammatory arthritis at least in a subset of patients, especially in view of its strong association with deficiency of vitamin D in many studies? Can the onset of inflammatory arthritis be delayed by treating a low vitamin D state in this setting? These questions have no answers at this moment.

[13] Further, vitamin D has been reported to attenuate inflammation in periodontal tissue induced by Porphyromonus gingivalis, again a strong triggering event for development of RA.[14] Such associations of low vitamin D state with many other systemic autoimmune diseases, including lupus, are also well known and readers will have no difficulty in finding Alectinib in vitro enough, and convincing, publications in this regard.[15, 16] Apart from its osteoimmunological implications, vitamin D deficiency and the renin angiotensin system (RAS) activity may represent two sides of the same

coin which is responsible for metabolic syndrome and high cardiovascular mortality, as hypothesized and reported by some.[17] This is all the more relevant as vitamin D is also reported to have a protective role against metabolic syndrome in RA.[18] An inverse relationship between vitamin D levels and C-reactive protein is yet another factor in imparting cardiovascular protection in RA.[19] In contrast, there is a query if vitamin D levels should be tested indiscriminately for every ache and pain in rheumatology and this was addressed in a study from Kuwait published in this issue of IJRD. While the authors report otherwise in this study, there are some elements of truth in the other school of thought too. Most of these studies have methodological flaws, heterogeneous cohort, smaller sample

size and are underpowered to address this issue. However, the majority of the reports from different populations have documented lower vitamin D levels in vague aches and pain than reference populations.[20-22] Correlation between low back pain in people BGB324 datasheet with modic changes and vitamin D insufficiency also

do exist in the literature.[23] A randomized controlled trial conducted among non-Western immigrants with nonspecific musculoskeletal pain in the Netherlands suggests modest benefit of vitamin D.[24] Low fantofarone vitamin D state in a cohort of fibromyalgia patients and good response to corrective treatment have been documented both in veiled, conservatively dressed, as well as in non-veiled subsets alike.[25] Even in the elderly, post-menopausal, as well as in mixed cohorts of patients with different rheumatic diseases, vitamin D showed clear improvement in musculoskeletal pain[26-28] and negative studies have been reported only occasionally.[29] To add further, vitamin D deficiency leading to hypersensitivity to pain in muscles via nerve endings has been described.[30] And finally, what is non-specific musculoskeletal pain (NSMP)? Is it a harbinger of evolving early inflammatory arthritis at least in a subset of patients, especially in view of its strong association with deficiency of vitamin D in many studies? Can the onset of inflammatory arthritis be delayed by treating a low vitamin D state in this setting? These questions have no answers at this moment.

Saline soils are pristine and unexplored habitats representing intriguing ecosystems expected to harbour

potential diazotrophs capable of adapting in extreme conditions, and these implicated organisms are largely obscure. Differential occurrence of diazotrophs was studied by the nifH gene-targeted clone library approach. Four nifH gene clone libraries were constructed from different soil niches, that is saline soils (low and high salinity; EC 3.8 and 7.1 ds m−1), and agricultural and rhizosphere soil. Additionally, the abundance of diazotrophic community members was assessed selleck chemicals llc using quantitative PCR. Results showed environment-dependent metabolic versatility and the presence of nitrogen-fixing bacteria affiliated with a range of taxa, encompassing members of the Alphaproteobacteria, Betaproteobacteria, Deltaproteobacteria, Gammaproteobacteria, Cyanobacteria and Firmicutes. The analyses unveiled the dominance of Alphaproteobacteria and Gammaproteobacteria (Pseudomonas,

Halorhodospira, Ectothiorhodospira, Bradyrhizobium, Agrobacterium, Amorphomonas) as nitrogen fixers in coastal–saline soil ecosystems, and Alphaproteobacteria and Betaproteobacteria (Bradyrhizobium, Azohydromonas, Azospirillum, Ideonella) in agricultural/rhizosphere ecosystems. The results revealed a repertoire of novel nitrogen-fixing Epacadostat research buy bacterial guilds particularly in saline soil ecosystems. “
“Chair of Food Safety, Faculty of Veterinary Medicine, LMU, Oberschleißheim, Germany Ground feeds for pigs were investigated for fungal contamination before

and after pelleting (subsamples in total n = 24) by cultural and molecular biological methods. A fungal-specific primer pair ITS1/ITS5.8R was used to amplify fungal DNA; PCR products were processed for the PCR-SSCP method. In the resulting acrylamide gel, more than 85% of DNA bands of ground feeds were preserved after pelleting. Twenty-two DNA bands were sequenced; all represented fungal DNA. The level of fungal DNA in ground feed samples was equivalent to 4.77–5.69 log10 CFU g−1, calculated by qPCR using a standard curve of Aspergillus flavus. In pelleted Florfenicol feed, the level of fungal DNA was in average ± 0.07 log10 different from ground feed. Quantified by cultural methods, the fresh ground feeds contained up to 4.51 log10 CFU g−1 culturable fungi, while there was < 2.83 log10 CFU g−1 detected in pelleted feeds. This result shows that, while the process of pelleting reduced the amount of living fungi dramatically, it did not affect the total fungal DNA in feed. Thus, the described methodology was able to reconstruct the fungal microbiota in feeds and reflected a considerable fungal contamination of raw materials such as grains. "
“Glyphosate is a widely used herbicide that inhibits 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) activity. Most plants and microbes are sensitive to glyphosate.

, 1990). The Vsr protein is an endonuclease that is necessary to remove the new thymine residue (Hennecke et al., 1991) and thus compensates for the mutagenic potential of 5mC. There is evidence that Dcm itself is required for robust very short patch repair of mismatched bacteriophage heteroplexes (Jones et al., 1987; Lieb, 1987; Zell & Fritz, 1987), but this relationship has not been observed in all reports (Sohail Ku-0059436 mw et al., 1990). Nonetheless, the sequence

5′CCWGG3′ is still a mutational hot-spot sequence, because not all mismatches are repaired (Lieb & Bhagwat, 1996). The biological role of the dcm gene and 5′CCWGG3′ cytosine DNA methylation in E. coli remains unclear. The dcm gene is not essential as mutant, deletion, and knockout strains are viable (Marinus & Morris, 1973; Baba et al., 2008). Interestingly, the dcm gene and cytosine

DNA methylation are absent from E. coli B (Doskocil & Sormova, 1965; Fujimoto et al., 1965), a host strain used extensively to study bacteriophages T1–T7 (Daegelen et al., 2009). Genome sequencing of E. coli B (REL606) shows that when compared to E. coli strain K-12 MG1665, it has an IS1-associated 41-kbp deletion from uvrY to hchA that comprises ~0.9% of the genome including the dcm gene and 21 flagellar genes Gefitinib research buy (Studier et al., 2009). The loss of the dcm operon in E. coli B may have been coupled to the loss of the nearby flagellar and chemotaxis genes, as strains that lack flagellar and chemotaxis genes have an advantage during laboratory evolution experiments (Asakura et al., 2011). Nonetheless, several Phosphatidylinositol diacylglycerol-lyase pieces of evidence suggest that Dcm has a role in modulating the activity of the EcoRII R-M system in K-12 strains, which also targets 5′CCWGG3′ sequences. Experiments by Takahashi et al. (2002) indicate that loss of a plasmid containing

the EcoRII methyltransferase and restriction enzyme genes is higher in dcm+ cells compared to dcm mutant cells, indicating that Dcm protects the genome against attack by this R-M system. Furthermore, Dcm protects the cell from postsegregational killing due to loss of the EcoRII R-M system (Ohno et al., 2008). Also, dcm partially protects DNA from cleavage during entry into a new host containing the EcoRII restriction enzyme (Hattman et al., 1973). However, it is unclear whether there are roles for Dcm beyond the role in the EcoRII R-M system. Therefore, we determined whether the dcm gene and 5mC were present in E. coli clinical strains and strains isolated from water and animal feces (environmental strains). We also tested the hypothesis that dcm influences the process of transcription, as cytosine-5 DNA methyltransferases often have this property. The E. coli Reference Collection (ECOR), a set of E. coli strains isolated from a variety of hosts and geographical locations (Ochman & Selander, 1984), was obtained from the ‘Shiga-toxin producing E. coli’ Center (STEC) at Michigan State University. Environmental strains of E.