In nine children with diarrhea of unknown etiology in Group C, eight had Streptococcus as the most dominant fecal bacterial genus at admission, one with S. lutetiensis, two with S. gallolyticus subsp. pasteurianus, two with Streptococcus salivarius, and

three with Streptococcus sp. (Figures 1 and 2, Table 1). We divided these nine children in Group C into two, according to the most dominant fecal bacterial species at admission. Group C1 included one child whose most dominant species was E. coli. The percentage of E. coli in the fecal microflora of NSC23766 mw Patient 036 (age 7 months) was increased from 87.10% at admission to 90.91% during treatment, and then dropped to 28.90% after recovery (Figure 2B), based on 445 analyzed 16 s rRNA gene sequences. PND-1186 order Figure 2 Percentage changes in fecal bacteria in children with diarrhea at admission and

during and after recovery. Only patients who had unknown etiology and provided three fecal samples were included. The bacterial species with fewer than five determined sequences, or <1% in a given sample, or unrecognized species are not shown. (A) The true percentage value of individual bacterial species in fecal samples of patients with diarrhea sampled at admission and during and after recovery. Each block was divided into three columns by white vertical lines, representing the fecal samples at admission and during and after recovery, respectively. The color value from red to yellow displayed the percentage (50% to 0%) of a given bacterial species in each sample. (B) The percentage changes Sotrastaurin cost medroxyprogesterone in individual bacterial species in fecal samples from patients with diarrhea during and after recovery compared with that at admission. Each block was divided into two columns by white vertical lines, representing the relative percentage changes of given bacterial species during and after recovery, compared with that in feces at admission. The color value from red to yellow to green displayed the percentage (50% to 0% to −50%) of

a given bacterial species in each sample. The negative percentage shows that the percentage of a given bacterial species was reduced compared with that detected at admission. Table 1 Features of study samples from children with diarrhea of unknown etiology Patient information Clinical presentation Stool routine analysis Patient and feces number Sampling date (after onset) Times of stool/day Characteristics of stool Temperature (°C) WBC* RBC* Occult blood 011-1 1 5 Watery Normal + ++ + 011-3 3 5 Loose         011-4 5 2 Formed         016-1 1 3-4 Bloody and mucoid 39.0°C ++ + +/− 016-3 3 3 Watery         016-6 ** 12 2 Formed         017-1 16 10 Watery Normal + ++ +/− 017-3 18 6 Watery         017-5 20 6 Watery         019-1 133 8-9 Bloody and mucoid Normal ++ ++ + 019-6 138 3 Loose         019-7** 143 3 Loose         021-1 33 6 Watery Normal + + – 021-4 35 5 Watery         021-7 38 4-5 Loose         023-1 20 6 Loose 38.

The DNA fragments were incubated with increasing amounts of purified BaeR GW786034 protein in presence of nonspecific competitor DNA (Salmon sperm) (Figure 4). The purified BaeR protein showed binding to the upstream region of acrD with increasing concentrations, which was detected as a smear (Figure 4A). A slight interaction between the acrAB promoter

and BaeR was detected at the highest protein concentration (64 pM), which could suggest an unspecific binding (Figure 4B). No interactions between the fragment of the promoter region of tolC and BaeR were detected (Figure 4C). These results show that BaeR binds to the acrD regulatory region and is probably involved in its regulation. Figure 4 Electrophoretic mobility shift analysis of BaeR interaction with Cy5-labeled DNA fragments. DNA fragments contain the promoter regions of (A) acrD (246 bp), Lazertinib manufacturer (B) acrA (205 bp) and (C) tolC (291 bp), respectively. Approximately 0.16 pmol of the DNA fragments were incubated with increasing amounts of His-tag purified BaeR (indicated at the top of each lane). The DNA-protein complexes were separated on 4% non-denaturing polyacrylamide gels. Induction of acrD through overexpression of BaeR Owing to the interaction between the acrD promoter region and BaeR observed during EMSA assays, we investigated whether overexpression of BaeR may induce

the expression of acrD. Therefore, we cloned baeR under an arabinose-inducible promoter (pBAD24.baeR) and performed learn more qRT-PCR analysis 1 hour after induction. Relative fold-changes in mRNA transcripts of acrA (0.8-fold), acrD (3.8-fold) and tolC (0.7-fold) were determined. The obtained data values correlate with the observed interaction of BaeR during EMSA indicating a specific binding of BaeR to the regulatory region of acrD. Discussion Bacteria have evolved energy-dependent PD184352 (CI-1040) multidrug efflux pumps in order to prevent intracellular accumulation of toxic compounds, including antimicrobials, antibiotics, dyes and detergents [6, 34]. In several enterobacteria, including the human pathogen E. coli and the plant pathogen E. amylovora,

the RND transporter AcrAB-TolC has been described as the major multidrug efflux system providing resistance towards lipophilic and amphiphilic substrates but not towards hydrophilic compounds [6, 16]. Another member of the RND family, AcrD, has been shown to efficiently efflux highly hydrophilic aminoglycosides from E. coli cells [13]. Here, we identified a gene encoding AcrD in E. amylovora Ea1189, which shows significant sequence homology to the cognate aminoglycoside efflux pump of E. coli and investigated the role of this transporter in the fire blight pathogen. Due to the high level of homology shared by AcrD from E. coli and E. amylovora, it was not surprising to find similar substrate specificities. Previous studies of AcrD in E.

The main objectives of the GenTEE network are to document and compare current practices and the state of genetic service provision in the participating eight emerging economies via a standardised

global survey (GenTEE survey) that allows comparison of services internationally across a number of key dimensions by using a core set of indicators selected by the GenTEE participants for their relevance Adriamycin and comparability. In addition, the GenTEE survey identifies current knowledge gaps and unmet service needs. The outline of the special issue Presented are four papers from the CAPABILITY project; two of them addressing conceptual approaches developed by the CAPABILITY consortium and two papers describing the outcomes of capacity building demonstration projects in Argentina and South Africa. Six papers are provided by GenTEE participants describing in a condensed way outcomes of the GenTEE survey in Argentina, Brazil, China,

Oman, the Philippines and South Africa. The IHCP will publish a comprehensive report on the outcome of the GenTEE survey later this year. This report will include the outcomes for the surveys conducted in Egypt and India which could not be included in this special issue. In their paper “Health needs assessment for medical genetic services for congenital disorders in middle-&low-income nations,” Selonsertib Arnold Christianson et.al. describe the CAPABILITY HNA approach. CAPABILITY HNA is an epidemiological-assisted find more systematic approach for providing health policy makers with data for informed decision making in order to plan, introduce and beneficially change health care services (genetic services) to improve both individual and population health. Florian Meier et al. explore ways how middle- and low-income countries could acquire the necessary capital to strengthen health care services/genetic services

via public–private partnerships (PPPs). So far, PPPs have been used exclusively in other health areas. In their paper “Public–private partnerships as a solution for integrating genetic services into health care of countries with low and middle incomes,” a first attempt PIK-5 is made to discuss the feasibility of transferring the concept of PPPs to genetic services and explore how the PPP model could be applied for infrastructure building services. The success of the CAPABILITY Argentina demonstration project is described by Cristina Barreiro et al. in “CHACO outreach project: The development of a primary health care based medical genetic service in an Argentinean province.” Based upon a systematic HNA for Argentina, the outreach project was conducted in one (Chaco) of the 10 Argentine provinces that lacked genetic services.

Conclusions We simulated the photoluminescence spectra of vertically grown pairs of quantum dots and observed that their size is a crucial factor to achieve coupling via magnetic field. Two sets of dots were examined: the first one does not couple because its dimensions MAPK Inhibitor Library concentration strengthen Coulomb interaction and disfavors diamagnetic shift. In contrast, the second one with larger dimensions exhibits a very different behavior as the magnetic field increases, showing the characteristic anticrossings of molecular coupling. The

presence of coupling is highly affected by the Coulomb interaction, regardless of the fact that its value is around 2 orders of magnitude smaller than the exciton energy. Moderate-low temperature (below the nitrogen boiling point) was found enough

to optically observe excited states, which is directly related to the small gap between hybridized states in the resonance region. From these results, we conclude that magnetically tuned tunneling coupling eases optical observation of excited states as compared to single-dot states. Furthermore, effective control on the energy, polarization, and intensity of emitted light, through externally applied magnetic field, has been shown which suggests that this type of on-demand HDAC inhibitor coupled nanostructures Akt activity is a relevant candidate for the implementation of quantum optoelectronic devices. Endnotes a For the electron (hole) g factor, we used −0.745 (−1.4). b The following parameters were used in the calculations: InAs (GaAs) eletron mass 0.023 m e (0.067 m e ), InAs (GaAs) hole mass 0.34 m e (0.34 m e ), and InAs (GaAs) confinement potential V 0=474 meV (258 meV). c Although the

top dot is larger than the bottom one, because of its heaviness, the hole has similar eigenenergies in each of them, and vertical strain effects (as reported in [14]) are likely to be more relevant than those of size. Thus, we assume the ground hole state to remain in the bottom those dot. d An interband gap of 800 meV was used in our calculations. Authors’ information NRF is a MSc degree holder and is a lecturer in the Physics Department of UAN. ASC is a Ph.D. degree holder and is a Senior Researcher and Professor in Universidad de Los Andes. HYR is a Ph.D. degree holder and is an Assistant Professor in the School of Physics of UPTC. Acknowledgements This work was financially supported by the Department of Physics of Universidad de Los Andes and the Research Division of UPTC. References 1. Doty MF, Scheibner M, Bracker AS, Gammon D: Optical spectroscopy of spins in coupled quantum dots . In Nanoscience and Technology. Volume 1. Edited by: Michler P. Berlin: Springer; 2009:330–366. 2. Krenner HJ, Sabathil M, Clark EC, Kress A, Bichler M, Abstreiter G, Finley JJ: Direct observation of controlled coupling in an individual quantum dot molecule . Phys Rev Lett 2005, 94:057402. 15783693CrossRef 3. Voskoboynikov O: Theory of diamagnetism in asymmetrical vertical quantum dot molecule .

Significant increases of blood flow to exercising muscles may provide training benefits for some athletes during certain types of competition or physical conditioning. For example, this website the high degree of leg pump might provide unique athletic conditioning benefits to those in the competitive bodybuilding field and others during particular phases of training. Conclusion Chronic supplementation of GPLC appears to provide benefits

that are dose dependent. While acute supplementation of 4.5 grams was previously shown to provide significant enhancement of anaerobic work capacity, the present study suggests that chronic supplementation of GPLC at 3.0 or 4.5 grams daily does not improve anaerobic performance of repeated high speed high intensity bouts and may actually produce detrimental effects with high velocity, high intensity exercise. However, these results also suggest that 1.5 g GPLC does provide enhancement of anaerobic capacity. These findings also suggest that long term supplementation with this dosage (1.5 g/day) results in significantly lower lactate accumulation with high intensity exercise.

Acknowledgements Funding for this work was provided by Sigma-tau HealthSciences, Inc. References 1. Hamman JJ, Kluess HA, Buckwalter JB, Clifford PS: Blood flow GANT61 price response to muscle contractions is more closely related to metabolic rate than contractile work. J Appl Physiol 2005, 98:2096–2100.CrossRef 2. Tschakovsky ME, Joyner MJ: Nitric oxide and muscle blood flow in exercise. Appl Physiol Nutr Metab 2007, 33:151–161.CrossRef 3. Adams MR, Forsyth CJ, Jessup mTOR inhibitor W, Robinson

J, Celermajer DS: Oral arginine inhibits platelet aggregation but does not enhance endothelium-dependent dilation in healthy young men. J Amer Col Cardiology 1995, 26:1054–1061.CrossRef 4. Bode-Boger SM, Boger RH, Galland A, Tsikas D, Frolich J: L-arginine-induced vasodilation in healthy humans: pharmacokinetic-pharmacodynamic Telomerase relationship. Br J Clin Pharmacol 1998, 46:489–497.CrossRefPubMed 5. Chin-Dusting JP, Alexander CT, Arnold PJ, Hodgson WC, Lux AS, Jennings GI: Effects of in vivo and in vitro L-arginine supplementation on healthy human vessels. J Cardiovasc Pharmacol 1996, 28:158–166.CrossRefPubMed 6. Bloomer RJ, Tschume LC, Smith WA: Glycine propionyl-L-carnitine modulates lipid peroxidation and nitric oxide in human subjects. Int J Vitam Nutr Res 2009, 79:131–41.CrossRefPubMed 7. Bloomer RJ, Smith WA, Fisher-Wellman KH: Glycine propionyl-L-carnitine increases plasma nitrate/nitrite in resistance trained men. J Int Soc Sports Nutr 2007,4(1):22.CrossRefPubMed 8. Jacobs PL, Goldstein ER, Blackburn W, Orem I, Hughes JJ: Glycine propionyl-L-carnitine produces enhanced anaerobic work capacity with reduced lactate accumulation in resistance trained males. J Int Soc Sports Nutr 2009, 6:9.CrossRefPubMed 9. Anderson P, Saltin B: Maximal perfusion of skeletal muscle in man.

22, 2.88, 2.32, 7.04 and 3.47 folds, respectively.

Figure 5 Effects of DNMT1 silencing on gene methylation and mRNA expression of seven tumor suppressor genes in Siha cells assayed by MeDIP combined with Real-Time PCR. Except for FHIT and CHFR, the rest five suppressor genes CCNA1, PTEN, PAX1, SFRP4 and TSLC1 in transfected group displayed lower level of methylation with increased mRNA expression when compared with control group. (n = 3, **P < 0.01). Discussion DNMT1 silencing in cervical cancer cells could induce re-expression of most tumor suppressor genes by demethylating its promoter region, and co-silencing of DNMT1 and DNMT3b might perform a greater inhibitory effect on tumorigenesis [3]. Sowinska XAV-939 research buy [4] demonstrated that combined DNMT1 and DNMT3b Kinase Inhibitor Library datasheet siRNAs could enhance promoter demethylation and re-expression of

CXCL12 in MCF-7 breast cancer as well as AsPC1 in pancreatic carcinoma cell lines, and suggested that they acted synergistically in inhibiting CpG island hypermethylation of tumor suppressor genes. Rhee et al [5] reported that DNMT3b deletion in a colorectal cancer cell line reduced global DNA methylation by less than 3%, but co-silencing of both DNMT1 and DNMT3b nearly eliminated methyltransferase activity, and reduced genomic DNA methylation by greater than 95%. Thus, DNMT1 and DNMT3b play the significant role in promoter methylation of tumor suppressor genes and tumorigenesis in its early status. Urease Currently, functions and mechanisms of DNMTs in cervical cancer cells remained unclear, and whether DNMT1 and DNMT3b act synergistically or through other ways exploration CP-690550 ic50 efforts were still required study. In human bladder cancer cells, selective depletion of DNMT1 with siRNA induced demethylation and reactivation of the silenced tumor-suppressor gene CDKN2A [6]. RNAi-mediated knockdown of DNMT1 resulted in significant reduction of promoter methylation and re-expression of RASSF1A, p16, and HPP1 in HCC1954 breast cancer cells

[7]. In ovarian cancer cell line CP70, DNMT1 siRNA treatment led to a partial removal of DNA methylation from three inactive promoter CpG islands, TWIST, RASSF1A, and HIN-1, and restored the expression of these genes [8]. Thus, RNAi-mediated DNMT1 depletion in different tumor cells could induce demethylation of various tumor suppressor genes and enhance re-expression. However, contradictory results were reported even in the same cell line. Ting et al [9] found that hypermethylation of CDKN2A, SFPR1, GATA4 and GATA5 were still maintained in HCT116 colorectal cancer cells after transiently or stably depleted of DNMT1, and suggested that DNMT1 might not play the dominant effect which caused hypermethylation of CpG islands in tumor suppressor genes. Knockout of DNMT1 in HCT116 cells by homologous recombination only reduced global DNA methylation by 20% and p16 maintained completely methylated status.

In the present study, we have discovered by genetic and biochemical approaches that xanthosine phosphorylase (xapA; also known as purine nucleoside phosphorylase II [PNP-II], EC 2.4.2.1) is also capable of mTOR inhibitor review converting NAM to NR in E. coli. XapA was originally identified from E. coli, and known to catalyze the reversible ribosyltransfer on purine nucleosides including xanthosine, inosine and guanosine [35–37]. Our data has not only assigned a novel function to xapA, but also uncovered a potential new route in the NAD+

salvage, in which the pathway III is extended by using NAM as an alternative precursor in xapA-possessing organisms. Results Genetic SRT1720 cost disruption of NAD+ de novo biosynthesis and NAD+ salvage pathway I in Escherichia coli In an effort to uncover the new function of E. coli xapA in NAD+ salvage pathway from nicotinamide, we produced a set of gene knockout mutants deficient in previously defined NAD+ synthetic pathways, including NAD+

de novo and NAD+ salvage pathways I and III for genetic investigation purpose (see Table 1, Additional file 1: Figure S1 and Additional file 2: Table S1). We first generated a mutant strain deficient in NAD+ de novo pathway (BW25113ΔnadC) that was unable to survive in the M9 minimal medium, but could restore the growth to a level comparable to the wild-type BW25113 when NA or NAM was supplied to allow NAD+ synthesized via NAD+ salvage pathway I (Figure 2 and Ion Channel Ligand Library purchase Table 2). Table 1 Escherichia coli strains and plasmids used in this study Strains or plasmids Genotypes and comments Source or reference Strain DH5α Routine cloning host In-house collection BW25113 rrnB3 ΔlacZ4787 hsdR514 Δ(araBAD)567 Δ(rhaBAD)568 rph-1 CGSC* BW25113ΔnadC BW25113 with chromosomal nadC deletion This study BW25113ΔnadCΔpncA BW25113 with chromosomal nadC and pncA deletion This study BW25113ΔnadCΔpncAΔxapA Fossariinae BW25113 with chromosomal nadC, pncA, and xapA deletion This study BW25113ΔnadCΔpncAΔnadR BW25113 with chromosomal nadC, pncA, and nadR deletion This study

BW25113ΔnadCΔpncAΔxapAΔnadR BW25113 with chromosomal nadC, pncA, xapA and nadR deletion This study Plasmid pKD13 Gene knockout procedure CGSC* pKD46 Gene knockout procedure CGSC* pCP20 Gene knockout procedure CGSC* pBAD-hisA bla + In-house collection pBAD-EGFP pBAD-hisA with EGFP gene This study pBAD-xapA pBAD-hisA with xapA gene This study pET28a Kana + In-house collection pET28-xapA pET28a with xapA gene This study pEGFP-N2 Template for PCR amplification of EGFP gene In-house collection *CGSC is the E. coli Genetic Stock Center of Yale University. Figure 2 Growth of wild-type Escherichia coli (BW25113) and mutants in LB or M9 agar plates supplied with NAM or NA. Strains in area I-VI represent BW25113, BW25113ΔnadC, BW25113ΔnadCΔpncA, BW25113ΔnadCΔpncAΔxapA, BW25113ΔnadCΔpncAΔnadR and BW25113ΔnadCΔpncAΔxapAΔnadR, respectively.

Among the thirty genomes, the search yielded at least one putative operator sequence upstream of more than 30 genes involved in a variety of biological processes e.g. DNA repair, transport, virulence and antibiotic resistance (Table 1). Table 1 In silico predicted LexA binding sites in C. difficile find more ribotypes           Various toxinotypes Toxinotype V Toxinotype 0/nontoxinogenic Luminespib ic50           O33 O27 O75 O17 O78 126 OO9 OO1 O12 OO5 O87 O14 O53 Gene accession number GENE Product LexA BOX Distance 1 strain 8 strains 2 strains 1 strain 3 strains 2 strains 1 strain 3 strains 3 strains 3 strains 1 strain 1 strain 1 strain CDR20291_1854 lexA Transcriptional regulator. LexA repressor GAAC….GTTT −51/-91 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_1169 recA Protein RecA (Recombinase A) GAAC….GTTT −39/-41 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_2696 ruvC Crossover junction endodeoxyribonuclease

GAAC….GTTT −65 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_3234 uvrB Excinuclease ABC subunit B GAAC….GTTC −30 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_0487 rusA Putative RusA-like endodeoxyribonuclease GAAC….GTTT −122 1 4 1 1 3 2 NO NO 1 NO NO 1 NO CDR20291_2024 trxB Thioredoxin reductase GAAC….GTTT −216 NO NO {Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|buy Anti-infection Compound Library|Anti-infection Compound Library ic50|Anti-infection Compound Library price|Anti-infection Compound Library cost|Anti-infection Compound Library solubility dmso|Anti-infection Compound Library purchase|Anti-infection Compound Library manufacturer|Anti-infection Compound Library research buy|Anti-infection Compound Library order|Anti-infection Compound Library mouse|Anti-infection Compound Library chemical structure|Anti-infection Compound Library mw|Anti-infection Compound Library molecular weight|Anti-infection Compound Library datasheet|Anti-infection Compound Library supplier|Anti-infection Compound Library in vitro|Anti-infection Compound Library cell line|Anti-infection Compound Library concentration|Anti-infection Compound Library nmr|Anti-infection Compound Library in vivo|Anti-infection Compound Library clinical trial|Anti-infection Compound Library cell assay|Anti-infection Compound Library screening|Anti-infection Compound Library high throughput|buy Antiinfection Compound Library|Antiinfection Compound Library ic50|Antiinfection Compound Library price|Antiinfection Compound Library cost|Antiinfection Compound Library solubility dmso|Antiinfection Compound Library purchase|Antiinfection Compound Library manufacturer|Antiinfection Compound Library research buy|Antiinfection Compound Library order|Antiinfection Compound Library chemical structure|Antiinfection Compound Library datasheet|Antiinfection Compound Library supplier|Antiinfection Compound Library in vitro|Antiinfection Compound Library cell line|Antiinfection Compound Library concentration|Antiinfection Compound Library clinical trial|Antiinfection Compound Library cell assay|Antiinfection Compound Library screening|Antiinfection Compound Library high throughput|Anti-infection Compound high throughput screening| NO NO NO NO 1 NO NO NO NO NO NO 63q42v1_580022 rps3 Putative 30S ribosomal protein S3 GAAC….GTTA −284 NG NG 1 NG NG NG NG 1 NG NG NG NO NO CDR20291_3107 sspB Small. acid-soluble spore protein beta GAAC….GTTC 34 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_0784 oppC ABC-type transport system. oligopeptide GAAC…GTTT −285/ -286 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_3532 soj Small walker A ATPase, chromosome replication GAAC….GTTT −226 NO 8 2 1 NO NO 1 3 3 3 NO 1 1 CDR20291_2297   Putative

multidrug efflux pump GAAC…TTTT −138 1 8 2 1 3 2 1 3 3 3 1 1 1 63q42v1_310170   ABC-type HA1077 multidrug-family GAAC….CTTT −154 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_3125 vanR Regulatory protein vanR GAAC….ATTT −222 NO 8 2 NO NO NO NO NO NO NO NO NO NO CDR20291_0083 rplR 50S ribosomal protein L18 GAAC….GTTT −261/ -262 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_0060 rpoB DNA-directed RNA polymerase subunit β GAAC…GTTT −42/-43 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_1619   Putative transcriptional regulator GAAC…GTTT 30/31 1 8 2 1 3 2 1 3 3 3 1 1 1 63q42v1_570034   Helix-turn-helix domain protein GAAC…CTTT −97 NG 3 NG 1 NG NG NG 1 NG 1 NG NG NG CDR20291_0882 potC ABC-type transport system. GAAC…GTTC −207 1 8 2 1 3 2 1 3 3 3 1 1 1 CDR20291_0584 tcdA Toxin A GAAC….GTTT −525 NG 8 2 NG 3 2 NG 3 3 3 1 1 1 CDR20291_3466   Putative cell wall hydrolase GAAC…GTTT −68 NO 8 NG NO NO NO NO NO NO NO NO NO NO CDR20291_2689   Putative membrane protein GAAC….

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