This eukaryotic-type degradation mechanism of alkane in G. thermoleovorans cells might reflect chaotic living cell systems of common ancestor under high temperature condition of the primitive earth. Evolutional relationship

between G. thermoleovorans and peroxisome in the eukaryotic cells are of great interest. Figure 7 Acyl-CoA oxidase activity of G. thermoleovorans B23. a, Induction of acyl-CoA oxidase activity by alkanes or fatty acids. G. thermoleovorans B23 was cultivated in the presence of alkanes or single fatty acid at 70°C for 5 days (open bar) and 10 days (closed bar). Cells grown on simple LBM were used as a negative control. Acyl-CoA oxidase activity was measured using tetradecanoyl-CoA as a substrate. One unit was defined as the amount of AZD1480 enzyme Luminespib producing 1 nmol of H2O2 in one min. b, Substrate specificity of acyl-CoA oxidase. Enzyme activity was compared each other

using acyl-CoA with various alkyl chain length. Conclusion We, for the first time, suggested that peroxisomal β-oxidation pathway exists in an extremely thermophilic alkane degrading Geobacillus thermoleovorans B23. This eukaryotic-type alkane degradation pathway in the bacterial cells might be a vestige of primitive living cell systems that would had evolved into eukaryotes. Methods Cells and plasmids An extremely thermophilic alkane-degrading bacterium, Geobacillus thermoleovorans B23 was previously isolated from a deep petroleum reservoir in Minami-aga Meloxicam oil field (Niigata, Japan, [1]). G. thermoleovorans type strain LEH-1 (ATCC43513) was purchased selleck chemicals llc from ATCC (American Type Culture Collection, Manassas,

VA, [22]) and used as a comparative strain. E. coli DH5α was used as a host strain for the gene cloning with a cloning vector pCR2.1 (Invitrogen Corp., San Diego, CA).E. coli strain XL1-Blue MRA (P2) was used as a host strain for construction of a phage library of B23 genome. Culture media Nutrient L-broth contained (per liter) 5 g of yeast extract (Difco, Detroit, MI), 10 g of Bacto-tryptone (Difco), and 5 g of NaCl (pH 7.2) was used for cultivation and storage of the strains. Cells were aerobically grown in a screw capped culture bottle without shaking at 70°C or 60°C for B23 and LEH-1, respectively. The bottle cap was opened once a day to avoid oxygen depletion. Solid medium was prepared by adding 1.5% agar or 4% gellan gum (Wako Pure Chemicals, Osaka, Japan). Mineral salts medium, LBM [23], was used for alkane degradation and protein induction experiments. LBM contained per liter; 0.25 g NaNO3, 0.25 g NH4Cl, 0.21 g Na2HPO4, 0.20 g MgSO4-7H2O, 0.09 g NaH2PO4, 0.04 g KCl, 0.02 g CaCl2, 1 mg FeSO4, 10 ml Trace mineral solution. Trace mineral solution contained per liter; 7 mg ZnSO4-7H2O, 1 mg H3BO4, 1 mg MoO3, 0.5 mg CuSO4-5H2O, 18 μg CoSO4-7H2O, 7 μg MnSO4-5H2O. Otherwise mentioned, LBM was supplemented with 1 ml (0.

g. glutamate). The pyruvate dehydrogenase also provides acetyl-CoA used in fatty acid biosynthesis. In addition, the presence of cbbZ in the cbb3 operon is associated with phosphoglycolate phosphatase activity, responsible for removal of phosphoglycolate, an undesirable product of the oxygenase activity of

RubisCO, that must be detoxified preferentially by rechanneling to 3-phosphoglycerate [13, 36]. The co-transcriptional connection between the cbb, pykA and trpEG genes in the cbb3 operon may reflect the substrate requirement www.selleckchem.com/products/Belinostat.html of anthranilate phosphoribosyltransferase for an activated pentose (5-phosphoribosyl 1-pyrophosphate) in order to proceed to the next step of tryptophan biosynthesis [42]. The production of the activated pentose would be stimulated by the activity of the operon. An alternate hypothesis is that the co-transcriptional connection represents a means for pyruvate regeneration since both pykA and trpE/G produce pyruvate. In addition

to the four cbb operons described herein, a fifth gene cluster has recently been detected in A. ferrooxidans that includes genes cbbM, cbbQ3 and cbbO3 predicted to encode form II of RubisCO and its associated chaperons, respectively [43]. The cluster also contains another putative cbbR divergently transcribed from cbbMQO. Future work will evaluate the role of this cluster in CO2 fixation. Acknowledgements This work was supported NVP-HSP990 manufacturer by a grant from Fondecyt 1090451, a Microsoft Sponsored Research Award, a Deutscher Akademischer Austausch

Dienst (DAAD) scholarship to ME, a CONICYT graduate student grant to J-PC and a grant from the Deutsche Forschungsgemeinschaft to BB. Electronic supplementary material Additional file 1: Prediction of secondary structure elements in CbbR of Acidithiobaillus ferrooxidans. Above: secondary structure predictions of alpha-helix, beta-sheet, HTH DNA binding domain, oligomerization domain and LysR-substrate like domain. Below: alignment of amino acid sequences from the HTH domain from several bacteria (abbreviations used can be found in Additional File 2) with the pfam domain00126. (PDF 65 KB) Additional file 2: Alignment and conservation Vorinostat solubility dmso of DNA sequences in the intergenic regions between cbbR and cbbL1 in autotrophic bacteria. The DNA sequences contain the cbb control elements including the operator, the operon promoter (pcbbL) and the promoter cbbR (pcbbR). The CbbR regulator bind to region R (recognition site) and the region A (activation site) of the cbb operator. The nucleotides conserved (TNA-N7/8-TNA, T-N11-A) for to bind CbbR are located in intergenic regions RI-1, RI-2 and RI-3. The prediction of the promoter and the sites for to bind σ70 are in the Selleck NCT-501 columns (sequences -35 and -10).

The autonomous replication of the pMyBK1 derivatives learn more in these species was confirmed by plasmid purification and back-transformation of E. coli with the purified plasmids. Transformation of Mmc with pCM-K3/4 also yielded many tetracycline resistant transformants, but no free plasmid could

be detected despite the positive PCR amplification of CDSB. These results suggest an integration of the pMyBK1 derivative into the host chromosome of this species, as it has been previously described for oriC plasmids [55]. Attempts to transform M. mycoides subsp. mycoides or Spiroplasma citri with pCM-K3 repeatedly failed. Interestingly, we also showed that pMyBK1 not only replicated in various mycoplasma species but was also able to express heterologous genes. The spiralin gene encoding the major surface protein of S. citri was inserted into the EcoRI site of pCM-K3 and the resulting plasmid pCM-K3-spi (Figure 2A) was successfully introduced into M. yeatsii GIH TS and Mcc California Kid. Expression of spiralin by the transformants was demonstrated by immunoblotting

(Additional file 6: Figure S3 for Mcc transformants, data not shown for M. yeatsii transformants). These results Dinaciclib molecular weight confirm and extend recently published results [25] indicating that pMyBK1 derivatives can be used as expression vectors in mycoplasma species of veterinary importance. General phylogeny of Rep sequences from mycoplasma plasmids Based on the availability of 25 Rep sequences of mycoplasma plasmids (Additional file 3: Table S3), it was possible to address how these sequences cluster in the PF299 supplier Phylogenetic tree constructed with a set of sequences including representatives of RCR plasmids from both Mollicutes and Firmicutes mafosfamide (Figure 6). A set of 62 amino acids sequence corresponding to the replication protein of 25 mycoplasma plasmids and of 37 representatives of the major RCR plasmid families, including those of the phytoplasma plasmids was selected for constructing

the phylogenetic tree. Phylogenetic analyses confirmed that, except for pMyBK1, all mycoplasma plasmids could be grouped within the pMV158 family (Figure 6). This result is consistent with the prediction, in these Rep sequences, of a Rep2 domain typical of this plasmid family. Yet, mycoplasma plasmids do not form a single, coherent group in this family but instead cluster into two distinct branches designated as groups 1 and 2. Rep proteins from groups 1 and 2 share only limited similarities and, the most divergent members in these groups are more distant between each other than they are from the streptococcal pMV158. Group 1 consists of highly similar proteins (identity ranging from 88 to 100%) and includes Rep proteins from Mmc and Mcc plasmids. Conversely, group 2 is more heterogeneous and includes Rep proteins from M. leachii, M. yeatsii, M. cottewii, Mmc and Mcc plasmids. Further phylogenetic analyses showed that group 2 could be split into two statistically-supported subgroups (2A and 2B).

Future studies are necessary to determine the optimal peri-operative treatment strategies for patients on anti-platelet agents and on thromboembolic prophylaxis when they undergo hip fracture surgery. Conflicts of interest Dr. Leung is the speaker for Synthes and has received research support

from Synthes. None of the other authors has a real or perceived conflict of interest or a disclosure of any personal this website or financial support. Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. References 1. Lu-Yao GL, Baron JA, Barrett JA, Fischer ES (1994) Treatment and survival among elderly Americans with hip fractures: a population-based study. Am J Public Health 84:1287CrossRefPubMed 2. Magaziner J, Simonsick EM, Kashner TM et al (1990) Predictors of functional recovery one year following hospital discharge for hip fracture: a prospective study. J Gerontol 45:M101PubMed 3. Magaziner J, Hawkes W, Hebel JR et al (2000)

Recovery from hip fracture in eight areas of function. J Gerontol A Biol Sci Med Sci 55A:M498–M507 4. Morris AH, Zuckerman JD (2002) National consensus conference on improving the continuum of care for patients with hip fracture. J Bone Joint Surg Am 84-A:670–674PubMed PLX3397 5. Morrison RS, Chassin MR, Siu AL (1998) The medical consultant’s role in caring for patients with hip fracture. Ann Intern Med 128:1010PubMed 6. Davis FM, Woolner DF, Frampton C et al (1987) Prospective, multi-centre trial of mortality following general or spinal anaesthesia for hip fracture surgery in the elderly. Br J Anaesth 59:1080CrossRefPubMed 7. Bredahl C, Nyholm B, Hindsholm KB et al (1992) Mortality after hip fracture: results of operation within 12 h of admission. Injury 23:83CrossRefPubMed 8. 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 39:261CrossRefPubMed 9. Bottle A, Aylin P (2006) Mortality associated with delay in operation after hip fracture: observational

study. BMJ 332:947CrossRefPubMed Loperamide 10. Shiga T, Wajima Z, Ohe Y (2008) Is operative delay associated with increased mortality of hip fracture patients? Systematic review, meta-analysis and meta-regression. Can J Anaesth 5:146 11. Anonymous (1994) Collaborative overview of Target Selective Inhibitor Library order randomized trials of anti-platelet therapy—III: reduction in venous thrombosis and pulmonary embolism by antiplatelet prophylaxis among surgical and medical patients. Antiplatelet Trialists’ Collaboration. BMJ 308:235 12. Merritt JC, Bhatt DL (2004) The efficacy and safety of perioperative antiplatelet therapy. J Thromb Thrombolysis 17:21–27CrossRefPubMed 13. Kaluza GL, Joseph J, Lee JR, Raizner ME, Raizner AE (2000) Catastrophic outcomes of noncardiac surgery soon after coronary stenting.

Moreover, the ORF 28 is homologous

to the ptmG gene of Campylobacter jejuni (Cj1324) which converts the CMP-Leg5Ac7Ac residue to CMP-5-acetamidino-7-acetamido-3,5,7,9-tetradeoxy-D-glycero-D-talo-nonulosonic acid (CMP-Leg5Am7Ac) [40], the dominant residue of the O-antigen of non-Sg1 strains of L. pneumophila[41]. A functional correlation of the ORFs of this region is supported by recent transcriptomic data of strain Paris in which the ORFs 21-17 and 28-22 were transcribed as operons [42]. Since all analyzed Sg1 strains and a broad number of non-Sg1 strains carry ORF 28 [35, 43, 44] it can be assumed that CMP-Leg5Am7Ac is a common residue of the L. pneumophila LPS Y-27632 supplier molecule which might subsequently become modified in a mAb-subgroup or even strain specific selleck products manner. Three clusters of the O-acetyltransferase Lag-1 A well ATM/ATR signaling pathway examined phenotype variation is linked to the presence and absence of the lag-1 gene. Lag-1 encodes for an O-acetyltransferase that conferred reactivity with mAb 3/1 and is exclusively found in Sg1 strains. Our results revealed three clusters of the lag-1 genes, although without any detectable relation to the mAb-subgroup switch which supports recent findings [45]

(Figure  2A). Lag-1 was previously reported to be involved in mAb-subgroup switches of different strains. However, this was generally due to gene deletion or loss-of-function mutations of lag-1[46–49]. Complete and functional lag-1 genes were present in all mAb 3/1+ strains and were absent in all mAb 3/1- Dynein strains. Besides that, the Philadelphia subgroup strains (Philadelphia 1 and Paris) as well as the Knoxville-subgroup strain Uppsala 3 carried a transposase and a partial duplication of ORF

2 adjacent to lag-1. Bernander et al. reported the region from ORF 2 to ORF 3 as unstable [46]. Looping out of the intermediate located lag-1 gene is assumed to be a potential consequence. Under in vitro conditions the deletion of the lag-1 gene occurred at with frequency of 10-6 to 10-7 (C. Lück, unpublished results). Detailed analysis of the region from ORF 2 to ORF 3 including lag-1 of these strains revealed remarkably high similarities of Uppsala 3 to the Philadelphia-subgroup strains Philadelphia 1 and Paris (>98-100%) whereas the remaining Knoxville-subgroup strains clustered in a different group (Table  3; Figure  2A). The high similarity of this 4 kb region between strain Uppsala 3 and the strains Paris and Philadelphia 1 may indicate horizontal gene transfer of this region. However, this had no impact on the specific mAb reactivity for all other analyzed Knoxville-subgroup strains. Horizontal gene transfer between strain Paris and Philadelphia 1 was recently reported for a large genome fragment which also harbored the LPS biosynthesis locus [32].

Additionally, the disfiguring scars caused by Leishmania keep patients hidden. An

estimated 1.5 million new cases of cutaneous leishmaniasis and 500,000 cases of visceral leishmaniasis occur annually, with approximately 12 million people currently infected [1]. Moreover, cases of Leishmania and human immunodeficiency virus co-infection are becoming more frequent [2, 3]. Leishmania (Leishmania) amazonensis infection results in diverse clinical manifestations, ranging from cutaneous to mucocutaneous or visceral involvement [4]. This is attributable to the genetic diversity of L. amazonensis strains, and this divergence extends to variations PFT�� solubility dmso of chromosome size [5]. The arsenal of drugs available for treating Leishmania infections is limited. The basic treatment consists of administering pentavalent antimonial compounds [6]. However, the choice

of medication depends Talazoparib on the species involved and type of clinical manifestation [7]. The usefulness of antileishmanial drugs has been limited by their toxicity, and treatment failure is often attributable to drug resistance [8]. To solve this problem, developing less toxic drugs and discovering cellular and molecular markers in parasites to identify the phenotype of chemoresistance against leishmanicidal drugs are necessary [8, 9]. These problems led to the development of additional antileishmanial drugs. Some drug-delivery systems, plants, and synthetic compounds are being developed as effective treatments for the disease [7]. Previous studies demonstrated the in vitro activity of parthenolide, a sesquiterpene lactone purified from Tanacetum parthenium, against promastigotes and intracellular Selleck GDC-0449 amastigotes (inside J774G8 macrophages) of L. amazonensis[10].

Moreover, significant Y-27632 2HCl alterations in promastigote forms were demonstrated by light microscopy and scanning and transmission electron microscopy [11]. We evaluated the activity of parthenolide against L. amazonensis axenic amastigotes and demonstrated a possible mechanism of action of this compound in this life stage of the parasite. Results Antileishmanial assays The addition of 4.0 μM parthenolide to the culture of axenic amastigotes induced growth arrest and partial cell lysis after 48 h (i.e., growth inhibition up to 90%). When the cells were treated with 2.0 μM parthenolide, the percentage of growth inhibition was approximately 70%. Parthenolide had an IC50 of 1.3 μM and IC90 of 3.3 μM after 72 h incubation (Figure 1A). Figure 1 Effects of parthenolide (A) and amphotericin B (B) on the growth of L. amazonensis axenic amastigotes. After treatment with different concentrations of the drugs, parasites were counted, and the percentage of parasite growth inhibition was determined daily for 120 h. The data indicate the average of the two independent experiments performed twice. Statistical analysis: the data of each incubation period were compared statistically at p < 0.05.

7 and 1.2 × 105, respectively. In contrast, the filled factor (FF) does not seem to depend on post-growth heat treatment. The chlorine doping of CdTe NGs and the related GB passivation following the CdCl2 heat treatment are thus beneficial for the photovoltaic properties. The best photovoltaic properties only result in a photo-conversion efficiency of about 0.01%: this is fairly low as compared to the photo-conversion efficiency of 4.74% for ZnO/CdSe [65], 4.15% for ZnO/CdS/CdSe [66], and 4.17% for ZnO/In2S3/CuInS2 NW arrays [67].

However, it has widely been reported that the photovoltaic properties of ZnO/CdTe core-shell NW arrays are poor [22, 24, 25, 27, 29, 32]. The low V OC may originate from the occurrence of cracks in the CuSCN thick layer acting as the hole-collecting layer, which could also increase the series resistance [32]. In contrast, the J SC depends, in addition to the incident spectral flux density, RG-7388 datasheet on the EQE, which is the MK5108 supplier number of collected charge carriers divided by the number of incident photons. The EQE for the annealed ZnO/CdTe core-shell NW arrays is about 2% above the bandgap energy of 1.5 eV for CdTe, as shown in Figure  8. Basically, the EQE is

equal to the internal quantum efficiency (IQE) multiplied by the light-harvesting efficiency. Still, the light-harvesting efficiency see more is fairly high in ZnO/CdTe core-shell NW arrays, as revealed in Figure  7a: the light-harvesting efficiency is typically larger than 90% at the energy of 2.36 eV (i.e., the wavelength of 525 nm at the maximum of the solar irradiance). This is in agreement with the systematic optical simulations of the ideal J SC by RCWA, which have emphasized the large

absorption capability of ZnO/CdTe core-shell NW arrays [20]. As a consequence, the low J SC and EQE arise from the poor IQE: this indicates that most of the photo-generated charge carriers in CdTe NGs is lost. The location where the charge carriers are photo-generated is given in Figure  7b, by the maps of the polychromatic radial optical generation rate. Interestingly, most of the charge carriers are actually photo-generated in the CdTe shell, owing to its bandgap energy of 1.5 eV in contrast to the wide bandgap energy of ZnO and CuSCN. A smaller proportion of PAK6 the incident light is still absorbed in the ZnO NWs, especially for lower wavelength. More importantly, the optical generation rate is significantly decreased from the bottom to the top of the ZnO/CdTe core-shell NW arrays, as shown in Figure  7b. The vast majority of charge carriers is even photo-generated at the extreme bottom of the ZnO/CdTe core-shell NW arrays inside the CdTe shell. It is expected that the main critical point for these solar cells is related to the collection of the photo-generated charge carriers. The absence of structural relationship (i.e.

Infect Immun 2002,70(6):2869–2876.CrossRefPubMed 43. Kjeldgaard M, Nissen P, Thirup S, Nyborg J: The crystal structure of elongation factor EF-Tu from Thermus aquaticus in the GTP conformation. Structure 1993,1(1):35–50.CrossRefPubMed 44. Pancholi V, Fischetti VA: A novel plasminogen/plasmin binding protein on PX-478 mw the surface of group A streptococci. Adv Exp Med Biol 1997, 418:597–599.PubMed 45. Wilkins JC, Beighton D, Homer KA: Effect of acidic pH on expression of surface-associated proteins of Streptococcus oralis. Appl Environ Microbiol 2003,69(9):5290–5296.CrossRefPubMed

46. Granato D, Bergonzelli GE, Pridmore RD, Marvin L, Rouvet M, Corthesy-Theulaz IE: Cell surface-associated elongation factor Tu mediates the attachment of Lactobacillus johnsonii NCC533 (La1) to human intestinal

cells and mucins. Infect Immun 2004,72(4):2160–2169.CrossRefPubMed 47. Jenkinson HF, Baker RA, Tannock GW: A binding-lipoprotein-dependent oligopeptide transport system in Streptococcus gordonii essential for uptake of hexa- and heptapeptides. J Bacteriol 1996,178(1):68–77.PubMed 48. Trivier D, Houdret N, Courcol RJ, Lamblin G, Roussel P, Davril M: The binding of surface proteins from Staphylococcus this website aureus to human bronchial mucins. Eur Respir J 1997,10(4):804–810.PubMed 49. Kessler RE, Yagi Y: Identification and partial characterization of a pheromone-induced adhesive Oxymatrine surface antigen of Streptococcus faecalis. J Bacteriol 1983,155(2):714–721.PubMed 50. Jenkinson HF, McNab R, Loach DM, Tannock GW: Lipoprotein receptors in oral streptococci. Dev Biol Stand 1995, 85:333–341.PubMed 51. Jenkinson HF, Terry SD, McNab R, Tannock GW: Inactivation of the gene encoding surface protein SspA in Streptococcus gordonii DL1 affects cell interactions with human salivary agglutinin and oral actinomyces. Infect Immun

1993,61(8):3199–3208.PubMed 52. Murray PA, Levine MJ, Tabak LA, Reddy MS: XL184 specificity of salivary-bacterial interactions: II. Evidence for a lectin on Streptococcus sanguis with specificity for a NeuAc alpha 2, 3Ga1 beta 1, 3Ga1NAc sequence. Biochem Biophys Res Commun 1982,106(2):390–396.CrossRefPubMed 53. Reddy MS, Levine MJ, Prakobphol A: Oligosaccharide structures of the low-molecular-weight salivary mucin from a normal individual and one with cystic fibrosis. J Dent Res 1985,64(1):33–36.CrossRefPubMed 54. Carnoy C, Scharfman A, Van Brussel E, Lamblin G, Ramphal R, Roussel P: Pseudomonas aeruginosa outer membrane adhesins for human respiratory mucus glycoproteins. Infect Immun 1994,62(5):1896–1900.PubMed Competing interests The authors declare that they have no competing interests.

This value ranged from 0 (no growth in the presence of antibiotic) to 1 (no inhibition by antibiotic), and was used in all subsequent analyses. It is desirable to reduce the AR readings over the time course to a single value characterizing the particular isolate. Therefore, all isolates were characterized by the smallest resistance value over the time course of growth. selleck products We tested all antibiotics at three concentrations, thereby producing three values of AR for each isolate. We presumed that the antibiotic concentration leading to the biggest variability in AR values between the isolates would be the most informative for characterizing

the resistance levels in the population. To evaluate the variability at different antibiotic concentrations, the pairwise differences in resistance values for all isolates were calculated and the values combined to give a sum total for each particular antibiotic concentration. The concentration with the biggest total was defined as the most informative and selected for further analysis. The informative concentrations were 100 μg mL-1 for ampicillin, 5 μg mL-1 for

chloramphenicol, 1 μg mL-1 for kanamycin, 0.5 μg mL-1 for norfloxacin, 5 μg mL-1 for tetracycline and 0.3 μg 4SC-202 price mL-1 for meropenem. Distribution of resistance We analyzed the prevalence of antibiotic resistance in the eight genera that were represented by more than 20 isolates each: Aeromonas with 57 isolates (represented by 3 Operational Taxonomic Units (OTU) as defined by the 16S rRNA sequence types), Pseudomonas

217 (7 OTUs), Stenotrophomonas 73 (5 OTUs), Chryseobacterium 86 (25 OTUs), Pedobacter 61 (7 OTUs), Flavobacterium 41 (11 OTUs), Microbacterium 37 (6 OTUs) and Brevundimonas oxyclozanide 23 (5 OTUs). The number of OTUs indicates that the actual species richness might be lower than can be estimated from the number of isolates. On the other hand, the similarity of the 16S rRNA sequences is not always a sensitive enough criterion to distinguish different species [38, 39]. In most cases, one OTU contains small number of isolates making it impossible to learn more analyze the data at OTU level. Therefore the subsequent analyses (Figure 2) were performed at the level of genus. Still, it is interesting to note that three major OTUs of Chrysobacterium had considerably different resistance patterns when compared between each other (Table 1). OTU “A”, containing 18 isolates is considerably more sensitive to ampicillin, meropenem (p value 10-5) and norfloxacin when compared to OTU “C”, containing 13 isolates. OTU “B”, containing 11 isolates was more sensitive to ampicillin, meropenem, norfloxacin and tetracycline when compared to OTU “C”. There were no significant differences between “A” and “B”. Figure 2 The average values of resistance coefficients in a specific genus as grouped by antibiotics (A) and genera (B). (A) The genera are organized by antibiotics tested.

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