CusF was identified in only five families and in 62% of them it c

CusF was identified in only five families and in 62% of them it co-localized with cusABC. However, the fact that in 22 organisms CusB and CusF were fused in a single gene do not compare with the role of CusF as a soluble carrier, a role that certainly deserves to be revised. In E. coli APEC 01 we identified a CusABC paralog, named SilABC which is plasmid borne and adjacent to PcoAB, with an apparent role in silver extrusion suggesting evolution by duplication and functional equivalence but metal-binding specialization. These analyses were performed with the aim to elucidate between Pevonedistat cell line two hypotheses for the concurrent evolution of well characterized

interacting protein sets in copper homeostasis: function dominance or protein-protein interaction dominance, The high presence correlation of CusABC support protein-protein interaction as the selection trait for the assembly with two caveats: CusC may still be functional in the absence TGF-beta cancer of CusAB (as happens in other RND groups, [43]). This idea is consistent with the fact that in a number of cases cusC was found to lie adjacent to genes encoding for RND complexes with other proposed specificities. Additionally it would be interesting to determine if the minimal set of an inner Captisol chemical structure membrane protein such CopA and a single outer membrane protein such as CusC

are sufficient for copper tolerance Sodium butyrate acquisition. In contrast, the low presence correlation between

PcoA/PcoC compared to the higher and unexpected correlation of PcoC with CueO may lead to observation that CueO functionally replaces PcoA on the interaction with PcoC. However, CueO and PcoA belong to the MCO structural family and, in spite of sharing low identity at the sequence level, their three dimensional structure is highly preserved as happens with the rest of the family members [44]. In both cases evidence support the protein-protein interaction hypothesis as the basic mechanisms for the evolution of the copper homeostasis systems supporting our theoretical treatment as metabolic networks [45]. Conclusions Our results suggest complex evolutionary dynamics and still unexplored interactions among different proteins to achieve copper homeostasis in gamma proteobacteria, challenging some of the molecular transport mechanism proposed for these systems. Methods Gamma proteobacterial genomes To carry out this analysis we analyzed 268 proteobacterial genomes available from the KEGG database (Release 56.0, October 1, 2010) [46, 47] (Aditional file 1). Protein sequences used as seeds for ortholog detection CopA from Escherichia coli K-12 MG1655 [KEGG:eco:b0484]; CueO from Escherichia coli O1:K1:H7 (APEC) [KEGG:ecv:APECO1_1862]; CueP from Salmonella enterica subsp.

3 2 [74] The number of clusters K was estimated by calculating t

3.2 [74]. The number of clusters K was estimated by calculating the ad hoc statistic ΔK[76]. ΔK was calculated for K = 1 through 10 using 5 Markov chains for each value of K. The simulations of Evanno et al. [76] showed that the highest value for ΔK reliably identified the optimum click here value of K. Chains were run for 500,000 steps following an initial

burn-in of 100,000 steps, using the admixture ancestry and correlated allele frequency models. Once the optimum value of K was identified, strains were assigned to clusters using assignment coefficients (proportion of cluster membership) generated from an additional run utilizing the RAD001 order linkage ancestry and correlated allele frequency models. A study of recombinant bacterial populations showed the linkage model of ancestry to produce the most accurate assignment scores in situations where there are multiple linked loci along contiguous sections of DNA [75]. The model assumes these sections, which could be recombinant, to be discrete units of inheritance. Markov chains were run see more for 2,000,000 steps following an initial burn-in of 500,000 steps. Acknowledgements We would like to thank staff from Cornell

University’s Quality Milk Production Services and Animal Health Diagnostic Centre for their contribution to sample and isolate collection. This study made use of PathogenTracker 2.0 ( http://​www.​microbtracker.​net), developed by Martin Wiedmann. This work was supported by the National Institute of Allergy and Infectious Disease, U.S.

National Institutes of Health, under Grant No. AI073368 awarded to M.J.S. Electronic supplementary material Additional file 1: Streptococcus RefSeq genome summary statistics. (DOC 102 KB) Additional file 2: S. canis annotation. (XLS 540 KB) Additional file 3: Additional Streptococcus genomes. (XLS 30 KB) Additional file 4: Insertion sites of putative integrative plasmid. (DOC 58 KB) Additional file 5: S. canis isolate MLST allele data. (DOC 87 KB) Additional file 6: Ln P(D) scores for Structure analysis. (DOC 206 Farnesyltransferase KB) Additional file 7: MLST PCR primer details. (DOC 118 KB) Additional file 8: Putative integrative plasmid PCR primer details. (XLS 24 KB) References 1. Devriese LA, Hommez J, Kilpper-Balz R, Schleifer KH: Streptococcus canis sp. nov.: a species of group G streptococci from animals. Int J Syst Bacteriol 1986,36(3):422–425.CrossRef 2. Vandamme P, Pot B, Falsen E, Kersters K, Devriese LA: Taxonomic study of Lancefield streptococcal groups C, G, and L ( Streptococcus dysgalactiae ) and proposal of S. dysgalactiae subsp. equisimilis subsp. nov. Int J Syst Bacteriol 1996,46(3):774–781.PubMedCrossRef 3. Murase T, Morita T, Sunagawa Y, Sawada M, Shimada A, Sato K, Hikasa Y: Isolation of Streptococcus canis from a Japanese raccoon dog with fibrinous pleuropneumonia. Vet Rec 2003,153(15):471–472.PubMedCrossRef 4.

Acta oncologica (Stockholm, Sweden) 2007, 46:975–981 CrossRef 6

Acta oncologica (Stockholm, Sweden) 2007, 46:975–981.CrossRef 6. Bilchik A, Nissan A, Wainberg Z, Shen P, McCarter M, Protic M, Howard R, Elashoff D, Tyler J, Peoples GE, et al.: Surgical quality

and nodal ultrastaging is associated with long-term disease-free survival in early colorectal cancer: an analysis of 2 international multicenter prospective trials. Ann Surg 252:467–474. discussion 474–466 7. Orntoft TF: [DNA check details microarrays (DNA chips) used in molecular medical research]. Ugeskr Laeger 2003, 165:786–790.PubMed 8. Anjomshoaa A, Nasri S, Humar B, McCall JL, Chatterjee A, Yoon HS, McNoe L, Black MA, Reeve AE: Slow proliferation as a biological feature of colorectal cancer metastasis. Br J Cancer 2009, 101:822–828.PubMedCrossRef 9. Dunn GP, Koebel CM, Schreiber RD: Interferons, immunity and cancer immunoediting. Nat Rev Immunol 2006, 6:836–848.PubMedCrossRef 10. Pages F, Berger A, Camus M, Sanchez-Cabo F, Costes A, Molidor R, Mlecnik B, Kirilovsky A, Nilsson M, learn more Damotte D, et al.: Effector memory T cells, early metastasis, and survival in colorectal cancer. N Engl J Med 2005, 353:2654–2666.PubMedCrossRef 11. Naito Y, Saito K, Shiiba K, Ohuchi A, Saigenji K, Nagura H, Ohtani H: CD8+ T cells infiltrated within cancer

cell nests as a prognostic factor in human colorectal cancer. Cancer Res 1998, 58:3491–3494.PubMed 12. Galon J, Costes A, Sanchez-Cabo F, Kirilovsky A, Mlecnik B, Lagorce-Pages C, Tosolini M, Camus M, Berger A, Wind P, et al.: Type, density, and location of immune cells within human colorectal tumors predict clinical outcome. Science 2006, 313:1960–1964.PubMedCrossRef 13. Lin YH, Friederichs Masitinib (AB1010) J, Black MA, Mages J, Rosenberg R, Guilford PJ, Phillips V, Thompson-Fawcett M, Kasabov

N, Toro T, et al.: Multiple gene expression classifiers from different array platforms predict poor prognosis of colorectal cancer. Clin Cancer Res 2007, 13:498–507.PubMedCrossRef 14. Ling KL, Pratap SE, Bates GJ, Singh B, Mortensen NJ, George BD, Warren BF, Piris J, Roncador G, Fox SB, et al.: Increased frequency of regulatory T cells in peripheral blood and tumour infiltrating lymphocytes in colorectal cancer patients. Cancer Immun 2007, 7:7.PubMed 15. Clarke SL, Betts GJ, Plant A, Wright KL, El-Shanawany TM, Harrop R, Torkington J, Rees BI, Williams GT, Gallimore AM, et al.: CD4+CD25+FOXP3+ regulatory T cells suppress anti-tumor immune responses in Selleck SN-38 patients with colorectal cancer. PLoS ONE 2006, 1:e129.PubMedCrossRef 16. Yaqub S, Henjum K, Mahic M, Jahnsen FL, Aandahl EM, Bjornbeth BA, Tasken K: Regulatory T cells in colorectal cancer patients suppress anti-tumor immune activity in a COX-2 dependent manner. Cancer Immunol Immunother 2008, 57:813–821.PubMedCrossRef 17. Frey DM, Droeser RA, Viehl CT, Zlobec I, Lugli A, Zingg U, Oertli D, Kettelhack C, Terracciano L, Tornillo L: High frequency of tumor-infiltrating FOXP3(+) regulatory T cells predicts improved survival in mismatch repair-proficient colorectal cancer patients.

2 V bias with 10 ms duration The mean value of current is 89 29 

2 V bias with 10 ms duration. The mean value of current is 89.29 μA with the standard deviation of 0.155. The current ratio of low-resistance to high-resistance state in this device is about 22.85 (which varied in 20 to 40 range for various

devices). Besides the high retention time, the device also shows good endurance when continuous reading cycles with small pulse duration is applied. The retention characteristics are extrapolated to 104 s, and a stable behavior is foreseen in both states of the device. Figure 3 Retention characteristics. The memory device shows a stable low-resistance state with for 103 s (blue line). Tariquidar research buy After switching to the high-resistance state by applying a 1.2-V write pulse of 10 ms duration, stable current is observed again. The dashed lines are the interpolation to 104 s (red line). For the control sample without the BLG contact, the device shows higher conduction with random switching, hysteresis, and significant variation from device to device. We attribute this irregular behavior in our control sample to the atomically rough interface between Ni and C60, as well as the electromigration of Ni atoms across C60/Ni interface. The switching mechanism in the reported WORM memory device with the BLG contact is not clearly understood yet. However, we hypothesize

selleckchem that BLG prevents the electromigration of Ni atoms into C60 film, thus stabilizing the device behavior. The transport characteristics do not show ohmic or space-charge-limited conduction. Similar devices using C60 molecules have been reported to have rewritable switching characteristics – quite different from our observation [19, 20]. click here Moreover, multilayer graphene electrodes used in devices with PI:PCBM composite as active material have also been recently reported to have mafosfamide WORM memory behavior, whereas with the metallic electrodes, rewritable switching characteristics have been

reported [21]. Although the channel materials are different in the two experiments, the connection between the use of graphene and WORM features is noteworthy and needs to be explored further. Carbon nanotube-based contact [22] has also been explored to eliminate electromigration, however, we believe that graphene nanomembrane provides a better interface due to its 2D nature. Conclusions We have fabricated a molecular memory device with atomically smooth BLG contacts. Covering Ni film with BLG shields the channel from metal surface irregularities and also prevents the electromigration of Ni atoms into the C60 film. The device switches from a low-resistance to a high-resistance state, followed by hysteresis in the first sweep cycle. In the subsequent sweep cycles, the device remains in the high-resistance state and no hysteresis is observed, thus showing WORM memory behavior. The switching voltages vary in 0.8 to 1.2 V bias range for various devices with the high-resistance to low-resistance ratio in 20 to 40 range.

The need for subsequent anti-platelet therapy following stent pla

The need for subsequent anti-platelet therapy following stent placement to assure patency limits the utility of these approaches in the multiply injured blunt trauma patient. Some of these patients are already coagulopathic and the addition of these agents can destabilize clots in solid organs leading to life-threatening hemorrhage, or propagate an intracerebral hemorrhage

with grave clinical click here consequences. In our patient the LDN-193189 price decision to proceed to coronary bypass was likely due to two factors. Most importantly, the dissection involved the left main coronary artery, which is preferentially treated surgically [23]. Secondly, our patient had a contraindication to percutaneous techniques because of his risk of bleeding. Our approach is supported by a number of successful cases already reported. Korach, Smayra, and Boland all report cases of motor vehicle collisions with resultant LAD coronary dissection that were successfully treated with surgical revascularization [9, 10, 13]. Harada had a similar success story, Ilomastat in vivo but the dissection was the left main coronary artery [8].

Redondo reported a mortality in the case of a 45 year-old female diagnosed with a left coronary artery dissection after a motor vehicle collision [11]. Attempts to treat with angioplasty and heparinization were complicated by fatal intra-abdominal hemorrhage. Coronary dissection after blunt chest trauma has been successfully treated with a more conservative approach. Hobelmann reported the case of a 32 year-old male who suffered an RCA dissection after

being elbowed in the chest during basketball [6]. The lesion was successfully treated with eptifibitide, heparin and stents. A focal right coronary artery lesion can be successfully stented, similar to the treatment of lesions in coronary artery disease [23]. Also, the risk of bleeding associated with the use of anticoagulation and anti-platelet agents was lower due to the isolated nature of the trauma. Hazeleger reported an LAD dissection 2 months after a tackle in football which was successfully treated with a stent [5]. Once again, left anterior descending artery lesions respond Vitamin B12 well to stent placement [23]. Also, the time interval from injury to diagnosis significantly reduces the risk of bleeding from anticoagulation necessary when stents are utilized. Conclusions Blunt thoracic injury is commonly encountered in a trauma center, and a small fraction of those patients will present with blunt cardiac injuries. The goal of evaluation should be identifying patients with clinically relevant complications related to the cardiac injury and providing the appropriate level of care to meet patients’ needs. We present a review of the diagnostic tools for evaluating blunt cardiac injury.

All cell lines were grown as monolayers of up to 80% confluence i

All cell lines were grown as monolayers of up to 80% confluence in RPMI 1640 supplemented with 10% FBS and 1% Penicillin/Streptomycin at 37°C, 5% GW3965 in vitro CO2 and humidified air. Growth inhibition experiments To assess antiproliferative effects, the total protein sulforhodamine B (SRB) assay was used as described previously [15]. In brief, cells were seeded in 96 well plates at a cell line specific density to ensure exponential growth throughout the whole period of the assay. These cell numbers were determined previously by cell growth kinetics. After 24 h, exponentially growing cells were exposed to serial dilutions

of each drug alone or drug combinations for the indicated times continuously. To investigate the influence of drug schedules drug A was added 24 h after cell seeding followed by drug B another 24 h later or vice versa. Corresponding control plates with single agents were treated in parallel. After 120 h total assay time, media was removed and cells were fixed with 10% TCA and processed according to the published SRB assay protocol [15]. Absorbency was measured at 570 nm using a 96-well plate reader (Rainbow, SLT, Germany). DNA gel electrophoresis To detect apoptosis by DNA gel electrophoresis the

floating cells after drug treatment with an IC90 of FWGE for 48 h were used. After washing cells twice with PBS they were lysed in lysis-buffer (100 mM TRIS-HCL (pH8.0), 20 mM EDTA, 0,8% SDS). Subsequent to treatment with RNaseA for 2 h at 37°C and proteinase K (Roche Molecular Biochemicals) overnight at 50°C, lysastes were mixed with DNA loading buffer. To separate DNA fragments, probes were run on a 1.5% agarose

gel followed by ethidium bromide staining and rinsing with destilled water. DNA ladders were visualized under UV light and 2-hydroxyphytanoyl-CoA lyase documented on a BioDocAnalyse instrument (Biometra). Data analysis Dose response curves were generated by Sigma Plot (Jandel check details Scientific, San Rafael, CA) and IC50 values were calculated based on the Hill equation. Drug interaction was assessed using the model of Drewinko [16]. In brief, a hypothetical curve was calculated by multiplying the ratio of treated and untreated control with the dose response data points of the single drug curve. Synergy could be assumed if the hypothetical curve runs above the combination curve and antagonism is indicated if the hypothetical curve runs below the combination curve. In case of additivity both curve were superimposed. Statistical significance was probed with the two tailed, unpaired student’s t-test. Significance was assumed at a p-value < 0.05.

Following treatment withdrawal, results obtained were in agreemen

Following Luminespib treatment withdrawal, results obtained were in agreement with this dual mode of action as they show a significant decrease in bALP and an increase in sCTX. These changes are already observed 3 months after click here treatment discontinuation, suggesting a relatively rapid release of strontium from bone. In the present analysis, patients who continued on strontium ranelate in the main treatment period and in the treatment-switch period showed a progressive increase in BMD throughout the entire 5-year period. The increase in lumbar BMD from M48 to end in the SR/SR group (1.2 ± 5.8%) is clinically significantly smaller

than in the placebo/SR group (5.3 ± 7.3%). Increase of bone density with strontium ranelate may be due to different effects: increase in bone mass, increase in the degree of mineralization,

or artifactual increase of BMD due to the presence of strontium in bone. Studies on bone biopsies have demonstrated that the degree of mineralization is not modified compared to placebo after selleck kinase inhibitor 3 years of treatment [38]. Regarding the bone strontium content, it has been demonstrated that bone strontium content reached a plateau after 3 years of treatment [39]. This plateau might explain at least partly the smaller increase in BMD after 4 years of treatment compared to the first year of treatment and suggested that strontium ranelate continue to increase bone mass despite the plateau observed in bone strontium content. Furthermore, a strong relationship between the increase in BMD and a subsequent reduction of the risk to have a new vertebral or hip fracture have been demonstrated in strontium ranelate-treated patients indicating that BMD may be of interest to monitor those patients for 3 years [40, 41]. After treatment withdrawal,

patients who switched to placebo IKBKE at 4 years experienced a significant reduction in BMD, showing effects of strontium ranelate to be progressively reversible and reflecting clearance of strontium from bone. Decrease observed after treatment cessation is also suggesting that BMD may be followed up after a treatment with strontium ranelate. After 3 years, strontium ranelate treatment was associated with significant beneficial effect on QoL, relative to placebo, assessed by QUALIOST®, a validated disease-targeted QoL instrument [24, 25, 42]. These results are confirmed after 4 years of treatment: Both the emotional and physical components of the global QUALIOST® score were improved in comparison to placebo (p = 0.012 and p = 0.034, respectively).

Nevertheless they have to be interpreted with caution and within

Nevertheless they have to be interpreted with caution and within their context. The strongest and most consistent results from VAE in Belnacasan clinical studies concern QoL and improved tolerability of conventional AZD6738 in vitro treatment. QoL questionnaires included mostly well established and

validated QoL instruments and one on psychosomatic self-regulation. The latter is a 16 item QoL instrument that measures competence and autonomy, in terms of the ability to actively adapt to stressful life situations and to restore well-being. [136] This tool has so far been exclusively used in studies focusing on complementary cancer treatments. Improvement was seen especially in relation to self-regulation, fatigue, MCC950 cell line sleep, nausea/vomiting, appetite, diarrhoea, energy, ability to work, enjoyment of life, depression, anxiety, pain, and general physical, emotional, and functional well-being (for more details see Kienle GS, Kiene H: Influence of mistletoe treatment on quality of life in cancer patients. A systematic review of controlled clinical studies. Submitted). Regarding the side effects of conventional oncology treatments, reduced hematopoetic

damage (i.e. leukopenia) and immuno-suppression was reported by some, but not by all studies. Similar, less chemotherapy-related events were observed in some but not in all studies. Validity of this evidence is quite good. 15 RCTs are available, four of them double-blinded (three of them showing a positive result) and one with an active control treatment. 5 RCTs reported following ICH-GCP guidelines and three of them comprised more

than 200 patients each. Questions remain regarding observation or reporting bias, which is of major importance in relation to subjectively assessed outcomes such as QoL and subjective symptoms. Treatment should therefore be blinded; but blinded subcutaneous VAE application can easily be correctly identified by doctors and patients [55, 137], due to its local reactions and mild flu-like symptoms. In the four blinded trials reviewed here, a considerable degree of unblinding was detected by asking patients and physicians Tyrosine-protein kinase BLK in one study [55]; and can be presumed in two other of these trials where substantially more VAE-treated patients reported local reactions than control patients [54, 57]. Other RCTs did not blind treatment application, as blinding is unreliable. Therefore questions will remain in “”blinded”" as well as in open trials even though in general cancer or non-cancer trials could not detect relevant improvements of QoL or disease symptoms due to suggestive administration of inert substances [138–140]. Nevertheless, the frequency, magnitude, duration and conditions of QoL or symptomatic improvement in the course of VAE treatment should be clarified in more detail.

tularensis strain SCHU S4 b Primer sequence of primer Tuf1705 in

tularensis strain SCHU S4. b Primer sequence of primer Tuf1705 in marker 20-ISFtu2 and TUL-435 in marker 22-lpnA seem to be incorrectly specified Lazertinib clinical trial in [56]. See [37] and [59] for the correct primer sequences. c Insertion element present in multiple copies in reference. Only first position and gene specified. Figure 1 Overview of primer specificity. Weighted score of primer specificity calculated with penalties

for mismatches and gaps, where zero indicates a perfect match. The first column of each marker represents the forward primer score and the second represents the reverse primer score. The score was calculated with PrimerProspector as follows: 3’ mismatch, 1 penalty per mismatch (length of 3’ region was set to 5), non-3’ mismatch, (0.4 penalty per mismatch), last base mismatch (penalty 3 per mismatch), non 3’ gap (penalty 1 per gap) and 3’ gap (penalty 3 per gap). The primer

specificities of the 38 DNA markers were calculated, resulting in scores ranging from 0 to 7.2 (Figure 1). Importantly, the calculation was performed for check details Francisella species besides those included in the publication from which the marker originated. A primer score of zero represented a perfect match without any mispriming events or gaps, while the maximal score of 7.2 corresponded buy Selinexor to two mismatches in the 3’ region and a gap of 10 bases within the region targeted by a primer (see marker 21-ISFtu2). All primer scores are presented in Figure 1 and summarised in Table 2. The limit for possible amplification Histone demethylase was assumed to be a score value of two, in agreement with the NCBI Primer-BLAST default primer specificity stringency setting. Scores below two (<2) are denoted as low score and score above two (≥2) are denoted as high score [30]. Evaluation of DNA markers The marker 01-16S [14] targeting 16S rRNA was the only marker with a low score (<1) for all the investigated genomes. A total of nine markers (01-16S, 03-16S-Itr-23S, 04-16S-Itr-23S,

08-fabH, 18-groEL 23-lpnA, 25-mdh, 30-prfb and 35-tpiA) had scores < 2 in all subspecies. However, some of these markers, e.g. 23-lpnA, showed a clear difference in scores between clade 1 and clade 2, as clade 1 yielded almost perfect matches, while scores in clade 2 were always > 1. Most of the included primers amplified sequences of F. tularensis (including subspecies tularensis, mediasiatica, and holarctica) and F. novicida of clade 1 and less frequently amplified sequences of F. noatunensis and F. philomiragia, of clade 2. Fifteen markers (05-aroA, 07-dnaA, 11-fopA-in, 12-fopA-out, 13-fopA, 14-FtM19, 15-FtM19, 19-iglC, 22-lpnA, 26-mutS, 27-parC, 31-putA, 36-tpiA, 37-trpE and 38-uup) gave low scores for clade 1 and high scores for clade 2. Marker 38-uup also had low scores in one isolate of philomiragia, and the marker 19-iglC had low scores in F. noatunensis subsp. orientalis and in two isolates of F. philomiragia.

Res Microbiol 1991, 142:541–549 PubMedCrossRef 26 Huff WE, Huff

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jejuni and Campylobacter coli bacteriophages. Lett Appl Microbiol 1989, 8:5–7.CrossRef 29. Connerton PL, Loc Carrillo CM, Swift C, Dillon E, Scott A, Rees CE, Dodd CE, Frost J, Connerton IF: Longitudinal study of Campylobacter

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of Campylobacter jejuni and Campylobacter Nutlin-3 mw coli colonizing broiler chickens. J Food Prot 2009, 72:733–740.PubMed 34. Loc Carrillo CM, Connerton PL, Pearson T, Connerton IF: Free-range layer chickens as a source of Campylobacter bacteriophage. Antonie Van Leeuwenhoek 2007, 92:275–284.PubMedCrossRef 35. Carvalho C, Susano M, Fernandes E, Santos S, Gannon B, Nicolau A, Gibbs P, Teixeira P, Azeredo J: Method for bacteriophage isolation against target Campylobacter strains. Lett Appl Microbiol 2009, 50:192–197.PubMedCrossRef 36. Atterbury RJ, Connerton PL, Dodd CE, Rees CE, Connerton IF: Application of host-specific bacteriophages to the surface of chicken skin leads to a reduction in recovery of Campylobacter jejuni. Appl Environ Microbiol 2003, 69:6302–6306.PubMedCrossRef 37. Lavigne R, Darius P, Summer E, Seto D, Mahadevan P, Nilsson A, Ackermann H, Kropinski A: Classification of Myoviridae bacteriophages using protein sequence similarity. BMC Microbiol 2009, 9:224.PubMedCrossRef 38. Rosenquist H, Sommer HM, Nielsen NL, Christensen BB: The effect of slaughter operations on the contamination of chicken carcasses with thermotolerant Campylobacter. Int J Food Microbiol 2006, 108:226–232.PubMedCrossRef 39.