In this group of recruits,

we selleck chemical found considerable dietary deficiency. First, despite the high selleck inhibitor energy needs during this period of training, the recruits consumed only 70% of the energy recommendations of the NSOR, with the NSF group reporting an 8.4% decrease in their BT total energy intake compared with the pre-induction total energy intake. This low intake may be explained by the presence of fundamental stressors in the military environment, such as periodic food restrictions, sleep deprivation, mental burden, and constant physical evaluations. These findings are in accordance with previous studies pointing to the fact that military personnel normally consume insufficient energy, whether or not they are provided with an adequate amount of food [33]. In this study, the deficient energy intake was not associated with a weight loss

but rather an increase of body weight during BT by 1.5%. This is also in line with previous studies, specifically that in this training program the gained weight was in lean body mass and not in fat [34]. We are concerned that our participants did not meet MDRI requirements. These deficiencies were observed for nearly every nutrient evaluated in the FFQ. The highest deficiencies were for vitamin D and calcium in the SF group, both around 60% of the MDRI before induction and click here also during BT. Of note, among the NSF group, vitamin D intake was the second most deficient variable, reported to be consumed at a level of 78.7% from MDRI before induction and at even a lower level of 59.6% during BT. In our

study, the SF recruits reported 41.0% less initial calcium and vitamin D intakes on induction day than the MDRI recommendations. Although vitamin D3 (cholecalciferol) is either formed in the skin after exposure to sunlight or obtained from nutritional sources, especially fatty fish [32], most IDF soldiers use Smoothened sunscreen and wear long-sleeved clothing during military training. This may limit vitamin D3 synthesis, and therefore, the importance of balanced nutritional intake, especially of vitamin D and calcium, should be emphasized, even though we did not actually find low serum levels of vitamin D. Release of PTH is controlled by the level of calcium in the blood, with low blood calcium levels causing an increase in PTH. The main purpose of this hormone is calcium homeostasis. It is therefore not surprising that in these healthy young recruits, we did not find any pathological PTH or calcium values. A slight trend towards higher levels of PTH in the 4-month BT may represent a lack of dietary calcium. However PTH differences between SF and NSF or between induction values and 4 or 6 month values were not significant.

Also, due to the relatively large size of DWCNTs (approximately 2.0-nm i.d.) AZD1152 supplier compared to single-walled CNTs (SWCNTs, 1.4 nm), the rectification of small ion pairs (i.e., KCl) was not seen, as was for the case of SWCNTs [42]. However, larger mobile anions such as ferricyanide, 2,6-naphthalenedisulfonic acid (NDS), and benzenesulfonate showed rectification (Table 1). The ionic current of potassium ferricyanide vs. transmembrane bias for as-made and modified DWCNT membranes is shown in Figure 6, with a summary of rectification factors in Table 2. The highest observed experimental rectification factor of ferricyanide was

14.4 for single-step grafting, which was 3.7 times as that of as-made membrane. Everolimus in vivo The rectification factor dropped with increasing ionic concentration, which was expected for the screening of charge on the gatekeepers at high ionic strength. The rectification factor dropped to 9.8 when the ferricyanide concentration increased from 10 to 50 mM. With the concentration increasing up to 100 mM, the rectification factor further dropped to 8.0. It seemed that rectification

was attributed to both charge and steric effects at low concentration. The steric effect was dominant at the high-concentration region. Table 1 Summary of ionic rectification factor on single-step modified DWCNT-dye membrane Concentration Rectification factor (mM) Potassium ferricyanide NDS Sodium benzenesulfonate 10 7.2 ± 0.3 3.1 ± 0.3 2.4 ± 0.2 50 6.4 ± 1 2.0 ± 0.1 Rapamycin concentration 2.0 ± 0.1 100 5.6 ± 1 2.3 ± 0.1 1.7 ± 0.1 Rectification factor was calculated by the ratio of ionic transport current at ±0.6-V bias. Linear scan was from −0.60 to +0.60 V with the scan rate at 50 mV/s. Figure 6 Ionic rectification curves click here on (A) as-made and (B) modified DWCNT membranes with potassium ferricyanide. Table 2 Comparison of ionic current rectification factor in K 3 Fe(CN) 6 solution Concentration of K3Fe (CN)6 Rectification factor (mM) As-made Single-step electrooxidation

of amine Electrochemical grafting of diazonium and coupling of dye Chemical grafting of diazonium and coupling of dye 10 3.9 ± 0.8 14.4 ± 0.6 2.9 ± 0.2 4.0 ± 0.4 50 4.4 ± 0.9 9.8 ± 0.3 2.9 ± 0.2 3.3 ± 0.07 100 3.4 ± 0.1 8.0 ± 0.4 3.2 ± 0.3 3.6 ± 0.2 Rectification factor was calculated by the ratio of ionic transport current at ±0.6-V bias. Linear scan was from −0.60 to + 0.60 V with the scan rate at 50 mV/s. On another modified membrane with one-step amine grafting, we compared the rectification factor of three different ions, namely ferricyanide, NDS, and sodium benzenesulfonate, to examine the role of anion size in being repelled by the modification of CNT tips. In Table 1, we saw that as the ion size was reduced, smaller rectification factors were seen, which were consistent with those of partially blocked ion channels. Similar to Table 2, as ionic strength was increased, the rectification factor decreased for all of the anions. It indicated that the rectification was partially attributed to the charge effect.

It remain has many factors influence the experimentation to cause the false positive results. Moreover, 85 patients were certainly few and follow-up time was short to be able to conclude firmly on any of the findings in our study, particularly using multivariate analysis. However, because of patients with negative expression of these genes indeed receive more benefit from platinum based chemotherapy in our study, the

combined detection of the mRNA expression of these genes might better individualize the efficacy of chemotherapy and improve survival in this common and vital cancer. Funding This research was supported by Guangxi Scientific research and technology development projects (Grant No. 10124001A-44) Acknowledgements This research was supported by Guangxi Scientific Lorlatinib price research and technology development projects (Grant No. 10124001A-44). Thanks for data sorting and processing by Guang-Yao Ma and Man-Hong Li. References 1. Chen W, Zhang S, Zou X: Evaluation on the incidence, mortality and tendency of lung cancer in China. Thoracic Cancer 2010, 1:35–40.CrossRef 2. Olaussen KA, Dunant A, Fouret P, Brambilla E, Andre F, Haddad V, Taranchon E, Filipits M, Pirker R, Popper HH, et al.: DNA repair by ERCC1 in non-small-cell lung cancer and cisplatin-based adjuvant chemotherapy. N Engl J Med 2006, 355:983–991.PubMedCrossRef buy CHIR98014 3. Takayama S, Sato T, Krajewski S, Kochel K,

Irie S, Milian JA, Reed JC: Cloning and functional analysis of BAG-1: A novel Bcl-2-binding protein with anti-cell death activity. Cell 1995, 80:279–284.PubMedCrossRef 4. Krajewska M, Turner BC, Shabaik A, Krajewski S, Reed JC: Expression of BAG-1 protein correlates with aggressive behavior

of prostate cancers. Prostate 2006, 66:801–810.PubMedCrossRef 5. Liu H, Liang Y, Li Y, Wang J, Wu H, Wang Y, Tang SC, Chen J, Zhou Q: Gene silencing of BAG-1 modulates apoptotic genes and sensitizes lung cancer cell lines to cisplatin-induced apoptosis. Cancer Biol Ther 2010, 9:832–840.PubMedCrossRef 6. Kennedy RD, Quinn JE, https://www.selleckchem.com/products/rocilinostat-acy-1215.html Johnston PG, Harkin DP: BRCA1: mechanisms of inactivation and implications for management of selleck inhibitor patients. Lancet 2002, 360:1007–1014.PubMedCrossRef 7. Bepler G, Gautam A, McIntyre LM, Beck AF, Chervinsky DS, Kim YC, Pitterle DM, Hyland A: Prognostic significance of molecular genetic aberrations on chromosome segment 11p15.5 in non-small-cell lung cancer. J Clin Oncol 2002, 20:1353–1360.PubMedCrossRef 8. Bepler G, Kusmartseva I, Sharma S, Gautam A, Cantor A, Sharma A, Simon G: RRM1 modulated in vitro and in vivo efficacy of gemcitabine and platinum in non-small-cell lung cancer. J Clin Oncol 2006, 24:4731–4737.PubMedCrossRef 9. Dumontet C, Isaac S, Souquet PJ, Bejui-Thivolet F, Pacheco Y, Peloux N, Frankfurter A, Luduena R, Perol M: Expression of class III beta tubulin in non-small cell lung cancer is correlated with resistance to taxane chemotherapy.

Three isolates were negative for one of the genes, two isolates negative for vcsC2 and one isolate negative for vcsV2. The primer binding regions in the genes of these isolates may be divergent leading to non-amplification, but it is also possible that the genes are deleted. It seemed that the pathogenicity of the majority of the isolates was due to the presence of the T3SS since 35 isolates possessed one or both T3SS genes (87.5%),which is different from that reported in Bangladesh (38.9%) [45] and in India (31.5%) [16]. The varying presence of virulence factors among different

non-O1/non-O139 strains may be associated with their ability S63845 mw to cause disease. Further studies are warranted. Conclusion Our study is the first

report which showed that non-O1/non-O139 V. cholerae was an important pathogen in China, selleck products causing diarrhoeal infections with an isolation rate of 1.2%. MLST revealed that a single ST, ST80, was predominant in Zhejiang Province. ST80 persisted over several years and appeared in different cities. It caused two outbreaks in recent years. Since the majority of the isolates were positive for T3SS but negative for any other virulence factors tested, the T3SS was likely to be the key virulence factor for these isolates. Resistance to commonly used antibiotics limits Doramapimod in vitro choice of drugs for treating non-O1/non-O139 V. cholerae infections. Our study highlights that non-O1/non-O139 V. all cholerae has been neglected as an important cause of diarrhoea in China and may be the same in other developing countries. Close monitoring of non-O1/non-O139 V. cholerae capable of causing outbreaks in China is necessary

to reduce the health burden of diarrhoeal infections caused by this pathogen. Methods Bacterial isolates Faecal samples from sporadic and outbreak cases were collected by local hospitals as part of standard patients care over a five year period from diarrhoeal patients at local hospitals in Zhejiang Province, China, and were sent to Zhejiang Provincial CDC laboratory for isolation of V. cholerae. Potential V. cholerae isolates from the faecal samples were grown onto No. 4 Agar (1% sodium citrate, 0.5% pig gall powder, 0.003% rivano powder, 0.2% sodium sulphite, 0.1% sodium lauryl sulphate, 0.001% potassium tellurite, and 500 μg/L gentamicin). All retrieved isolates were serologically tested for agglutination of O1 or O139 antisera (Denka Seiken, Japan) and all were shown to be negative. V. cholerae isolates were also obtained from an active surveillance program of enteric bacterial pathogens which was coordinated by Zhejiang Provincial CDC and was conducted in two Provincial hospitals in Hangzhou between May and December in 2010. Faecal specimens were obtained with written informed consent of the patients and with the approval of the Zhejiang Provincial CDC ethics committee, according to the medical research regulations of Ministry of Health, China.

The dotted horizontal line learn more represents the cut-off value for adherence. The dashed vertical line indicates the separation of the biofilm formation assay. vs: versus, ***P < 0.0001, **P < 0.001, black dot: isolate AC 7070, black triangle: isolate AC 1181. The analysis of biofilm formation demonstrated that all strains have the

capability to adhere to polystyrene surfaces and form biofilms (Fig. 4). Isolates 10672, AC1135 and strain DSM 16831 revealed the highest biofilm formation; remarkably, strain DSM 16831 had no capacity to invade cells. Correlation analysis of adherence to or invasion of endothelial cells and biofilm formation revealed no correlation. Additionally, no correlation was found between adherence to different ECM proteins and biofilm formation. Discussion and Conclusions S. gallolyticus click here is an important pathogen with an underestimated relevance causing IE. The frequent changes in the taxonomy resulted in an inadequate or incorrect identification of the causative pathogens, because non-experts were often not aware of the new nomenclature (e.g. [42]). In contrast to Tozasertib other streptococci, little is known about virulence factors and pathogenesis. The adherence of circulating bacteria to damaged heart tissues and subsequent colonization and persistence of bacteria are the crucial factors in streptococcal IE. The prevention of tissue colonization, with special

attention to targeting therapy against ECM-binding, potentially provides a promising alternative in human medicine [43]. Therefore, we analyzed the factors which contribute to S. check gallolyticus adhesion and invasion in IE using an experimental in vitro cell culture model. Investigation

of the adhesion to ECM proteins identified or confirmed putative adhesive sites on the endothelial cell surface. Additionally, virulence factors were detected and biofilm formation was analyzed in order to identify different strain characteristics. Most S. gallolyticus strains tested in this study adhere to and invade endothelial cells. The diversity in adhesion and invasion characteristics appears considerably higher for invasion. Strain DSM 16831 exclusively demonstrated no invasive capability. Invasion was also not induced using higher concentrations of bacteria, usage of primary endothelial cells or mechanical stretched cells. In contrast, strain DSM 13808 present a considerably high invasion. The distinct behaviour of these two strains may be due to the fact that they were the only strains tested that were isolated from non-human sources. In general, the observed differences may reflect distinctions in the bacterial equipment with virulence factors or gene expression of virulence factors. We have shown that isolate represent a different distribution of the virulence-associated genes gtf, fimB and pilB. However, the presence of a putative virulence gene does not necessarily indicate expression. For example, Stipp et al.

Although charcoaling a living tree is forbidden in all tribal groups, to do

so is a powerful temptation to resist because charcoal means money for poor people. Ma‘aza people continued charcoaling until what they described selleck screening library as a decade-long drought afflicted them during the 1950s. As ephemeral pasture failed altogether in their homeland and adjacent Ababda lands to the south, they recognized that their acacia reserves were critically low. Numerous families left the desert and settled around the eastern margin of the Nile Valley opposite Beni Suef during the drought, but those who remained adopted a complete ban against cutting larger branches and fed their animals mainly with shaken leaves and pods. The Ma‘aza took a number of steps to keep their existing acacia resources and stave off destruction of living trees. One was to emphasize Evofosfamide nmr territorial and kinship rights and responsibilities to acacias based more on lineage (a sub-clan), household and CFTRinh-172 chemical structure individual than on tribe and clan. Acacias that belonged collectively to clan members remained so nominally but were subdivided into effective properties of their families, according to rights within traditional law (‘urf Ar.). They proclaimed protected groves of trees on a family-by-family,

wadi-by-wadi basis (Hobbs 1989). The claimant’s direct male descendants, and thus eventually his entire lineage, became responsible for protection in the future. These ‘lineage preserves’ were intended to serve as a kind of drought insurance that would protect the desert way of life in any future emergency. Ma‘aza people today insist that acacia trees rescued them and enabled their way of life to survive the 1950s. Due to

push and pull factors driving and drawing Ma‘aza people out of the desert, that way of life has all but ended. As recently as the 1980s many hundreds of Ma‘aza tribespeople, mostly of the Khushmaan clan, practiced nomadic pastoralism. Only a handful of families do so today. With another prolonged dry spell and a boom in Red Sea tourism in the 1990s, most of the desert-dwellers were drawn into a state of “soft sedentarization” at 14 encampments Arachidonate 15-lipoxygenase (mahatta) on the coastal plain near Hurghada (Hobbs and Tsunemi 2007). Egyptian guides bring international tourists on half day “safaris” from beach hotels to see “how the real Bedouin live”. In 2013, on the eve of the coup and subsequent violence that wracked Egypt’s tourism industry, about 200 Ma‘aza families were encamped at these sites. A few kept sheep and goats in penned areas there, but most of their income came from tourism at the stations and from wage labor in Hurghada. Acacias on the cultural landscape of the Ma‘aza at present have several distinctive features. While their numbers are small compared with populations further south, there are several dispersed groves of trees.

Type 1 SHEAST has 12 VE-821 datasheet nucleotide non-synonymous substitutions including one in the initiation codon; type 2 SHEAST lacks the first 8 codons of EAST1 sequence [16]. The focus of the study was to investigate the astA gene sequence present in

tEPEC and aEPEC strains. The strains were collected in different cities of Brazil in different periods of time and in a previous study poor relatedness was observed by RAPD analysis of 118 strains belonging to this collection [13]. Results and discussion We examined 222 EPEC strains (70 typical and 152 atypical) for the presence of the astA gene by PCR using primers that anneal to the 5’ ends of the EAEC 042 astA gene sequence [16]. Those strains were isolated from diarrheic and non diarrheic Brazilian children in previous studies [17–20]. As shown in Table  1, 11 (16%) tEPEC and 43 (28%) Ulixertinib price aEPEC strains were positive in the PCR assay. Among the aEPEC PCR-positive strains, 13 belonged to the O26 and O119 serogroups. Table 1 EPEC- astA strains isolated from diarrheic and non-diarrheic children EPEC Serotype No. of strains (positive/total)     Diarrheic

selleck kinase inhibitor children Non-diarrheic children Total of children tEPEC O55:NM;HND 0/13 0/1 0/14   O86:NM;H34 0/2 0 0/2   O111:NM;H2,HND 4/9 0 4/9   O119:NM;H6;HND 2/22 0/3 2/25   O127:NM;H6 0/1 2/3 2/4   Other serotypesa 3/14 0/2 3/16 Subtotal 9/61 2/9 11/70 aEPEC O26:H11;HND 6/10 0/2 6/12   O55:HND 2/3 1/2 3/5   O111:NM 2/2 1/2 3/4   O114:NM 0 0/1 0/1   O119:H2;HND 7/9 0/3 7/12   O126:NM 0/1 0 0/1   O127:NM;H40 0/3 0/1 0/4   O128:NM 0/3 0 0/3   O142:NM;H2 1/8 0 1/8   Other serotypesb 18/68 5/34 23/102 Subtotal 36/107 7/45 43/152 Total 45/168 9/54 54/222 aO2:H2;H45; O101:H33; O145:HND; O157:HND; O162:H33; ONT:H45; ONT:HND. bO4:HND; O15:HND O33:H6; O35:H19; O37:HND; O49:HND; O61:HND; O63:HND; O79:HND; O85:H40; O96:HND; O98:HND; O101:NM; O103:NM; O105:H7; O108:H31; O109:H54; O117:HND; O132:HND; O141:HND; O1523H2; O156:H16; O157:HND; O167:H6; O169:H6; Morin Hydrate O175:HND;ONT:NM; ONT:H18; ONT:HND. Note: NM, nommotile, ND, nondetermined, ONT, nontypeable. The 54 astA gene

PCR products were sequenced. Twenty five strains, 7 tEPEC and 18 aEPEC, carried the DNA sequence identical to the EAST1 gene (042-type EAST1) (Figure  1). A subgroup of 7 aEPEC strains presented a variant type of the 042-type EAST1 gene sequence, with four non-synonymous nucleotide substitutions. Nine other strains, including one typical, carried either the sequence identical to type 1 SHEAST (7 strains) or to type 2 SHEAST (two strains). The remaining 13 strains carried mutated sequences of the 042-type EAST1 (five strains), type 1 SHEAST (two strains) or type 2 SHEAST (six strains) genes.

Nano Lett 2011, 11:1952–1956.CrossRef 19. Ma DDD, Lee CS, Au FCK, Tong SY, Lee ST: Small-diameter silicon nanowire surfaces. Science 2003, 299:1874–1877.CrossRef 20. Schmidt V, JQ-EZ-05 solubility dmso Wittemann JV, Senz S, Gosele U: Silicon nanowires: a review on aspects

GSK1210151A of their growth and their electrical properties. Adv Mater 2009, 21:2681–2702.CrossRef 21. Liu HI, Biegelsen DK, Ponce FA, Johnson NM, Pease RFW: Self-limiting oxidation for fabricating sub-5 nm silicon nanowires. Appl Phys Lett 1994, 64:1383–1385.CrossRef 22. Buttner CC, Zacharias M: Retarded oxidation of Si nanowires. Appl Phys Lett 2006, 89:263106.CrossRef 23. Walavalkar SS, Hofmann CE, Homyk AP, Henry MD, Atwater HA, Scherer A: Tunable visible and near-IR emission from sub-10 nm etched single-crystal Si nanopillars. Nano Lett 2010, 10:4423–4428.CrossRef 24. Wang T, Yu B, Liu Y, Guo Q, Sheng K, Deen MJ: Fabrication of vertically stacked single-crystalline Si nanowires

using self-limiting oxidation. Nanotechnology 2012, 23:015307.CrossRef 25. Fang H, Wu Y, Zhao JH, Zhu J: Silver catalysis in the fabrication of silicon nanowire arrays. Nanotechnology 2006, 17:3768–3774.CrossRef 26. Huang ZP, Fang H, Zhu J: Fabrication of silicon nanowire arrays with controlled diameter, length, and density. Adv Mater 2007, 19:744–748.CrossRef 27. Lin LH, Guo SP, Sun XZ, Feng JY, Wang Y: Synthesis and photoluminescence properties of porous silicon nanowire arrays. Nanoscale Res Lett 2010, 5:1822–1828.CrossRef 28. Liu Selleckchem PND-1186 RY, Zhang FT, Con C, Cui B, Sun BQ: Lithography-free fabrication of silicon nanowire and nanohole arrays by metal-assisted chemical etching. Nanoscale Res Lett 2013, 8:1–8.CrossRef 29. Haginoya C, Ishibashi M, Koike Ribonucleotide reductase K: Nanostructure array fabrication with a size-controllable natural lithography. Appl Phys Lett 1997, 71:2934–2936.CrossRef

30. Cui H, Wang CX, Yang GW: Origin of self-limiting oxidation of Si nanowires. Nano Lett 2008, 8:2731–2737.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions SS carried out the fabrication and characterization of the study and drafted the manuscript. LL conceived of the study, participated in its design and preparation, analyzed the results, and helped draft the manuscript. JF participated in the design of the study and helped draft the manuscript. ZL and ZZ participated in the design and coordination of the study. All authors read and approved the final manuscript.”
“Background Graphene molecules were first extracted from a graphite crystal by a simple micromechanical approach (mechanical cleavage) [1, 2]. During the graphite crystal peeling out process, the applied mechanical stress causes the separation of the graphene layers, contrasting the interlayer interaction forces. This procedure is known as the Scotch type or drawing method since the mechanical exfoliation resembles writing with a pencil.

Angiogenesis, the establishment of new blood vessels from preexisting blood, is thought to be required for process of tumorigenesis and metastasis and may prove to be a useful

prognostic marker for prostate cancer [25]. A notable finding is that PSMA, an angiogenic endothelial cell which is like one of several peptidases that play a role in angiogenesis. PSMA Dasatinib purchase expression was specifically detected on the neovasculature of many other prostates not related tumors, suggesting the possibility that PSMA may also functionally contribute to angiogenesis of primary and metastatic cancers [26, 27].Therefore, it has been suggested that PSMA may be utilized both as VE-821 nmr a marker and as a therapeutic target [26, 6]. In prostate cancer, a significant correlation between PSMA expression and angiogenesis has been shown [26, 28]. However, the biological role of both angiogenesis [29] and PSMA expression in PC is still unclear for there are, indeed, studies in which the presence of these molecules is deprived of any prognostic significance [30]. Interestingly, in vitro and in vivo investigation, it was revealed that PSA suppresses angiogenesis and, therefore, tumor growth and PC invasiveness by activating the angiostatin-like fragments [31, 32]. The present study was undertaken to relate the co-expression of prostate-associated antigens, PSMA and PSA, with the degree of vascularization in normal and pathologic

(hyperplasia and cancer) prostate tissues to elucidate their possible role in tumor progression. On the basis of the heterogeneity in PSMA and PSA expression along prostatic tumor progression, we suggested the presence of various profiles of these this website prostate-associated antigens in each prostatic group (NP, BPH and PC).

This led us to better investigate the association between the two markers in each OSBPL9 prostatic group. The ultimate question was which, if any, of these factors could provide additional information regarding the biology of prostate tumorigenesis. Materials and methods Prostates were obtained from: (i) transurethral resections from 44 men (aged from 61 to 85 years) diagnosed clinically and histopathologically with Benign Prostate Hyperplasia (BPH); (ii) radical prostatectomy from 39 men (aged from 57 to 90 years) diagnosed with prostate cancer (PC) (dominant Gleason grade ≥7); and (iii) histologically normal prostates (NP) obtained at autopsy (8-10 hours after death) from 6 men (aged from 21 to 40 years) without histories or reproductive, endocrine or related diseases. All pathological, clinical and personal data were anonymized and separated from any personal identifiers. This study was made with the consent of the patients’ relatives or their family in autopsy cases. All the procedures followed were examined and approved by the Hospital of La Rabta of Tunis, the Hospital of Charles Nicolle of Tunis and the Military Hospital of Tunis (HMPIT) (Tunisia).

International Archives of Occupational and Environmental Health1999,72:443–450.CrossRefPubMed 6. Brown BJ, Leff LG:Comparison of fatty acid methyl ester analysis with the click here use of API 20E

and NFT strips for identification of aquatic bacteria. Applied Environmental Microbiology1996,62(6):2183–2185. 7. Francis CA, Obraztsova AY, Tebo BM:Dissimilatory metal reduction by the facultative anaerobe Pantoea agglomerans SP1. Applied and environmental microbiology2000,66(2):543–548.CrossRefPubMed 8. Wodzinski RS, Umholtz TE, Beer SV:Mechanisms of inhibition of E. amylovora by E. herbicola in vitro and in vivo. J Appl Bacteriol1994,76:22–29. 9. Johnson KB, Stockwell VO:Management of fire blight: a case study in microbial ecology. Annu Rev Phytopathol1998,36:227–248.CrossRefPubMed 10. Braun-Kiewnick A, Jacobsen BJ, Sands DC:Biological control of Pseudomonas syringae pv. syringae , the causative agent of basal kernel blight of barley, by antagonistic Pantoea agglomerans.Phytopathology2000,90:368–375.CrossRefPubMed 11. Nunes C, Usall J, Teixidó N, Fons E, Viñas I:Post-harvest

biological control by Pantoea agglomerans (CPA-2) on Golden Delicious apples. J Appl Microbiol2002,92:247–255.CrossRefPubMed 12. Bonaterra A, Camps J, Montesinos E:Osmotically induced trehalose and glycine betaine accumulation improves tolerance to dessication, survival AC220 mouse and efficacy of the postharvest biocontrol agent Pantoea agglomerans EPS125. FEMS Microbiol Lett2005,250:1–8.CrossRefPubMed 13. Bonaterra

A, Mari M, Casalini L, Montesinos E:Biological control of Monilinia laxa and Rhizopus stolonifer in postharvest of stone fruit by Pantoea agglomerans EPS125 and putative mechanisms of antagonism. Int J Food Microbiol2003,84:93–104.PubMed 14. Francés J, Bonaterra A, Moreno MC, Cabrefiga J, Badosa E, Montesinos E:Pathogen aggressiveness and postharvest biocontrol efficiency in Pantoea agglomerans.Postharvest Biol Technol2006,39(3):299–307.CrossRef RVX-208 15. Vanneste JL, Cornish DC, Yu J, Voyle MD:P10c: a new biological control agent for control of fire blight which can be sprayed or distributed using honey bees. Acta Hortic2002,590:231–235. 16. Ishimaru CA, Klos EJ, Brubaker RR:Multiple antibiotic production by Erwinia herbicola.Phytopathology1988,78:746–750.CrossRef 17. Pusey PL, Stockwell VO, Rudell DR:Antibiosis and acidification by Pantoea agglomerans strain E325 may contribute to suppression of Erwinia amylovora.Phytopathology2008,98(10):1136–1143.CrossRefPubMed 18. Stockwell VO, Johnson KB, Sugar D, Loper JE:Antibiosis contributes to biological control of fire blight by Pantoea agglomerans strain Eh252 in orchards. Phytopathology2002,92(11):1202–1209.CrossRefPubMed 19. Vanneste JL, Yu J, Cornish DA:Presence of genes homologous to those necessary for synthesis of microcin MccEh252 in EPZ-6438 mouse strains of Pantoea agglomerans.Acta Hort2008,793:391–396. 20.