Homology searches revealed that the plasmid (designated pMK100) found in S. Infantis (S20) exhibited 100% homology with

qnrB19-carrying plasmids including pSGI15, a Atezolizumab small ColE plasmid identified recently in S. enterica serovar Typhimurium isolated in Germany (Hammerl et al., 2010), and a qnrB19-containing plasmid pPAB19 from an S. Infantis clinical isolate recovered in Argentina (GenBank accession number GQ412195). The plasmid purified from isolate S75 (designated pMK101) was found to be 97% similar to these latter plasmids. The dissimilarity noted was mapped to an insertion located between nucleotide positions 896 and 957. Remarkably, the latter DNA sequence was identical to one found in a pBC633 from a K. pneumoniae strain KN633 (accession number EU176012), a urinary isolate from Colombia displaying carbapenem resistance and reported in 2005. This plasmid of approximately 15.5 kb carried a blaKPC−2 gene encoding a class A carbapenemase (Villegas et

al., 2006). The additional Lumacaftor nmr DNA sequence contained in the plasmid from the isolate S75 was located between the qnrB19 gene and orf2, and was found to be homologous with a region of pBC633. Furthermore, nucleotide sequence similarity was observed in the region upstream of the inserted fragment, possibly facilitating the incorporation of the new DNA fragment. The fact that pBC633 was found only in Colombia indicates that the homology found here may not be coincidental. It is interesting to speculate that pMK101 (the plasmid from isolate S75) is chimeric and may have emerged as a result of a recombination event that led to the horizontal acquisition of a fragment from another plasmid containing blaKPC−2. The process is likely to have occurred in a bacterium simultaneously hosting Astemizole a plasmid similar to or identical to pBC633, as well as a small ColE-like plasmid such as pMK100. While blaKPC−2 genes are frequent in K. pneumoniae and only sporadic in other Enterobacteriaceae, there are insufficient data to conclude what species was the primary host of the new plasmid structure (Villegas et al., 2006; Pournaras et al., 2009). In addition, it is noteworthy

that pBC633 containing a blaKPC−2 gene was found on a transposon Tn4401 with multiple insertion sequence (IS) elements that have likely contributed to its emergence (Naas et al., 2008). Of particular concern is the possibility of the emergence of chimeric plasmids carrying both qnr genes and blaKPC−2 that could compromise the clinical value of fluoroquinolones and virtually all β-lactams. In view of this, monitoring of phenotypic resistance as well as associated mechanisms and mobility is essential. Furthermore, the occurrence of both blaKPC−2 and qnr in Colombia and their associated plasmids is likely to be under-reported as a result of poor surveillance as well as diagnostic challenges associated with the low-level resistance conferred (Villegas et al., 2006).

In addition, two flavin-binding monooxygenases were found to be upregulated during growth on alkanes indicative of two novel pathways likely to be involved in alkane degradation by A. borkumensis (ABO_0282, ABO_1097, Table 1). BMN673 Moreover, we detected the up-expression of two genes similar to the ones involved in the degradation of halogenated alkanes in other bacteria, namely haloacid dehalogenase-like hydrolase dhlA (ABO_1537, Table 1) and haloalkane dehalogenase dhmA (ABO_2415,

Table 1). If the first enzyme is known to convert haloalkanes to corresponding alcohols and halides, the second one catalyzes hydrolytic cleavage of carbon-halogen bonds in halogenated aliphatic compounds, leading to the formation of primary alcohols, halide ions, and protons. Alkane-induced coexpression of these enzymes mediating the breakdown of haloalkanes, alongside the induction of enzymes degrading aliphatic alkanes, signifies unspecific upregulation of expression, probably reflecting the presence of halogenated alkanes in sea water. Additionally, we found alkane-induced

expression of aldehyde reductase (ABO_2414, Table 1). This gene is predicted to be involved in the metabolic activation of polycyclic aromatic hydrocarbons (PAHs), as shown recently for human aldehyde reductase AKR1A1 (Palackal et al., 2001). However, as yet, A. borkumensis has not been shown to either degrade or transform PAHs, and thus requires further experimentation to explore what coexpression Doxorubicin of this gene alongside those mediating the degradation of aliphatic alkanes may signify for the degradation of alkanes or petroleum. These data allow us to update the list of enzymatic systems shown before by our proteomic study to be potentially involved in the initial terminal oxidation of alkanes by A. borkumensis (Figs 1 and 2). Attachment of A. borkumensis to hydrocarbons and its molecular mechanisms have not yet been studied, although such abilities are likely to form part of the specific ecological adaptation of this bacterium. EM observation of Alcanivorax SK2 indeed indicates that this organism forms biofilm-supporting structures during growth on alkanes (Fig.

Ixazomib cost 3). Cells grown on alkane seem to more connect to each other rather than to the solid surface of the carrier slide, and they are shorter and rounder, and produce considerable amount of extracellular polymeric substances (EPS), which appears to support the three-dimensional structure of a biofilm. After 10 days of growth, alkane-grown cells develop a biofilm, which exhibits a pronounced three-dimensional architecture supported by extracellular matrix (Fig. 3). The argument of an alkane-induced formation of EPS is supported by alkane-induced up-expression of gmhA (ABO_0584). GmhA encodes a phosphoheptose isomerases that mediates the synthesis of heptose, a conserved component of outer membrane lipopolysaccharide, that for example in Yersinia, was shown to contribute to the formation of biofilms (Darby et al., 2005).

In addition, two flavin-binding monooxygenases were found to be upregulated during growth on alkanes indicative of two novel pathways likely to be involved in alkane degradation by A. borkumensis (ABO_0282, ABO_1097, Table 1). Kinase Inhibitor Library screening Moreover, we detected the up-expression of two genes similar to the ones involved in the degradation of halogenated alkanes in other bacteria, namely haloacid dehalogenase-like hydrolase dhlA (ABO_1537, Table 1) and haloalkane dehalogenase dhmA (ABO_2415,

Table 1). If the first enzyme is known to convert haloalkanes to corresponding alcohols and halides, the second one catalyzes hydrolytic cleavage of carbon-halogen bonds in halogenated aliphatic compounds, leading to the formation of primary alcohols, halide ions, and protons. Alkane-induced coexpression of these enzymes mediating the breakdown of haloalkanes, alongside the induction of enzymes degrading aliphatic alkanes, signifies unspecific upregulation of expression, probably reflecting the presence of halogenated alkanes in sea water. Additionally, we found alkane-induced

expression of aldehyde reductase (ABO_2414, Table 1). This gene is predicted to be involved in the metabolic activation of polycyclic aromatic hydrocarbons (PAHs), as shown recently for human aldehyde reductase AKR1A1 (Palackal et al., 2001). However, as yet, A. borkumensis has not been shown to either degrade or transform PAHs, and thus requires further experimentation to explore what coexpression Liproxstatin-1 order of this gene alongside those mediating the degradation of aliphatic alkanes may signify for the degradation of alkanes or petroleum. These data allow us to update the list of enzymatic systems shown before by our proteomic study to be potentially involved in the initial terminal oxidation of alkanes by A. borkumensis (Figs 1 and 2). Attachment of A. borkumensis to hydrocarbons and its molecular mechanisms have not yet been studied, although such abilities are likely to form part of the specific ecological adaptation of this bacterium. EM observation of Alcanivorax SK2 indeed indicates that this organism forms biofilm-supporting structures during growth on alkanes (Fig.

TCL 3). Cells grown on alkane seem to more connect to each other rather than to the solid surface of the carrier slide, and they are shorter and rounder, and produce considerable amount of extracellular polymeric substances (EPS), which appears to support the three-dimensional structure of a biofilm. After 10 days of growth, alkane-grown cells develop a biofilm, which exhibits a pronounced three-dimensional architecture supported by extracellular matrix (Fig. 3). The argument of an alkane-induced formation of EPS is supported by alkane-induced up-expression of gmhA (ABO_0584). GmhA encodes a phosphoheptose isomerases that mediates the synthesis of heptose, a conserved component of outer membrane lipopolysaccharide, that for example in Yersinia, was shown to contribute to the formation of biofilms (Darby et al., 2005).

7 mg/kg, respectively.

Some readers may argue that these high doses of oral midazolam are candidates for deep sedation which, although not reported in the studies, may have been measurable if equipments such as bispectral index monitors were to be used to verify the depth of sedation. Minor side effects were much more common and seen in 14% of all RCT studies with nausea/vomiting, transient desaturations and paradoxical reactions being the chief complaints. Further analysis of the relationship between oral midazolam dosage and prevalence of symptoms was felt to be unwise due R788 datasheet to the generally poor quality of the data. The frequency of transient desaturations emphasises the importance of adequate monitoring during sedation. Of the six studies reporting a transient desaturation, two did not provide a figure for the lowest oxygen saturation level reached[14, 39], whereas the remaining four studies reported that oxygen saturation reached low levels ranging from 78% to 94%[17, 23, 25, 36]. The importance of safety in sedation is paramount and the authors advise the use of pulse oximetry

and the availability of emergency equipment as standard. What constitutes a significant side effect? An arbitrary description was made for this review which some readers may disagree with; however, given the data available, we felt it was the best compromise. Clearly, an inability to maintain an airway or persistent desaturation should be considered as significant but what about transient desaturations? We felt that if these were easily

correctable through head repositioning, selleckchem then they should be considered as minor, and this sort of transient desaturation could be due to a range of reasons including breath holding or crying. It is important to recognise that all the side effects recorded here were very ‘clinician-centred’, Liothyronine Sodium that is, they could be considered as anything that might interfere with provision of the treatment. It might be interesting as part of any future work to look at patient-centred measures and perhaps get patients’ views as to what events they would consider to be significant. In general, it would be helpful if more generally agreed descriptions of side effects existed that could be used in future studies, thus facilitating greater comparison between studies and between different methods of sedation. In conclusion, significant or major side effects associated with oral midazolam usage for behaviour management in children and adolescents requiring dental treatment appear to be rare. Minor events are more common but determining precise figures was complicated by poor reporting. Why this paper is important to paediatric dentists? There is currently little information available as to the safety of midazolam when used as an oral sedative in children needing dental treatment. This study revealed that significant side effects are uncommon.

A prebiotic is a nondigestible food ingredient that beneficially affects the host by selectively stimulating the growth and/or activity of one or a limited number of bacteria in the colon, thus improving the host health (Gibson & Roberfroid, 1995). The combination of suitable probiotics

and prebiotics enhances the survival and activity of the organism. The combination of prebiotic and probiotic has synergistic effects because in addition to promoting the growth of existing strains of Depsipeptide mw beneficial bacteria in the colon, synbiotics also act to improve the survival, implantation, and growth of newly added probiotic strains. The synbiotic concept has been widely used by European dairy drink and yoghurt manufacturers such as Aktifit (Emmi, Switzerland), Proghurt (Ja Naturlich Naturprodukte, Austria), Vifit (Belgium, UK), and Fysiq (the Netherlands; Niness, 1999). The combination of Bifidobacterium and oligofructose was reported to synergistically improve colon carcinogenesis in rats compared to when both were given individually NVP-BEZ235 cell line (Gallaher

& Khil, 1999). Another study reported that a synbiotic containing Pediococcus pentoseceus, Leuconostoc mesenteroides, Lactobacillus paracasei, and L. plantarum with four fermentable fibers namely β-glucan, inulin, pectin, and resistant starch reduced the occurrence of postoperation infections from 48% to 13% in 66 liver transplant patients (Rayes et al., 2005). Most of the claims on benefits of different synbiotics are on general health (Gibson & Roberfroid, 1995). There have yet been any clinical trials on suitable combinations of synbiotics that specifically target reduction in serum cholesterol level in animals and humans. Bifidobacteria and Lactobacilli are the most frequent target organisms for prebiotics. Although there is growing interesting development of new functional foods

with synbiotics, the concept of synbiotics has been studied to a limited extent and needs further investigations. Only a few human studies have been carried out on the effectiveness of synbiotics (Morelli et al., 2003). There are evidences from well-conducted acetylcholine clinical trials of beneficial health effects from probiotics in a range of clinical conditions. The concept of ‘synbiotics’ has recently been proposed to characterize health-enhancing food and supplements used as functional food ingredients in humans, and with the advent of the functional food concept, it is clear that there is an important niche for these probiotic-based approaches. Although from the ongoing research, more of promising potential health effects of probiotics are being observed, more standardized and verifiable clinical studies are needed to demonstrate the safety, efficacy, and limitations of a putative probiotic, to determine effects on the immune system in healthy and diseased individuals and effects of long-term consumption, and to resolve whether it is superior to existing therapies.

The need for knowledge and preparedness is especially critical in the case of individuals with preexisting medical conditions. These patients may be at increased risk for developing altitude-related illness or decompensation of their underlying disease with altitude-related changes in physiology. This article reviews the effects of altitude in relation to a selection of common medical VX-770 research buy conditions and gives recommendations

for how people with these disorders can protect their health at altitude. There is a significant amount of individual variability in the effects of altitude on blood pressure. In the majority of people there is a small alpha adrenergic–mediated increase in blood pressure proportional to elevation gain,21 the effect of which is not clinically significant until above 3,000 m.2,22,23 However, in some people, there is a pathological reaction to high altitude which results in large blood pressure increases.5,22 A work by Häsler and colleagues24 suggests racial differences in the blood pressure response to altitude. Black mountaineers experienced a progressive decrease in systolic blood pressure (SBP) with increasing altitude whereas the matched white subjects experienced increasing SBP. Furthermore, bilanders who divide their time between sea level and

high altitude residences experience significantly higher mean arterial pressure at their high altitude dwelling compared to sea level.25 In all people, the extent of pressure change depends ICG-001 chemical structure on the degree of hypoxic stress, cold, diet, exercise, and genetics.22 Over-reactive sympathetic responses

during sleep may cause periodic breathing which increases the risk of exacerbating hypertension and causing cardiac arrhythmias.5 Hypertension is also an independent risk factor for sudden cardiac death (SCD) during mountain sports.26 Despite these risks, well-controlled hypertension is not a contraindication to high altitude old travel27 or physical activity performed at altitude.23 Aneroid sphygmomanometers have been validated for use at high altitude (4,370 m).28 Patients with poorly controlled blood pressure should monitor their blood pressure while at altitude6 and be made aware of the potential for sudden, large fluctuations in blood pressure.2,22 A plan for medication adjustments should be prepared in advance and should include increasing the dose of the patient’s usual antihypertensives as a first-line strategy for uncontrolled hypertension. Alpha-adrenergic blockers and nifedipine are the drugs of choice if hypertension remains severe.2,5 The development of hypotension may necessitate a later medication reduction with acclimatization to altitude.6 Patients taking diuretics should exercise caution in avoiding dehydration and electrolyte depletion. Furthermore, beta-blockers limit the heart rate response to increased activity and interfere with thermoregulation in response to heat or cold.

Supplementation of diet with dairy products fermented with LAB has the potential to reduce serum cholesterol levels in humans and animals (Pulusoni & Rao, 1983). A significant decrease in serum cholesterol level in rats fed milk fermented with L. acidophilus has been reported (Grunewald, 1982). Mann (1977) showed that large dietary intake of yogurt lowered the cholesterolemia

in humans. Experiments by Gilliland et al. Ulixertinib solubility dmso (1985) have shown that dietary elevation of plasma cholesterol levels can be prevented by the introduction of a L. acidophilus strain that is bile resistant and assimilates cholesterol. These findings were supported by Pereira & Gibson (2002) who demonstrated that Idasanutlin ic50 probiotic strains were able to assimilate cholesterol in the presence

of bile into their cellular membranes. Results, however, were influenced greatly by the bacterial growth stage, and inoculum using resting cells did not interact with cholesterol as also shown by studies conducted by Dambekodi & Gilliland (1998). St-Onge et al. (2000) extensively reviewed the existing studies from animal and human studies which detected that moderate cholesterol lowering was attributable to the consumption of fermented products containing probiotic bacteria. Studies by Gopal et al. (1996) also showed cholesterol removal by Bifidobacterium spp. and L. acidophilus. The possible mechanisms of action of probiotics are cholesterol assimilation by bacteria, deconjugation of bile salts, cholesterol binding to bacterial cell walls, and reduction in cholesterol biosynthesis (Pulusoni & Rao, 1983; Pereira & Gibson, 2002). The role of gut flora in the pathology of insulin resistance (type 2 diabetes) and obesity has been well documented by Ley et al. (2005). Animal and human studies have suggested that gut flora enhances the body weight gain and increases the insulin resistance, and these phenotypes

are N-acetylglucosamine-1-phosphate transferase transmittable with gut flora during the implantation studies of microbiota from obese to normal and germ-free mice (Ley et al., 2006; Turnbaugh et al., 2006). The mechanisms associated with gut flora–mediated pathology of obesity and diabetes are through (1) increased energy harvest, (2) increased blood LPS levels (endotoxemia), and (3) low-grade inflammation (Delzenne et al., 2011). Therefore, modulation of gut flora has been considered as a potential target to treat against obesity and diabetes. Probiotics are novel gut flora modulators, and their role in the prevention of and treatment for diabetes and obesity has been implicated in recent past by Yadav et al. (2007a, b, 2008). Yadav et al.

Fissures can be reliably examined with LF and by visual inspection on school premises if certain special arrangements are made. “
“International Journal of Paediatric Dentistry 2011 Aim.  To assess the relation between type of traumatic injury and use of pacifier at the time of a fall accident in 0- to 2-year olds. Material and methods.  click here The study draws on data from the database on traumatic dental injuries at the Department of Oral and Maxillofacial Surgery, Copenhagen University Hospital. Results.  The study includes 1125

patients ≤2 years of age, representing a total of 1886 injuries. A total of 176 patients had fallen while using a pacifier, whereas 949 children suffered a fall without using a pacifier. In the pacifier group, 11.9% had crown fractures compared with 20.0% of children who had fallen without a pacifier (P = 0.012). Tooth displacement (lateral luxation, extrusion or avulsion) was relatively more frequent in children falling with a pacifier compared to children falling without a pacifier (64.8%vs 54.8%; P = 0.014).

Furthermore, soft tissue injury was less frequent among the former (28.4%vs 38.3%; P = 0.013). Conclusions.  Injuries occurring Pifithrin-�� datasheet while using a pacifier tend to be tooth displacement rather than fractures. This is in accordance with the theoretical consideration that a blunt impact tends to favour displacement, whereas a sharp impact tends to favour fractures of the hard dental tissues. Urease “
“Early childhood caries (ECC) is a multifactorial disease resulting mainly from a time-specific interaction of micro-organisms with sugars on a tooth surface. The purpose of this study was to assess the relationship of dietary intake, as measured by the Healthy Eating Index-2005 (HEI-2005) to ECC. Cross-sectional analytical study. Sixty preschool children were equally divided into three groups according to their caries experience [Group 1: caries-free children, group 2: children with ECC, group 3: children with severe early childhood caries (S-ECC)]. The decayed (non-cavitated or cavitated), missing (due to caries) and filled tooth surfaces (dmfs) score was determined

through visual dental examination for each child. Questionnaires were collected recording the demographic characteristics of the families as well as 24-h food recall forms capturing the dietary intake of the children during the previous day. Accordingly, the HEI-2005 score was calculated for each child. The caries experience of the children in this study was significantly associated with their age. Caries-free children showed significantly higher ‘Whole fruit’, ‘Milk’, ‘Sodium’ and total HEI-2005 scores. The study findings illustrate the prominent protective role played by healthful dietary practices against dental caries in preschool children. “
“Welcome to Volume 24 of the International Journal of Paediatric Dentistry. In 2013, the Journal has received 578 manuscripts from 57 countries.

“
“The membrane-bound alcohol dehydrogenase of Gluconacetobacter diazotrophicus contains one pyrroloquinoline quinone moiety (PQQ), one [2Fe-2S] cluster, and four c-type cytochromes. Here, we describe a novel and inactive enzyme. ADHi, similarly to ADHa, is a heterodimer of 72- and 44-kDa subunits

and contains the expected prosthetic groups. However, ADHa showed a threefold molecular mass as compared to ADHi. Noteworthy, the PQQ, the [2Fe-2S] and most of the cytochromes in purified ADHi is in the oxidized form, contrasting with AZD1208 manufacturer ADHa where the PQQ-semiquinone is detected and the [2Fe-2S] cluster as well as the cytochromes c remained fully reduced after purification. Reduction kinetics of the ferricyanide-oxidized enzymes showed that while ADHa was brought back by ethanol to its full reduction state, in ADHi, only one-quarter of the total heme c was reduced. The dithionite-reduced ADHi was largely oxidized by ubiquinone-2, thus indicating that intramolecular electron transfer is not impaired in ADHi. The acidic pH of the medium might be deleterious for the membrane-bound ADH by causing conformational changes leading to changes in the relative orientation of heme groups and shift of corresponding redox potential to higher values. This would hamper electron transfer resulting in the low activity observed in ADHi. In Gluconacetobacter diazotrophicus,

the PQQ-dependent enzymes – ethanol dehydrogenase (ADH) selleck screening library and aldehyde dehydrogenase (ALDH) – are located in the cytoplasmic membrane and oriented toward the periplasmic space (Matsushita et al., 1992). ADH and ALDH catalyze the two sequential oxidation reactions that convert ethanol to acetic acid; both enzymes transfer electrons to membrane ubiquinone. The ethanol-oxidizing ability in acetic acid bacteria can be easily changed and sometimes lost during cultivation, especially in prolonged shaking Tacrolimus (FK506) cultures

of Acetobacter aceti (Muraoka et al., 1982; Ohmori et al., 1982) and Acetobacter pasteurianus (Takemura et al., 1991). Under these conditions, spontaneous mutants unable to oxidize ethanol emerge with high frequency. In Gluconobacter suboxydans, genetic instability has not been detected (Matsushita et al., 1995); instead, a dramatic decay in ADH activity has been observed under particular cultivation conditions, such as low pH and/or with high aeration. The presence of an ADH with a very low enzyme activity level (named as inactive ADH) has been reported (Matsushita et al., 1995). Gómez-Manzo et al. (2008, 2010) have already purified and characterized a highly active ADH (ADHa) from N2-grown Ga. diazotrophicus, using forced aeration and physiological acidification caused by growth. In the present work, we purified and characterized an ADH with very low enzyme activity (ADHi). A comparative study of the molecular and catalytic properties of the active and inactive forms of ADH from Ga.

We assessed the production of OMVs from K. pneumoniae ATCC 13883 during in vitro culture. Bacteria were cultured in LB broth, and OMVs were purified from culture supernatants. TEM analysis showed that K. pneumoniae-derived vesicles were spherical bilayered structures with diameters of 20–200 nm (Fig. 1a). No bacteria or protein contaminants were observed. The small-sized OMVs with diameters of approximately 20–30 nm were commonly observed, whereas relatively

large-sized vesicles with diameters of > 50 nm were less commonly observed. This result suggests that K. pneumoniae produces and secretes OMVs into the extracellular milieu during in vitro culture. Klebsiella pneumoniae OMVs were subjected to SDS-PAGE. Many protein bands were identified in the K. pneumoniae OMVs, but the protein profiles were different between OMVs and whole-cell lysates (Fig. 1b), selleck chemicals llc suggesting the absence of bacterial contaminants. Proteomic analysis was conducted to identify proteins in the OMVs from K. pneumoniae ATCC 13883. We identified

159 proteins in the K. pneumoniae OMVs (Supporting Information, Table S1). The proteins identified in the K. pneumoniae Tamoxifen OMVs were predicted to occur in the extracellular space (n = 13), outer membrane (n = 24), periplasmic space (n = 25), inner membrane (n = 13) and cytoplasm (n = 84). Of the proteins identified in the K. pneumoniae OMVs, the outer membrane protein X, murein lipoprotein, phage shock protein: Nintedanib (BIBF 1120) activates phage shock-protein expression, putative uncharacterized protein ygdR and 30S ribosomal protein S20 were the most abundant among the proteins located in the

outer membrane, periplasmic space, inner membrane, extracellular space and cytoplasm, respectively. These results suggest that K. pneumoniae OMVs contain numerous proteins originating from inner membrane and cytoplasm as well as outer membrane and periplasmic space. OMVs are naturally secreted products of Gram-negative bacteria, and OMV production appears to be a conserved process among Gram-negative bacteria (Beveridge, 1999; Kuehn & Kesty, 2005; Kulp & Kuehn, 2010). Additionally, Gram-positive bacteria such as Staphylococcus aureus and Bacillus anthracis also produce membrane-derived vesicles (Lee et al., 2009; Rivera et al., 2010; Gurung et al., 2011). Deatherage et al. (2009) proposed the OMV biogenesis model in Salmonella typhimurium. During bacterial growth and division, localized reductions in the density of outer membrane–peptidoglycan and outer membrane–peptidoglycan–inner membrane associations result in the bulging and release of the outer membrane as OMVs. Based on this model, OMVs only reflect the outer membrane and periplasmic components. However, cytoplasmic and inner membrane proteins have been identified in OMVs from E. coli (Lee et al., 2008), H. pylori (Olofsson et al., 2010) and Acinetobacter baumannii (Kwon et al., 2009).