Because antigen recognition

may vary greatly among patients, we examined in detail the reactivity of individual serum samples to each antigen. For this analysis, we selected the clones for the 58 ORFs of C. pneumoniae that exhibited positive signals in the initial immunoscreening; the serum samples that contained the highest titers in the ELISA assays were used as primary antibodies. The selected serum samples are indicated BIBW2992 ic50 by an asterisk in Table 1. A great variability was noted in the number of antigens detected using various combinations of individual serum samples as the primary antibody and isotype-specific anti-human immunoglobulins as the secondary antibodies (Fig. 3). Among the 58 ORFs tested, positive signals were detected for the antigens in a total of 39 ORFs by the combination selleck kinase inhibitor of at least one patient’s serum sample as the primary antibody and one of the isotype-specific anti-IgA, anti-IgG, or anti-IgM as the secondary antibody. Although anti-C. pneumoniae IgA in No. 4-3 serum, anti-C. pneumoniae IgG in No. 3-2 and 5-2, and anti-C. pneumoniae

IgM in No. 6 and 8 produced negative results in both the ELISA tests, some ORFs were clearly recognized as antigens. These results indicated that the serum sample definitely contains IgA, IgG, and IgM antibodies against the proteins encoded by some ORFs. We summarized the data for positive ORFs and have listed their orthologs and homologs from C. trachomatis in Fig. 3b. Among the 39 ORFs, we identified 11 ORFs as antigens (Cpj0147, Cpj0159, Cpj0178, Cpj0186, Cpj0268, Cpj0308, Cpj0472, Cpj0677, Cpj0678, Cpj1056, and Cpj1070) that do not have orthologs in the C. trachomatis genome. Among the other 19 ORFs, which were not detected by any individual serum sample (Fig. 3a and b), but were detected by pooled serum sample (Fig. 2), nine ORFs (Cpj0067, Cpj0181, Cpj0214, Cpj0224, Cpj0225, Cpj0339, Cpj0355, Cpj0356, and Cpj0457) do not have orthologs in the C. trachomatis genome (Fig. 3b). We believe that these 20 ORFs without orthologs in the C. trachomatis

genome represent strongly immunogenic antigens that are highly Inositol monophosphatase 1 specific to C. pneumoniae. In this study, we intended to identify novel C. pneumoniae-specific antigens by screening the C. pneumoniae genome. We applied a bioinformatics approach for annotation taxonomy that allowed us to concentrate on a subset of proteins with unknown functions. To identify the antigens recognized by the antibodies in the patients with primary C. pneumoniae infection, we designed a screening system to use patients’ serum samples as immunological probes for the genomic screening of a C. pneumoniae-ORF expression library. We measured the titers of the isotype-specific immunoglobulins using the commercially available ELISA kits HITAZYME and Medac. These kits gave both negative and positive results for antibody titers of IgA, IgG, and IgM.

1 19.9 0.0 Overall, 70.6% of contractors and employers agreed with the statement that ‘becoming an HLP has been worthwhile from a business http://www.selleckchem.com/products/PD-0325901.html perspective’, and 91.5% felt it was ‘worthwhile in terms of staff development’. The results demonstrate that commissioners value the HLP concept as this could provide a mechanism to increase volume, quality and reliability of community pharmacy services to meet local health needs. For reasons of commercial confidentiality

no ‘hard’ data was available on the effect of HLP on income. However, HLP uptake in additional pharmacies may be evidence in itself of the benefits to the business. Public health teams understood the potential of the HLP concept in helping to improve the health of the local population. The results of the contractor/employer survey showed that the overall effect

of HLP implementation was positive for all types of community pharmacy; whilst the benefits experienced varied between different types, there was something in HLP for everyone. Rebecca Venables1, Hannah Batchelor1, Heather Stirling1,2, John Marriott1 1University of Birmingham, Birmingham, UK, 2University Hospitals Coventry and Warwickshire, Coventry, UK The age at which a child transitions from liquids to tablets is influenced by nurses, pharmacists, doctors and paediatric patients The mean age at which paediatric consultants and pharmacists considered prescribing or dispensing tablets for children was lower than for GPs Greater awareness regarding the use of tablets in younger selleck products children in

specialist paediatric centres needs to be communicated into primary care Celecoxib which could result in benefits for patients in terms of convenience and for GPs in reducing costs. The choice to use a solid or liquid preparation may be influenced by healthcare professionals or children/parents/carers. There has been very limited work done outside of HIV populations to determine the factors that influence child preference to take solid dosage forms. Similarly, little is known about the factors (including child age) that may influence decisions to prescribe, supply and administer solid dosage forms to paediatric patients. Literature to date has not reported healthcare professionals’ views of tablet use versus child age. A mixed methods (quantitative and qualitative) questionnaire was distributed to paediatric: consultants, pharmacists, nurses and also GPs during routine CPD training sessions at University Hospitals Coventry and Warwickshire and Birmingham Children’s Hospital. This questionnaire had approval from NRES as well as the University of Birmingham ethics committee (FormPIC Project). Statistical analysis used ANOVA followed by Tukey’s HSD post-hoc test (conducted using IBM SPSS 20). The age at which tablets were considered to be appropriate for use in children was lower amongst the specialist healthcare professionals compared to GPs as shown in figure 1.

The standard tests commonly used for this purpose in 6-OHDA-lesioned rats, the cylinder and stepping tests and amphetamine-induced rotation, were found to be less useful as tools to monitor lesion severity in mice. Based

on the present data we have devised a set of behavioural criteria that can be used to distinguish between mice with varying degrees of cell loss induced by 6-OHDA lesions of the nigrostriatal pathway. http://www.selleckchem.com/Androgen-Receptor.html Our study is the first to characterise in detail the intranigral 6-OHDA lesion model in the mouse. The commonly used drug-induced rotation tests, cylinder test and stepping test were evaluated and compared, along with a novel task, the corridor task, for the assessment of sensorimotor deficits

on the side opposite to the lesion. The results confirm the usefulness of the intranigral lesion model in mice. The intranigral 6-OHDA lesion compares favourably with available alternatives, i.e. injections of 6-OHDA into the MFB, which are highly effective but complicated by a high death rate among the injected mice, and injections of 6-OHDA into the striatum, which tend to be less effective overall in inducing stable and severe behavioural deficits. Due to the small size of the mouse brain the 6-OHDA lesions tend to be much more variable in mice than in rats, regardless of the injection site. This is a serious problem in experimental studies, VX-809 in vitro particularly in studies that involve functional recovery over time, where profound and stable baseline deficits are important. In 6-OHDA-lesioned rats behavioural tests (most commonly amphetamine or apomorphine rotation) are generally used to preselect animals that exhibit

sufficiently severe nigrostriatal lesions to be included in the study. Similar selection criteria have so far been lacking for Decitabine 6-OHDA-lesioned mice. In the mild lesion group the average loss of TH+ neurons in the SN was 72%. These animals showed no deficits in any of the behavioural tests, which may be explained by the fact that the VTA remained largely intact (mean cell loss 17%). As a consequence, the overall density of the TH+ innervation in the striatum was only reduced by 36%, insufficient to induce any detectable deficits in either drug-induced or spontaneous motor tests. Inspection of the scatter plots in Fig. 5 and supporting Figs S1 and S2 suggests that significant motor asymmetry in the apomorphine and amphetamine rotation tests, and significant deficits in the corridor test, are seen only in mice with > 60% loss of striatal TH+ innervation (dorsal and ventral parts combined, including NAc), caused by the loss of > 75% of the TH+ cells in the SN and a > 20% loss of TH+ cells in the VTA. Only apomorphine-induced rotation and the corridor task were able to further subdivide mice with more extensive lesions and distinguish between the intermediate and severe lesion groups.

The Mycobacteria were the first bacteria shown to have multiple chaperonins (Kong et al., 1993; Lund, 2001). In M. tuberculosis there are two chaperonin genes, one (cpn60.1)

in an operon with the cochaperonin gene cpn10 and the other (cpn60.2) elsewhere on the chromosome (Kong et al., 1993). The latter encodes Hsp65 and its nomenclature as cpn60.2 genes reflect its distinct non-operon-encoded genomic localisation. Surprisingly, however, deletion studies in Mycobacterium smegmatis, M. tuberculosis and Mycobacterium bovis BCG XL184 mouse have shown that cpn60.2, and not cpn60.1, encodes the essential chaperonin, despite the latter being operon-encoded with cpn10 as in E. coli (Ojha et al., 2005; Hu et al., 2008; Wang et al., 2011). This has led to some debate about the functional equivalence of the mycobacterial cpn60 and SB203580 concentration the groEL genes (Lund, 2009). This controversy has not been resolved by the conflicting results obtained from studies on the oligomerisation of recombinant products of the different cpn60 genes and the crystal structures of their gene products (Qamra & Mande, 2004; Qamra et al., 2004; Lund, 2009). More recently, Lund and colleagues have addressed the questions posed by the presence

of multiple Cpn60 proteins and their state of oligomerisation by undertaking a detailed genetic and biophysical characterisation of the chaperonins from M. tuberculosis and M. smegmatis (Fan et al., 2012). These studies present evidence supporting the evolution of novel function for the cpn60.1 genes and show that the cpn60.2-encoded proteins are highly likely to function as oligomers in vivo as they assemble into oligomers in the presence of high salt and nucleotides. They also show that Cpn60.2 from both M. tuberculosis and M. smegmatis

is able much to replace GroEL in E. coli, when expressed with either the cochaperonin GroES or the cognate cochaperonin Cpn10. However neither Cpn60.1 nor Cpn60.3, a third chaperonin homologue found in M. smegmatis, was able to complement GroEL in E. coli. These studies also addressed the question of oligomerisation using a number of biophysical techniques and confirmed earlier structural studies showing that, under normal physiological conditions, the purified chaperonins are largely monomers or dimers (Qamra et al., 2004; Fan et al., 2012). However, as monomeric GroEL is nonfunctional (Hartl & Hayer-Hartl, 2002), they examined oligomer formation under a range of conditions and showed oligomerisation in the presence of high concentrations of ammonium salts and either ATP or ADP. Under these conditions, the ATPase activity of the chaperonins increased and the oligomers formed had molecular masses consistent with the typical GroEL tetra-decameric structure of a double ring with seven subunits each. Finally, they showed that substitution of the 22 amino acids at the N-terminus of cpn60.

On arrival, they still complained of itching, episodes of cough, and weakness. P.F. also showed transient urticaria. Eosinophilia was still present (absolute count 8,270 mm−3, 55% for S.F. and 8,700 mm−3, 60% for P.F.). Rhabditoid larvae of S stercoralis were found in one of five stool samples provided Pifithrin-�� ic50 by S.F. but in none of the five samples provided by P.F. (using

Ritchie’s fecal enrichment technique). Serology (an in-house IFAT for S stercoralis, with 97.4% sensitivity and 97.9% specificity),6 was positive, at minimum titer (ie, 1/20), only for S.F., whereas P.F. had a negative result. Fecal culture for S stercoralis resulted positive for both. Patients were treated with ivermectin, 200 µg/kg/d for 2 days, repeated after 1 month. All clinical signs disappeared. After 6 months, both patients were asymptomatic, with normal eosinophil count. Serology was found positive at minimum titer (1/20 ) in both patients 1 month after discharge and resulted

negative 3 and 6 months after treatment. We describe here the clinical and biological characteristics of acute strongyloidiasis, in a couple of travelers. This early invasive phase of human strongyloidiasis has never been reported in clinical settings, to our knowledge. Our two patients give the opportunity to more precisely describe this phase of the disease. Strongyloidiasis was probably acquired in Thailand Ibrutinib clinical trial where the disease prevalence, depending on the diagnostic technique and population under study, ranges from 2.3 to 19.2% (respectively in schoolchildren from West-Central Thailand and Thai workers who pursue overseas employment).7,8 Patients did not visit any other disease-endemic country before. We identified Koh Samui Island as the most likely site of infection. Indeed no bare skin exposure to humid soil was reported by the patients in Apulia where they came Isoconazole from or during travel in Malaysia, Singapore, and Bangkok where the patients always wore shoes. In contrast, during the last 4 days spent in the tourist resort in Koh Samui Island, they reported walking barefoot on the

grass around the bungalow. As Koh Samui is a very important touristic place, we may assume that other exposed travelers could have similarly acquired strongyloidiasis, an infection which goes largely under-reported. Little is known about the clinical manifestations of acute strongyloidiasis. Freedman gives a description of experimental infections in humans.9 Interestingly, he noticed a transient skin reaction at the site of larval entry that appears almost immediately after exposure to the larvae and lasted 1 to 21 days depending on the study. Within 10 days after exposure, a larval migration syndrome or Loeffler’s-like syndrome with pulmonary symptoms (cough, tracheal irritation, and asthma) and skin signs (acute urticaria and itching) may occur.

The additional M184I mutation was observed in the plasma RNA but not in the proviral DNA, and confers high-level resistance to 3TC. This patient was treated with d4T, abacavir (ABC) and LPV/r combination therapy for 1 year before being changed to a 3TC+TDF+LPV/r regimen because of poor compliance.

Patient 33 had the M46M/I mixed population in the PR gene at the therapy-naïve stage. The plasma viral load was undetectable under HAART in most cases, GSK-3 beta pathway but follow-up analysis of the proviral resistance mutations showed the presence of mutations detected at the therapy-naïve stage without additional mutations, except in the sequence from patient 36. Overall, comparison of resistance mutation patterns in GSK2118436 ic50 CD4 cells with plasma RNA data or follow-up data for CD4 cells revealed similar results for the RT and PR genes, with one or two discrepant mutations. The analysis of DNA resistance evolution in all treated patients showed that the proportion of new mutations was 22%

(n=6) (P<0.0001 for the difference from 0), and these included three new key mutations. However, the appearance of new mutations was not correlated with the time elapsed between sample collections. A logistic regression was performed and a P value of 0.34 [unitary odds ratio (OR) 1.03; global OR 3.24] was obtained. All the other covariates (patient characteristics and use of antiretroviral therapy) were found not to influence the incidence rate of new mutations. The comparison of pre-HAART RNA genotyping with post-treatment DNA sequencing gave calculated prevalences of detected Cyclin-dependent kinase 3 mutations of 59 and 78%, respectively. The proportion of detected mutations (19%) in the DNA was significantly higher than in the pre-HAART RNA by the χ2 test

(P<0.0001), with moderately good agreement between the two methods in terms of the number of detected mutations (kappa coefficient 0.56). A kappa coefficient of 0.50 indicated moderately good agreement in terms of predicted drug activity between the pretreatment RNA and pretreatment DNA mutation profiles, and a kappa coefficient of 0.40 indicated only fairly good agreement between the pretreatment RNA and post-treatment DNA mutation profiles, as a result of the accumulation of new mutations. Genotyping for HIV-1 drug resistance mutations is routinely performed on a plasma sample. At present, guidelines do not recommend HIV-1 drug resistance testing on cellular proviral DNA. The proviral compartment archives the various strains, either wild-type or drug-resistant, that arise during infection. The long-term persistence of archived drug-resistant DNA may jeopardize the efficacy of targeted drugs, and represents the ‘resistance potential’ profile of a patient [40]. This is important when switching antiretroviral agents or initiating treatment in patients without available historical data or conserved samples.

, 2012). One of the differences

between CYT ASW and LN ASW media is the presence of tryptone and yeast extract in CYT ASW. The importance of these factors was tested by adding tryptone or yeast extract at the same proportion (0.5 or 1.0 g L−1) as in CYT ASW medium. For those media (LN Ye ASW and LN Tryp ASW), iridescence profiles were similar to those observed on CYT ASW or MA. Gliding motility was visible for iridescent colonies after 72 h of growth. Cellulophaga lytica is potentially exposed to salinity variations and hypersaline conditions in its biotope. As shown in Table 2B, C. lytica’s iridescence was conserved even at high (sub-lethal) NaCl concentrations. As growth was inhibited under hypersaline conditions, red iridescence was more visible. Changes in agar Androgen Receptor high throughput screening concentration potentially affect several HKI-272 molecular weight physico-chemical parameters such as moisture, hydrostatic and osmotic pressures, and solidity of the surface. On soft agar plates (0.25–0.50%), colonies had a particular smooth aspect and no iridescence

was observed (Fig. 4). However, after 72 h of growth on 0.5% agar plate, iridescence could be observed on the inner part of the colony. In this specific condition, a second phase of growth and gliding motility may occur on older cells used as a support. The optimum agar concentration was 1.5%. At concentration higher than 2.0%, growth was lowered and Bumetanide no iridescence was observed. These conditions were favorable for agarolysis but unfavorable for gliding motility. Natural or in vitro conditions that favor or inhibit the unique iridescence of C. lytica colonies are unknown. We thus examined the effect of key environmental factors to determine the possible conservation of the iridescence in the natural environment. Cellulophaga lytica is a nonphotosynthetic bacterium which potentially encounters a plethora of light or dark conditions in its natural habitats (tidal flats, rocks,

pelagic zones…). Accordingly, we found that C. lytica’s iridescence seems biologically uninfluenced by light exposure, even if light is physically essential for the phenomenon. Drop tests permitted to follow colors’ apparitions linked with population density level. Under growth-limited conditions (e.g. 24 h under hypoxia), low cell density colonies appeared red. A higher cell density was needed to generate bright green-dominant iridescence. However, iridescence could be lost in the inner parts of the colonies, may be owing to an altered physiology of the older cells or a too high cell density. As already described in higher organisms, changes in the color of iridescence are owing to modifications in structure dimensions. Such hypothesis is currently being investigated in C. lytica in our laboratory. Interestingly, seawater was required for iridescence. The only presence of seasalts with agar (LN ASW medium) allowed both growth and iridescence.

Such recovery appears to be complete, as the acuity of the deprived eyes following treatment is indistinguishable from that typical of a normal eye. Finally, we investigated whether the treatment with valproic acid was able to increase histone acetylation in the visual cortex by Western blot using antibodies for histone H3 and its Lys 9 acetylated form. Fig. 4

shows that robust acetylation could be observed in tissue samples of the visual cortex 2 h after an i.p. injection of valproic acid, either in naïve rats or at the end of http://www.selleckchem.com/products/AG-014699.html the protocol of VPA treatment lasting 25 days used for the behavioral experiments (Kruskal–Wallis one-way anova, H2 = 10.677, P = 0.005; post hoc Dunn’s test, chronic Trametinib molecular weight valproic versus vehicle, P < 0.05; acute valproic versus vehicle, P < 0.05. Vehicle, n = 6 samples; acute valproic acid, n = 4 samples; chronic valproic acid, n = 6 samples). These data indicate that the amount of histone acetylation induced in the visual cortex by a VPA i.p. injection remained constant for the whole duration of the treatment. The main finding of this study is that visual acuity of the amblyopic eye recovered to normal values in rats treated with HDAC inhibitors.

This effect could be observed both with electrophysiological and behavioral techniques. In saline-treated rats, no spontaneous recovery of visual acuity was present, in agreement with previous studies showing little

or no increase in visual acuity after reopening the deprived eye in adult rats (Prusky et al., 2000; Iny et al., 2006; Pizzorusso et al., 2006; He et al., 2007; Sale et al., 2007; Maya Vetencourt et al., 2008; Morishita & Hensch, 2008). Studies performed in kittens have shown that the recovery of deprived eye acuity achieved with RS during the SP can occur in concomitance with an impairment of visual acuity of the previously nondeprived Montelukast Sodium eye (Kind et al., 2002). Intriguingly, our VEP acuity data indicated that visual acuity of the nondeprived eye was not affected by visual deprivation induced by the RS procedure in HDAC inhibitor-treated animals. Although it is not known whether RS during the SP causes an impairment of visual acuity of the previously nondeprived eye also in rats, it could be possible that the increased plasticity induced by HDAC inhibitors do not entirely reinstate the plasticity present during the SP. To inhibit HDACs we used valproic acid, a drug that has different targets in neuronal cells other than HDACs. In particular, valproic acid is a clinically used anticonvulsant and mood stabilizer in bipolar disorder and is known to elevate levels of the inhibitory neurotransmitter GABA by direct inhibition of GABA transaminase and succinic semialdehyde dehydrogenase, which are enzymes responsible for GABA breakdown.

1 mM. The O2 uptake rate was expressed as nanomoles per minute per milligram of protein. The rates were corrected for endogenous oxygen consumption. Cells grown in MSM in the presence of phenanthrene (1 g L−1) were harvested at the mid-exponential phase by centrifugation at 8000 g for 10 min at 4 °C. The pellet was washed twice with 10 volumes of 50 mM potassium phosphate buffer (pH 7.2) and resuspended in two volumes of the same buffer. The cell suspension was ultrasonicated (Labsonic-L, Braun Biotech International) for 10 min at 4 °C in 10 pulses and then centrifuged at 20 000 g for 20 min at 4 °C. The supernatant was used as cell-free enzymes for further studies. Protein was measured using the Bradford method

(1976) with bovine serum albumin as the standard. The enzymatic transformations of various substrates were carried out by recording DAPT nmr cell-free-extract-catalyzed changes in UV-visible spectra on a Cary 100 Bio UV-visible spectrophotometer

(Varian Australia Pty Ltd) using 1 cm path-length quartz cuvettes. The sample and reference cuvettes contained 50 mM potassium phosphate buffer (pH 7.0) in 1-mL volume. The sample cuvette also contained either 2-hydroxy-1-naphthoic acid (50 nmol), salicylaldehyde (50 nmol) or catechol (30 nmol). Data were analyzed using the Varian Cary win uv Scan application software. The metabolites were resolved mTOR inhibitor by HPLC using a Shimadzu model LC20-AT pump system (Shimadzu Corp., Kyoto, Japan) equipped with a diode array model SIL-M20A detector and an analytical Phenomenex C18 reverse-phase column (Phenomenex Inc., Torrance, CA) attached to a model SIL-20A autosampler. Metabolites were eluted at a flow rate of 1 mL min−1 and detected at 254 nm. UV-visible absorbance spectra were obtained online. The biodegraded products of phenanthrene were eluted with a methanol–water gradient as follows: an initial gradient

from 50 : 50 to 95 : 5 (v/v) in 45 min, isocratic for the next 10 min and then back to 50 : 50 (v/v) in 5 min, followed by isocratic for further 3 min. Metabolites were identified by comparing their retention times with those of the authentic compounds 17-DMAG (Alvespimycin) HCl analyzed under the same set of conditions. GC-MS analysis of phenanthrene and its degradation products was performed using a Thermo Scientific model TraceGC Ultra column (Thermo Fischer Scientific Inc., NYSE: TMO) with a model PolarisQ mass spectrometer equipped with a 30 m × 0.25 mm (0.25 μm film thickness) DB-5MS capillary column. The ion source was maintained at 230 °C and both the inlet temperature as well as the transfer line temperature were maintained at 280 °C. The temperature program gave a 2-min hold at 70 °C, an increase to 200 °C at 10 °C min−1, followed by hold for 1 min at 200 °C, further increase to 325 °C at 5 °C min−1 and a 15-min hold at 325 °C. The injection volume was 1 μL, and the carrier gas was helium (1 mL min−1). The mass spectrometer was operated at an electron ionization energy of 70 eV.

This raises the possibility that a number of different protein families can bind and modulate the activity of FtsZ and/or MreB. The interaction between YgfX and MreB, however, could not be detected by Y2H in this study. It is likely because of the presence of large activating or BD, fused to N-terminal of YgfX and MreB, respectively. It is equally possible that the lack of the interaction is because of the low expression of YgfX in yeast. It was previously shown that the apparent interaction

between YeeV and MreB was 10-fold less than the interaction between YeeV BKM120 in vivo and FtsZ (Tan et al., 2011). In the case of YgfX, even the interaction with FtsZ, measured by β-galactosidase assay, was not as strong as the interaction between YeeV and FtsZ (data not shown). This apparent weaker interaction is unlikely due to a weak physical binding of YgfX with target proteins in E. coli, as the rate at which YgfX and YeeV cause morphological defects in E. coli was approximately the same. Commonly, the regulation of the toxin activity occurs in two different ways: one through physical sequestration of toxin by antitoxin and the other by the autoregulatory mechanism of the toxin gene by the TA complex (Zhang et al., 2003; Makarova et al., 2006; Motiejūnaite et al., 2007). Although the toxicity of YgfX was neutralized by the co-expression of YgfY, the mechanism of how YgfY neutralizes

the YgfX toxicity remains unknown. Interestingly, we could not detect the physical interaction between YgfX and YgfY, suggesting that YgfY may exert its antitoxin function at the level of transcription or by an unknown mechanism; notably, the X-ray structure of YgfY has been determined (Lim et al., 2005), selleck screening library predicting that YgfY is a DNA-binding protein. These observations are also similar to what was observed for yeeUV; YeeU and YeeV Nitroxoline do not physically interact. The mode of neutralization of YeeV toxicity by YeeU is also predicted to involve the regulation at the level of transcription (Brown & Shaw, 2003). Intriguingly, despite the lack of sequence similarity, YgfX and YeeV show the same mode of toxicity, and YgfY and YeeU share a similar mode of antitoxin mechanism. Interestingly,

however, YeeV is a soluble protein, while YgfX is an inner membrane protein. Based on this different localization pattern, it is possible that YgfX may be able to exert its toxic function in a more specified manner than YeeV, as discussed above. Further study is necessary to characterize the physiological role of ygfYX. So far, no phenotype has been shown to be associated with the deletion of ygfYX. We speculate that this TA system may be involved in cell growth regulation under stress conditions, as in other TA systems. For instance, the expression of YgfYX is affected by norfloxacin, an inhibitor of DNA gyrase (Jeong et al., 2006). It is interesting to further investigate the importance of YgfYX under such conditions. The authors thank Dr Peter Tupa for critical reading of the manuscript.