Although some bacterial OTUs were detected on seeds, cotyledons a

Although some bacterial OTUs were detected on seeds, cotyledons and plants, the breadth of new sequences indicates the importance of multiple sources outside the seed in shaping phyllosphere PD-1 inhibitor community. Most classified sequences were from previously undescribed taxa, highlighting the benefits of pyrosequencing in describing seed diversity and phyllosphere bacterial communities.

Bacterial community richness increased from 250 different OTUs for spinach seeds and cotyledons, to 800 OTUs for seedlings. To our knowledge this is the first comprehensive characterization of the spinach microbiome, complementing previous culture-based and clone library studies. “
“Horizontal gene transfer by conjugation is common among bacterial populations in soil. It is well known that the host range of plasmids depends on several factors, including the identity of the plasmid host cell. In the present study,

however, we demonstrate that the composition of the recipient community is also determining for TSA HDAC order the dissemination of a conjugative plasmid. We isolated 15 different bacterial strains from soil and assessed the conjugation frequencies of the IncP1 plasmid, pKJK10, by flow cytometry, from two different donors, Escherichia coli and Pseudomonas putida, to either 15 different bacterial strains or to the mixed community composed of all the 15 strains. We detected transfer of pKJK10 from P. putida to Stenotrophomonas rhizophila in a diparental mating, but no transfer was observed to

the mixed community. In contrast, for E. coli, transfer was observed only to the mixed community, where Ochrobactrum rhizosphaerae was identified as the dominating plasmid recipient. Our results indicate that the presence of a bacterial community impacts the plasmid permissiveness by affecting the ability of strains to receive the conjugative plasmid. Horizontal gene transfer (HTG) is a driving force in bacterial evolution as it allows bacteria to rapidly acquire complex new traits. Plasmids are one of the key vectors of HTG, enabling genetic exchange between bacterial cells mafosfamide across species and domain barriers (Poole, 2009; Boto, 2010), and they very often encode genes that confer adaptive traits to their host, such as antibiotic resistance, biodegradation pathways and virulence (de la Cruz & Davies, 2000). Transfer of these traits by conjugation requires the donor and the recipient cells to be in direct contact. Different abiotic and biotic factors affect the range of conjugal exchange of genetic material between environmental bacteria, such as nutrient availability, spatial architecture of the bacterial community, plasmid donor and recipient relatedness and plasmid host type (van Elsas & Bailey, 2002; De Gelder et al., 2005; Sørensen et al., 2005; Seoane et al., 2011). The fraction of the cells in a community capable of receiving and maintaining conjugative plasmids is highly dependent on several of these factors and has been described as the plasmid permissiveness (Musovic, 2010).

CPs (n = 22) were recruited through professional pharmacy network

CPs (n = 22) were recruited through professional pharmacy networks. The evaluation had five component phases: prospective audit of emergency supply requests for prescribed medicines; interviews by five PRs with community pharmacist (CP) service providers; follow-up interviews with service users recruited by CPs; interactive feedback sessions (undertaken by seven PRs) with local medical practice teams; and a wider stakeholder workshop. Data from all phases provide an understanding of the service from multiple perspectives, enhancing the validity and reliability of the study outcomes. A favourable opinion was received by NHS and University Ethics Committees.

Twenty-two pharmacies in North West England participated in the study with diversity in ownership type, location and opening hours as well as in pharmacist experience, gender and length of time since selleck products registration. Clinical audit data revealed the extent of emergency

supply activity, with a total of 526 medicines items requested by 450 patients over two 4-week periods. Trends show peak periods over the Bank Holiday, either side of the weekend and at weekend-opening pharmacies. Higher proportions of requests were made for older patients and for medicines used in long-term conditions, broadly mirroring the demographics and therapeutic areas for all prescriptions. Patient difficulties in renewing repeat medication was a major reason for requests and the majority high throughput screening assay of medicines are ‘loaned’ to the patient

in anticipation of a NHS prescription. Subsequently, views were elicited from 26 CPs with experience of dealing with requests for emergency supplies; 25 service-users who received an emergency supply of prescribed medicine; staff at 6 medical practices; and 11 stakeholders with a wider knowledge of pharmacy, healthcare services and policy across the North West. Data from service providers and users indicated a positive impact on medicines adherence through continuation of supply, with Molecular motor no need to access out-of-hours or urgent care services. CP, medical practice and wider stakeholders supported provision of emergency supplies being established as a formal NHS service at community pharmacies as in Scotland. This research indicates that community pharmacies are providing an important service which ensures continued prescribed treatment and reduces overall burden to the wider NHS, particularly out-of-hours and urgent care services. Commissioners are urged to recognise this opportunity to utilise pharmacists’ expertise beyond routine dispensing and supply of medicines and the advantages of establishing a national, NHS emergency supply service from community pharmacies. 1. Statutory Instruments. The Human Medicines Regulations 2012 No.1916. London: The Stationery Office; 2012. 2. Royal Pharmaceutical Society. Medicines, Ethics and Practice: The Professional Guide for Pharmacists. Number 37. London; 2013. I. Altmana,b, A. MacAdama, G.

2C), but not subtypes without the splice site 4 insert The speci

2C), but not subtypes without the splice site 4 insert. The specific interaction with NRXs containing the splice site 4 insert was also observed by the immunoblot analysis (Fig. 2A). In contrast, the extracellular domain of LRRTM2 fused to the Fc fragment (LRRTM2-Fc) bound to HEK293 cells expressing NRX1β(S4−), but not to cells expressing NRX1β(S4+) (Fig. 2D). The extracellular domain of NL1(−) fused to the Fc fragment, i.e., NL1(−) Fc, bound to HEK293 cells expressing NRX1β(S4−) or NRX1β(S4+) (Fig. 2D). The addition of HA-Cbln1, but not HA-CS-Cbln1, significantly inhibited the binding

between NL1(−)-Fc and NRX1β(S4+), whereas it did not affect the binding between NL1(−)-Fc and NRX1β(S4−) (Fig. 2E). Together, these results indicate that, unlike LRRTM2 and NL1(−), hexametric Cbln1 binds to α- and β-isoforms of Everolimus datasheet NRXs in a manner I-BET-762 solubility dmso dependent on the splice site 4 insert, which probably determines the interaction

with Cbln1. The binding of NLs and LRRTMs to NRXs has been reported to require extracellular Ca2+ (Ko et al., 2009; Siddiqui et al., 2010), which binds to the interface between these molecules (Koehnke et al., 2008). To examine whether the binding of Cbln1 to NRX(S4+) was also sensitive to extracellular Ca2+, we performed a cell-based binding assay in a medium containing low (56 nm, according to Ca-ethylene glycol tetra-acetic acid calculator) (Schoenmakers et al.,

1992) Ca2+ concentrations. The binding of NL1(−)-Fc to HEK293 cells expressing NRX1β(S4+) under normal Ca2+ concentrations completely disappeared under low Ca2+ concentrations (Fig. 3A and B). Similarly, the binding of LRRTM2-Fc to NRX1β(S4−) was completely inhibited under low Ca2+ concentrations (Fig. 3C and D). In contrast, binding of Cbln1 to NRX1β(S4+) was observed even under low extracellular Ca2+ concentrations (Fig. 3E and F), suggesting that the mode of interaction between NRX1β(S4+) and Cbln1 was distinct from that between NRX1β(S4+) Phosphoprotein phosphatase and NL1(−). To further confirm the distinct binding mode of Cbln1 to NRX1β(S4+), we mutated Ca2+ binding sites of NRX1β(S4+) (Fabrichny et al., 2007; Reissner et al., 2008). Even under normal extracellular Ca2+ concentrations, NL1(−)-Fc did not bind to HEK293 cells expressing NRX1β(S4+)N238A in which an alanine residue replaced an asparagine residue at position 238 or cells expressing NRX1β(S4+)D137A in which an alanine residue replaced an aspartate residue at position 137 (Fig. 3B and G). In contrast, HA-Cbln1 bound to HEK293 cells expressing NRX1β(S4+)D137A or NRX1β(S4+)N238A in a manner similar to cells expressing wild-type NRX1β(S4+) (Fig. 3F and H). To examine whether Ca2+ concentrations did not affect the direct binding between Cbln1 and NRX1β(S4+), we performed an in vitro binding assay using HA-Cbln1 and NRX1β(S4+)-Fc or CD4-Fc.

[21-24] Moreover and to the best of our knowledge, there has neve

[21-24] Moreover and to the best of our knowledge, there has never been a published case of selleck inhibitor a travel-related death in a healthy person who has received appropriate PrEP in an industrialized country rather than a developing country.[32] If using the same principle as that used for animal handlers, many of these travel-related rabies deaths could have been prevented

with adequate PrEP using a WHO- recommended regime without necessarily receiving appropriate rabies PEP. Thus, providing rabies PrEP may do more than simplify the post-exposure management of the exposed traveler. Using animal bites and rabies exposure as an illustration, we can see that the assessment of travel-related risk and uncertainty is a complex process requiring effective risk communication between the provider and traveler. The pre-travel encounter should start with a “risk conversation.” More effort needs to be directed to this core function of travel medicine practice, but research MLN0128 mw such as that by Rossi and Genton is a good

start.[8] The author states that he has no conflicts of interest to declare. “
“Background. Travelers with diabetes mellitus to developing countries are thought to have symptomatic infectious diseases more often and longer than travelers without diabetes. Evidence for this is needed. This study evaluates whether travelers with diabetes are at increased risk of symptomatic infectious diseases. Methods. A prospective study was performed between October 2003 and February 2008 among adult medication-dependent travelers with diabetes, with their healthy travel companions without diabetes serving as matched controls. Thus, travelers with diabetes and controls were assumed to have comparable exposure to infection. Data on symptoms of infectious diseases were recorded by using mafosfamide a structured diary. Results. Among 70 travelers with insulin-dependent

diabetes, the incidence of travel-related diarrhea was 0.99 per person-month, and the median number of symptomatic days 1.54 per month. For their 70 controls, figures were 0.74 and 1.57, respectively (p > 0.05). Among 82 travelers with non-insulin-dependent diabetes, incidence was 0.75, and the median number of symptomatic days was 1.68. For their 82 controls, figures were 0.70 and 1.68, respectively (p > 0.05). As for other symptoms, no significant travel-related differences were found. Only 17% of travelers with diabetes suffering from diarrhea used their stand-by antibiotics. Conclusions. Medication-dependent travelers with diabetes traveling to developing countries do not have symptomatic infectious diseases more often or longer than travelers without diabetes.

This classification of amygdala subregions into a corticomedial a

This classification of amygdala subregions into a corticomedial and a basolateral part is reasonable from a functional perspective (Maren & Quirk, 2004; LeDoux, 2007; Ehrlich et al., 2009; Pape & Pare, 2010) and in terms of comparability to the few existing fMRI studies that previously reported functional dissociations of amygdala subregions in humans on the basis of high-resolution selleck products fMRI (Davis

et al., 2010; Gamer et al., 2010; Bach et al., 2011; Boll et al., 2011; Prevost et al., 2011). The US expectancy ratings as well as the SCRs indicated that volunteers successfully learned the CS–US contingencies (see Figs 2A and B). A 2 × 3 repeated-measures anova with factors phase (acquisition and reversal) and condition (CS–, CS50 and CS100) revealed a significant phase-by-condition interaction for behavioural (F2,40 = 107.05, P < 0.001) and autonomic (F2,36 = 9.06, P < 0.01) measurements. During acquisition, the averaged expectancy ratings were significantly higher for CS50 as compared with CS– (t20 = 7.55, P < 0.001) and the highest values were observed

CT99021 price in the CS100 condition differing significantly from CS– and CS50 expectancy scores, respectively (CS100 >  CS–: t20 = 21.39, P < 0.001; CS100 >  CS50: t20 = 6.55, P < 0.001). In the reversal stage, US expectancies were successfully reversed in accordance with the new contingency affiliations (new CS100 >  new CS–: t20 = 13.68, P < 0.001; new CS100 > new CS50: t20 = 6.58, P < 0.001; new CS50 >  new CS–: t20 = 3.23, P < 0.01). Likewise, the SCRs were higher for CS100 and CS50 as compared with CS– during acquisition (CS100 >  CS–: t18 = 2.84, P < 0.05; CS50 >  CS–: t18 = 4.04, P < 0.001). The SCRs did not differ significantly from each other in the CS100 and CS50 condition (t18 < 1). In the reversal stage, greater SCR amplitudes to the new CS50 were observed as compared with the new CS– (t18 = 2.49, P < 0.05), but no significant difference was found for a comparison of the new CS100 vs. the new CS– (t18 < 1). We suppose that this latter finding is related to a general habituation effect of SCRs

over time (main ALOX15 effect phase: F1,18 = 6.35, P < 0.05). Just as during acquisition, no significant difference was observed for a comparison of the new CS100 and the new CS50 condition in the reversal stage (t18 < 1). Table 1 summarizes the fit parameters and model deviances for the baseline, the RW and the hybrid model for all fitting procedures applied. As the results show, the RW and the hybrid model outperformed the random baseline model. Furthermore, the hybrid model provided a significantly more accurate explanation of behaviour than did the RW model if fitted across conditions (Table 1A), and if each of the conditions was fitted separately to the data (Table 1B). Comparing both fitting alternatives against each other showed that the condition-wise fitted hybrid model provided the best behavioural fit (Table 1C).

These two sequences were flanked by SbfI and SfiI restriction sit

These two sequences were flanked by SbfI and SfiI restriction sites, and separated in between by two nonidentical FauI restriction

sites. The three roGFPs were amplified by PCR, adding the respective FauI sites. These constructs were then ligated between the KAR2 leader and the HDEL sequences, and introduced into the same pPuzzle vector as that used for the cytosolic expression. The integration locus for the ER constructs was the 5′ region of the P. pastoris enolase gene. The plasmid containing the gene PDI1 (encoding protein disulfide isomerase; Inan et al., 2006) was generated by PCR using P. pastoris genomic DNA as a template and SbfI and SfiI as restriction sites. The gene was cloned into a pPuzzle vector containing the Zeocin resistance marker, and was expressed under the control of the GAP1 promoter. The vector was integrated into the native PDI1 gene locus see more of the P. pastoris genome after linearization in the respective sequence. Electrocompetent P. pastoris host strains were transformed using a BioRad Minipulser. Conditions for the pulsing included a cuvette with a 2-mm gap, a charging voltage of 2000 V and a pulse length of 4 ms. After 2-h regeneration on YPD (per liter: 20 g yeast extract, 10 g soy peptone, 20 g glucose), cells were cultivated for 48 h and at 30 °C on YPD-agar KU-57788 plates (per liter: 20 g yeast extract, 10 g soy peptone, 20 g glucose, 20 g agar-agar) containing 25 μg mL−1

Zeocin or 100 μg mL−1 Hygromycin (both Invivogen), respectively. Shake-flask experiments were carried out in 100-mL shake flasks incubating at 28 °C at 170 r.p.m. For each strain, 12–15 individual clones were used to inoculate 10 mL of freshly prepared minimal medium. The medium used in these experiments was M2 minimal medium containing per liter: 20 g of glucose, 20 g of citric acid, 3.15 g of (NH4)2HPO4, 0.03 g of CaCl2·2H2O, 0.8 g of KCl, 0.5 g of MgSO4·7H2O,

2 mL of biotin (0.2 g L−1) and 1.5 mL of trace salts stock solution. The pH was set to 5.0 with 5 M KOH solution. Trace salts stock solution contained per liter: 6.0 g of CuSO4·5H2O, Phosphatidylethanolamine N-methyltransferase 0.08 g of NaI, 3.0 g of MnSO4·H2O, 0.2 g of Na2MoO4·2H2O, 0.02 g of H3BO3, 0.5 g of CoCl2, 20.0 g of ZnCl2, 5.0 g of FeSO4·7H2O and 5.0 mL of H2SO4 (95–98% w/w). A protocol for the determination of the redox state using rxYFP in S. cerevisiae (Ostergaard et al., 2004) served as a template for the establishment of a redox-measuring procedure in living P. pastoris cells. The culture (840 μL) with an OD of approximately 30 was used for determination of the redox ratio. Redox measurements in the cytosol were performed with and without addition of the cell-solubilizing agent digitonin. Comparison of both experiments yielded the same results; therefore, further experiments were performed without digitonin. For the ER, digitonin was not added to the cells, because it would lead to a whole-cell lysis, which was not desirable in this case.

The volume corresponding to 200-μg protein from the cytosols was

The volume corresponding to 200-μg protein from the cytosols was loaded from the culture media, cytosols, and cell walls in 6.5% polyacrylamide gels to perform the electrophoresis. The α-HA and α-Cdc2 antibodies were used at a 1 : 5000 dilution. In order to gain information about the requirements for agglutination, the AI of spk1Δ, spm1Δ, dni1Δ, cfr1Δ, sec8-1, and exo70Δ mutants induced to mate in liquid medium was estimated. Wild-type

(WT) and map4Δ strains were used as controls. As shown in Fig. 1a, in the cultures from the BGB324 order dni1Δ and exo70Δ mutants, agglutination took place as efficiently as in the WT. In the case of the cfr1Δ and spm1Δ mutants, the AI was lower than that in the WT; however, mating aggregates were observed in these cultures, indicating that agglutination had taken place. The AI for the spk1Δ and the sec8-1 mutants was similar to that of the negative control map4Δ (Fig. 1a). We then determined whether the agglutination efficiency was correlated with the level of Map4p by observing under the fluorescence microscope cells from the mutants and the WT strain that had been induced to mate in liquid medium. Map4p localizes at the tip of the shmoos and at the mating bridge of the zygotes in the WT strain (Sharifmoghadam et al., 2006; Sharifmoghadam & Valdivieso, 2008). As shown in Fig. 1b, Map4p was readily observed in the cfr1Δ, exo70Δ, spm1Δ, and dni1Δ

mutants; agglutinin exhibited a weak fluorescent signal in the sec8-1 cells, and it could not PD0325901 ic50 be observed in the spk1Δ cells. Western blot analyses were performed to determine the level of Map4p in the culture media, the cytosols, and cell walls of the Sucrase WT, exo70Δ, sec8-1, and spk1Δ cells more precisely. Map4p was not detected in the culture media from any of the strains (Sharifmoghadam & Valdivieso, 2008 and results not shown). As shown in Fig. 1c, the level of agglutinin in the cytosol from the WT and sec8-1 strains was low; it was undetectable in the spk1Δ strain, and was high in the exo70Δ strain. In the cell walls of the WT and exo70Δ strains, the level of Map4p was similar, while this level was lower

in the sec8-1 mutant and was undetectable in the spk1Δ mutant. These results suggest that in the WT strain, Map4p is incorporated rapidly into the cell wall, where the protein accumulates; thus, most of the protein is detected in the cell walls. In the exo70Δ mutant, Map4p incorporates into the cell wall less efficiently than in the WT strain, and so it accumulates in the cytosol, although the amount of agglutinin that accumulates in the cell wall is similar in both strains. In the sec8-1 mutant, a low amount of Map4p incorporates into the cell wall. All the above results showed that the MAP kinase Spk1p and the exocyst subunit Sec8p were required for proper Map4p synthesis and delivery to the cell wall, while the exocyst subunit Exo70p was not.

To investigate sodium-dependent growth, ‘sodium-free M9’ was prep

To investigate sodium-dependent growth, ‘sodium-free M9’ was prepared by replacing EPZ015666 ic50 all sodium salts in M9 (this is around 50 mM Na+ in normal M9) with their potassium equivalents and replacing agar with 0.8% agarose; the sodium-free M9 medium still contained approximately 50 μM sodium from the Amp used for selection. M9 agarose plates required longer incubation

times (up to 4 days) for single colonies to grow. All experiments involving the WT and the ΔnanT strains used cells transformed with the empty vector, i.e. pWKS30. The presence of the vector did not affect the growth phenotypes of either strain (not shown). Starter cultures were prepared as described for the growth experiments, except that o/n growths were carried out in M9 Amp supplemented with 2 mg mL−1 glucose and 1 mM IPTG. Overnight cultures were diluted to an OD650 nm of 0.1 in the

same medium and allowed to grow at 37 °C until they reached an OD650 nm of 0.5, when they were harvested, washed four times in M9, resuspended in the same buffer at a final OD650 nm of 3 and stored LDK378 clinical trial on ice till use. For Neu5Ac uptake assays, cells were diluted 10-fold in M9 prewarmed at 37 °C and allowed to acclimatize for 2 min, with stirring before initiating the assays by adding of varying amounts of [14C]-Neu5Ac (Sigma) appropriately diluted with unlabelled Neu5Ac. The uptake assay and total protein quantification were then performed as described in Severi et al. (2008), except that 200 μL of cell suspensions were immobilized instead of 400 μL. [14C]-Neu5Ac was normally used at a final concentration of 0.5–2 μM and isotopically diluted (up to 100 ×) with unlabelled Neu5Ac when required. Ks and Vmax values were calculated by fitting the experimental data for uptake rates to a hyperbolic Michaelis–Menton equation using sigmaplot. To assay sodium-dependent Neu5Ac uptake, cells were prepared as for a standard uptake assay, except that sodium-free M9 (see the previous section) was used as both washing and

assay buffers. Salts, i.e. NaCl, KCl and LiCl, were added at a final Adenosine concentration of 100 mM during the acclimitization phase. The assay was performed as described above with a concentration of 100 μM total Neu5Ac. Cold chase experiments were performed as described in Mulligan et al. (2009), using SEVY1 cells transformed with the appropriate plasmids. To assess the suitability of an E. coliΔnanT strain for the functional characterization of hypothetical Neu5Ac transporters, we first examined cells expressing either nanT itself or the known siaPQM TRAP transporter genes from H. influenzae cloned into a low-copy-number vector under the control of an IPTG-inducible promoter.

The PCR product was blunt-end cloned into the SmaI site of pWKS30

The PCR product was blunt-end cloned into the SmaI site of pWKS30 (Wang & Kushner, 1991) to form pYSCN. The ΔyscN mutant was made electrocompetent as previously described (Conchas & Carniel, 1990) and transformed with either vector alone or pYSCN. Transformants were selected by growth on LB Lennox agar with ampicillin (50 μg mL−1). The effect of growth on the parental, IWR-1 nmr ΔyscN mutant, and pLcr− strains by incubation at 37 °C with induction of the low calcium response (Straley et al., 1993) was monitored by optical density (OD620 nm). Strains were initially grown overnight at 28 °C in HI broth at 150 r.p.m. They were then diluted to an OD of approximately

0.05 in 50 mL of HI broth supplemented with either CaCl2 or MOX. The cultures were grown for 1 h at 28 °C and then elevated to 37 °C. At hourly intervals, the OD was determined. All growth curves were

performed in triplicate. Yersinia pestis strains were grown in HI broth at 28 °C for 8 h and then diluted 1/20 in HI broth containing MOX. The fresh cultures were grown for 1 h at 28 °C, switched to 37 °C, and grown overnight. The cultures were then pelleted, supernatants collected, and pellets washed. The pellets were then suspended in water with MPBio Lysing Matrix B (MP Biomedicals, Solon, NVP-LDE225 datasheet OH), bead beat for 40 s with a FastPrep FP120 Cell Disrupter (Thermo Fisher Scientific, Pittsburg, PA), chilled on ice, bead beat again for 40 s, microfuged for 5 m, and then filtered.

The preparation was then sterility checked by plating a portion of the sample on sheep blood agar plates. The Y. pestis supernatants and uninoculated HI broth + MOX were concentrated by passage through a centrifugal filter device (Amicon Ultra-10K; Millipore, Billerica, MA), heat fixed (95 °C for 30 min), and sterility checked as described above. The protein concentrations from the samples were determined using the BCA Protein Assay Kit (Pierce, Rockford, IL) as per the manufacturer’s recommendations. Sitaxentan Samples (approximately 1 μg in 2 μL) were spotted onto PVDF membrane. The membranes were blocked with 7% skim milk in PBS containing 0.1% Tween 20 (PBST). Monoclonal antibody to LcrV (DiMezzo et al., 2009) was used at a dilution of 1 : 5000 in PBST, and secondary rabbit anti-mouse horseradish peroxidase labeled antibody was used at a dilution of 1 : 5000. Reactions were visualized using 4-chloronaphthol/3,3′-diaminobenzidine (Thermo Fisher Scientific, Rockford, IL). The Y. pestis strains were prepared for mouse vaccinations or challenges as previously described (Anderson et al., 1996), except that the bacteria were suspended in 10 mM potassium phosphate buffered saline (KPBS) solution rather than HI broth. To demonstrate loss of virulence and complementation of the mutant, groups of 10 naïve female Swiss–Webster mice were challenged s.c. with CO92 wild type, ΔyscN, ΔyscN + pWKS30, or ΔyscN + pYSCN at 0.2 mL aliquots.

Between 24% and 41% of the respondents indicated their inability

Between 24% and 41% of the respondents indicated their inability to determine the appropriate treatment modality for children with high and low caries risk. Majority of the students failed to differentiate between the caries-preventive practice for children with high and low risk of caries: preventive strategies for children with high caries risk were also

used for those with low caries risk. Age, gender, knowledge of caries prevention measures, and self-perceived competency in providing caries-preventive care were not associated with student’s capacity to provide caries-preventive practice for children. PLX4032 price Caries-preventive practice among dental students in Nigeria could be improved. It may be important to explore the possible role of problem-based learning EPZ-6438 cost approach in addressing this challenge. Dental

caries has been defined as ‘localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation’[1]. Although the disease is not life threatening, it is a matter of great concern in dental public health circles because of its high prevalence in some of the developing countries[2, 3], its consequences such as pain and dysfunction, its impacts on the quality of life at all ages, and its social and economic burdens[4, 5]. The burden of caries is high among children living in Nigeria. Unfortunately, there is only one national study on the caries in children in Nigeria and this was conducted in 1995. The survey showed that 30% and 43% of 12- and 15-year-old children had caries. The DMFT for the 12- and 15- year-olds was 0.7 and 1.2 respectively, with very low level of restorative care[6]. The multiple regional studies in the Sclareol country continue to show that the prevalence of dental caries in the permanent dentition remains high ranging from 13.9% in Ile-Ife to 33.0% in Benin, 15.5% to 35.5% in Enugu, 5.7% to 30.8% in Lagos, and 11.2% in Ibadan[7-16] (O. O. Sofola, M. O. Folayan, A. B. Oginni, personal communication). In the primary dentition, the prevalence ranges from 10.9% in Ile-Ife to 6.4%

to 22.5% in Lagos[7, 8, 11, 15-18]. Not only is the prevalence high, the level of untreated caries in the permanent dentition is also high, ranging from 77.2% in Ile-Ife to 98.6% in Benin, and 49.5% to 85.5% in Enugu[7, 12-14]. In Lagos, the restorative index ranged from 0.3% to 1%[8, 16], whereas the treatment index is 5.7%[7]. The Met Need Index in Ibadan was 0.11[8]. The prevalence of untreated caries in the primary dentition also remained high ranging from 92% in Ile-Ife to 95.6% in Lagos[3, 7, 16, 18]. As implementation of a curative and restorative approach to combat dental caries at the population level does not appear to be cost-effective in many countries[5], the World Health Organization (WHO) has put more emphasis on prevention in setting global oral health goals for the year 2020[19].