Signals were passed through an impedance adapter Seliciclib price and were amplified 1000 × using a home-made amplifier. They were displayed on a Fluke Combiscope oscilloscope and fed to an analog–digital interface (CED 1401; Cambridge Electronic Design, Cambridge, UK) connected to a computer. Data were collected and analysed with Spike 2 software (Cambridge Electronic Design). After some recordings, slices were fixed for 60 min by immersion in a phosphate-buffered paraformaldehyde–picric acid solution [KH2PO4, 75 mm; NaH2PO4, 85 mm; paraformaldehyde, 4% (wt/vol); and saturated aqueous picric acid, 14% (vol/vol); pH 7.4]. The slices were then washed six to eight times and

kept overnight in a 0.1 m phosphate-buffered sucrose (PBS) solution [KH2PO4, 30 mm; NaH2PO4, 70 mm; supplemented with sucrose, 30%

(wt/vol); pH 7.4] before being stored at −20 °C in a cryoprotectant solution. The immunocytochemistry was performed on free-floating sections. Slices were washed overnight in PBS and then rinsed three times for 5 min in PBS. Endogenous peroxidases were inhibited by bathing slices in H2O2 (0.6% dilution in Crizotinib PBS) for 20 min followed by three rinses in PBS with 0.1% Triton (PBST) for 5 min. Slices were first incubated in normal goat serum, 5% in PBST, for 30 min, then in mouse anti-tryptophan hydroxylase (TPH; 1 : 1000; T0678 from Sigma–Aldrich) and Streptavidin–FITC (A/500; DakoCytomation, Denmark) for 36 h at 4 °C to detect TPH and biocytin, respectively. To follow TPH visualization, they were then washed three Rho times for 5 min in PBST, incubated for 1 h in a 1% blocking solution from the Tyramide Signal Amplification kit (Invitrogen), incubated for 4 h at room temperature with the goat anti-mouse antibody conjugated with HRP (1 : 100; from the Tyramide Signal Amplification kit, Invitrogen), rinsed three times for 15 min in PBST and incubated for 20 min at room temperature in Tyramide-Alexa 546 (1 : 100 in amplification buffer with 0.0015% H2O2). Finally, slices were rinsed three times for 5 min in PBS with Hoechst (1 : 6000),

mounted on microscope slides and coverslipped with Vectashield® Hard Set mounting Medium with DAPI (5H-150). Slices were observed using an Olympus Fluoview FV1000 confocal system equipped with an Olympus IX81 inverted microscope. Images were stored using ImageJ software. All data were analysed using Statistica° (Statsoft°, Tulsa, OK, USA) and are expressed as means ± SEM. Differences were considered significant at P < 0.05. Patch-clamp data were analysed using a Kruskal–Wallis test to compare several groups of values because of heterogeneity of the variances. A Mann–Whitney U-test was subsequently used as a post hoc test. Data from intracellular and extracellular experiments were analysed using mixed anovas.

multiformis: Nmul; Polaromonas: Pola. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Vibrio cholerae colonizes the human intestine and causes the acute diarrheal disease cholera. Flagellar-mediated

chemotaxis contributes to intestinal colonization as well as infectivity. The virulence-regulatory protein ToxT activates transcription of the genes encoding the major virulence factors cholera toxin and toxin coregulated pilus. ToxT additionally activates transcription of two genes, tcpI and acfB, located within the Vibrio Pathogenicity Island predicted to encode methyl-accepting chemoreceptors. find more We show that disruption of either tcpI or acfB individually does not noticeably affect V. cholerae intestinal colonization within the infant mouse, but disruption of both tcpI and acfB leads to a decrease in intestinal colonization. These results suggest that TcpI and AcfB may have overlapping or redundant chemotactic functions that contribute to V. cholerae intestinal GSK J4 colonization. Vibrio cholerae causes the acute diarrheal disease cholera in humans. The bacteria are acquired by the ingestion of contaminated water or food, and colonize the intestine. Vibrio cholerae expresses virulence factors

within the intestinal tract that lead to disease symptoms, most notably the cholera toxin (CT), which is responsible for the acute Urocanase watery diarrhea characteristic of cholera (Holmgren & Svennerholm, 1989). The organisms also express the toxin coregulated

pilus (TCP), a Type IV pilus that is required for intestinal colonization (Taylor et al., 1987). A regulatory cascade commonly referred to as the ToxR regulon coordinately regulates the expression of CT and TCP in response to environmental signals within the host (for a review, see Childers & Klose, 2007). Activation of the ToxR regulon culminates in the expression of the regulatory protein ToxT, which then directly activates transcription of the genes encoding CT and TCP (DiRita et al., 1991). The toxT and tcp genes lie within a cluster of horizontally acquired virulence genes in the Vibrio Pathogenicity Island (VPI) (Karaolis et al., 1998), while the ctx genes are within the lysogenic bacteriophage CTXφ (Waldor & Mekalanos, 1996). Bacterial chemotaxis is accomplished by a number of proteins that constitute a signaling cascade. Methyl-accepting chemoreceptors (MCP) are membrane-spanning proteins that undergo a conformational change upon binding a chemoattractant or a repellant, and this stimulates a signaling cascade that ultimately results in the formation of a phosphorylated chemotaxis protein CheY that interacts with the flagellum and switches the rotation from counterclockwise to clockwise (for a review, see Baker et al., 2006).

Conflicts of interest: SV has received travel grants from Abbott, BMS, Boehringer-Ingelheim, Gilead Sciences, Roche, Tibotec and ViiV Healthcare.

FW has received travel grants from Abbott, BMS, Boehringer-Ingelheim, Gilead Sciences, Roche, Tibotec and ViiV Healthcare. GM has received research grants from Abbott, Ardea Biosciences, Bionor, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Merck, Pfizer, Theratechnologies and Tibotec. He has received honoraria as a speaker and/or advisor from Astellas, Boehringer-Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, GSK126 solubility dmso Merck, Pfizer, Theratechnologies, Tibotec and ViiV Healthcare. FR received research funding or honoraria from, or consulted for, Bristol-Myers Squibb, Gilead Sciences and Roche. DJ has received

research grants from Tibotec, ViiV and Vertex. He has received honoraria as a speaker from Tibotec, BMS, Merck, BIPI and Gilead and as a consultant for Tibotec, Roche and Gilead. SM has received research grants from Roche and has served on advisory boards for ViiV, BMS and Gilead. He has received honoraria as a speaker from Roche, Tibotec, BMS and Gilead. CK has received travel grants, conference fees or consultancy fees from Abbott, Bristol-Myers Squibb, Gilead, GlaxoSmithKline, Janssen and MSD. MF has served as a scientific advisor for, and/or received honoraria for speaking engagements from, Abbott, Boehringer Ibrutinib molecular weight Ingelheim, Bristol-Myers Squibb, Gilead, GlaxoSmithKline, Theratechnologies, Rucaparib Tibotec and ViiV Healthcare. LS has received lecture fees, travelling expenses and payment of registration fees from Roche, Bristol-Myers Squibb, MSD, Gilead and Boehringer Ingelheim. DH has received research grants from Pfizer, Tibotec, Gilead and Bionor, and honoraria for advisory boards/consulting from Tibotec, Pfizer, ViiV, Gilead, Monogram and Merck. EDJ has served on the speakers bureau for Gilead Sciences, Merck, Tibotec and Virco and has received honoraria for consulting from Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Merck, Tibotec, and Vertex Pharmaceuticals. He has received research support from

Abbott Laboratories, Achillion, Avexa, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Hoffman LaRoche Laboratories, Merck, Pfizer, Schering Plough, Taimed, Tobira, Tibotec and Vertex. PR has served as a scientific advisor to Boehringer Ingelheim Pharmaceuticals, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Merck & Co., Theratechnologies, Tibotec Therapeutics and Tobira Therapeutics. He has served on data and safety monitoring boards and endpoint adjudication committees for Tibotec Therapeutics and has received honoraria for speaking engagements at scientific conferences from Boehringer Ingelheim Pharmaceuticals, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline and Theratechnologies.

The exact mechanism of the anti-inflammatory activity of S. boulardii extract is not clear. However, in light of these results, it is tempting to speculate that the leading mechanism involves the modulation of neutrophils’ response. IL-8 influenced only chemotaxis and the activation of neutrophils, while the spectrum of IL-1β activity is wide and includes the activation of T helper, NK cells

and macrophages, maturation and proliferation of B cells. Slight stimulation of IL-1β and IL-8 expression in Caco-2 cells by S. boulardii extract may not indicate an inflammatory reaction, but rather the stimulation of the host defense. Induction of IL-8 expression by nonpathogenic microorganisms such as Saccharomyces cerevisiae R428 in vitro (Saegusa et al., 2004, 2007) or Escherichia coli Nissle 1917 (Lammers et al., 2002) was shown previously, and is believed to be beneficial for the normal state of the host immune system preparing for pathogen infection. Further studies are needed to fully understand the mechanism of S. boulardii action against C. albicans hyphae formation and adhesion to intestinal cell lines. We are now determining the chemical structure of active molecule/s secreted by S. boulardii, which will BTK signaling inhibitors allow further elucidation of the mechanism of its biological activity. This work was partly supported

by a grant from Biocodex, France. “
“Normally, Lactobacillus brevis has two glutamate decarboxylase (GAD) genes; gadA and gadB. Using PCR, we cloned the gadA gene from L. brevis strain NCL912, a high yield strain for the production of gamma-aminobutyric acid (GABA). However, despite using 61 different primer pairs, including degenerate primers

from conserved regions, we were unable to use PCR to clone gadB from the NCL912 strain. Furthermore, we could not clone it by genomic walking over 3000 bp downstream of the aldo-keto reductase gene, a single-copy gene that is located 1003 bp upstream of gadB in L. brevis ATCC367. Altogether, the data suggest that L. brevis NCL912 does not contain a gadB gene. By genomic walking, we cloned regions upstream and downstream of the gadA gene to obtain a 4615 bp DNA fragment that included the complete gadA locus. The locus contained the GAD gene (gadA) and the glutamate:GABA antiporter gene (gadC), which appear to be Paclitaxel price transcribed in an operon (gadCA), and a transcriptional regulator (gadR) of gadCA. During whole fed-batch fermentation, the expression of gadR, gadC and gadA was synchronized and correlated well with GABA production. The gadA locus we cloned from NCL912 has reduced homology compared with gadA loci of other L. brevis strains, and these differences might explain the ability of NCL912 to produce higher levels of GABA in culture. “
“We studied the effect of hydrogen peroxide (H2O2) stress on the anaerobic sulfate-reducing bacterium Desulfovibrio vulgaris Hildenborough. In a lactate/sulfate medium, growth was affected from 0.1 mM H2O2 and totally inhibited at 0.7 mM.

The procedure is described as follows. Cells were grown in ASSPL to early log phase (OD600 nm of 0.15–0.2) and harvested by centrifugation. Harvested cells were washed twice with cold electroporation buffer (10% glycerol+1 mM MgCl2) and centrifuged at 4000 g for 10 min at 4 °C. The cell pellet was resuspended in the same electroporation buffer to 1/50 volume of the original culture. Eighty microliters of this cell suspension was mixed with 2 μg of genomic DNA or PCR amplicon on ice and transferred to a precooled 0.1-cm gap electroporation cuvette (BTX, Harvard Apparatus). The cell–DNA mixture was subjected to electroporation

at field Selleckchem Pirfenidone strength of 20 kV cm−1, capacitance of 25 μF, and resistance of 200 Ω. Following electroporation, the cells were immediately diluted in 1 mL of THL medium and incubated anaerobically for 16 h at 37 °C then plated on THL agar plates

supplemented with 1 mg mL−1 streptomycin. Colonies would appear after 24–48 h. Using this protocol, we were able to consistently obtain 9–12 colonies μg−1 mutant genomic DNA, which was two to three times higher than the number of colonies from the wild-type DNA (3–5 colonies μg−1 DNA and these colonies are spontaneous mutants). This result suggested that at least half of the streptomycin-resistant colonies obtained using the mutant DNA contained introduced mutations while the rest may have originated from spontaneous mutation. We could not obtain consistent transformation results when using other parameter combinations mentioned in Materials and methods. Dabrafenib mw With the optimized protocol, we next tested whether PCR-generated DNA could be used to transform V. parvula PK1910. PCR amplicons were generated with the primers rpsLup-F and rpsLdn-R (Table 2 and Fig. 1) using the wild-type and the spontaneous streptomycin-resistant strains SR1 (AAG to AAC mutation) and SR2 (AAG to AAT mutation) as templates. The amplicons were named rpsL-WT, rpsL-SR1, and rpsL-SR2, respectively (Fig. 1). The three PCR amplicons were transformed into PK1910 Selleckchem Cisplatin with the procedure described above. In five

separate experiments, we obtained similar results as the transformation with genomic DNA: there were always about two times more colonies in the transformation with the mutant DNA than with the wild-type DNA. For one of these experiments, we sequenced the rpsL gene of all the colonies that appeared on the plates. As shown in Table 3, most colonies in the rpsL-SR1 transformation have AAC mutation in codon 43, while most colonies in the rpsL-SR2 transformation have AAT mutation in codon 43. The colonies in rpsL-WT transformation, representing the spontaneous mutation, have a similar distribution of the AAC or AAT mutation in codon 43. This result strongly suggests that DNA-mediated transformation had occurred in V.

In this study, we investigated Sirolimus mouse the presence of Tn6188 within the genus Listeria spp. Our screening indicates that the distribution of Tn6188 may be limited to L. monocytogenes.

We confirm that QacH is responsible for the observed increase in tolerance by complementation of a qacH deletion mutant and introducing qacH in a Tn6188 negative strain. We investigated the transporter’s substrate spectrum by determining minimal inhibitory concentrations (MICs) and showed that QacH also confers higher tolerance towards other QACs and ethidium bromide (EtBr). This result was supported by increased expression of qacH in the presence of the various substrates as determined by quantitative reverse transcriptase PCR (qRT-PCR). In addition, we detected expression of a Tn6188 transposase gene and circular forms Vincristine nmr of Tn6188, suggesting activity and possible transfer of this transposon. “
“A 530-kb megaplasmid pPag3 contributing 10.8% of the total genome of Pantoea vagans biocontrol strain C9-1

was sequenced. A rare nonpigmented variant C9-1W was obtained and shown to have lost pPag3, but retained all other plasmids (pPag1, pPag2). Phenotypic characterization of the variant confirmed the function of several annotated genes that may influence ecological fitness and efficacy. Metabolic profiling revealed important plasmid-based carbon utilization phenotypes. Plasmid loss resulted in thiamine auxotrophy, absence of carotenoid pigmentation, desferrioxamine diffusible siderophore biosynthesis, inherent ampicillin resistance and expression of AI-1 quorum-sensing signaling. This confirmed the functional expression of the corresponding genes located on pPag3 in P. vagans. Pantoea is a diverse genus, with most species considered to be ubiquitous plant epiphytes and often isolated from a wide range ADP ribosylation factor of other environmental habitats (e.g., soil, water,

insect/animal gut and clinical samples). Some plant isolates have demonstrated strong beneficial activity as biological control agents for pre- and postharvest fungal and bacterial diseases (Braun-Kiewnick et al., 2000; Bonaterra et al., 2005; Francés et al., 2006). The type species, Pantoea agglomerans, has undergone extensive taxonomic rearrangement emerging from the Enterobacter agglomerans–Erwinia herbicola complex (Ewing & Fife, 1972; Rezzonico et al., 2009). Recently, several closely related species, such as P. vagans, have been newly described based on molecular analysis (e.g., multilocus sequence analysis, DNA–DNA hybridization) (Brady et al., 2008, 2009; Rezzonico et al., 2009). Strain C9-1 is an important biocontrol agent (Ishimaru et al., 1988; Johnson & Stockwell, 1998) that is registered in the United States and Canada as Blight Ban C9-1 (NuFarms America).

[5] Anticoagulation

in older patients poses unique challenges because they are simultaneously at higher risk for recurrent thromboembolism and major bleeding, including catastrophic intracranial haemorrhage.[6-8] Older patients may be at increased risk for anticoagulant-related bleeding because of the increased prevalence of comorbidity and polypharmacy, increased vascular RG7204 cost and endothelial fragility, dietary inadequacies and increased sensitivity to warfarin.[9, 10] The limitations of warfarin necessitate regular monitoring of the International Normalised Ratio (INR) and dose adjustment. The efficacy and safety of warfarin therapy is strongly linked to the proportion of time that patients spend in the target INR range (time in therapeutic range; TTR).[11, 12] Unfortunately, many patients who are prescribed warfarin and managed in community settings, including those residing in aged-care facilities (ACFs), spend a considerable proportion of their time outside of the therapeutic range.[2, 13, 14] Barriers to optimal INR control in ACFs may include

difficulties arranging for pathology providers to visit the ACF, the time taken for the general practitioner (GP) to be notified of the INR result and the time taken for the GP to adjust the warfarin dose, if required, and alert or visit the ACF to implement changes.[15] Point-of-care (POC) coagulometers, BMS-354825 ic50 which measure the prothrombin time from capillary whole blood and provide an INR reading within minutes, are becoming increasingly popular. They can be used by patients to enable self-monitoring of

warfarin and in primary care settings as an alternative to traditional laboratory determination of the INR. Use of such devices can benefit both patients and primary care physicians in managing anticoagulation therapy.[16, 17] The combination PRKACG of POC monitoring and telemedicine may assist in improving access to regular INR monitoring and the communication of results in primary care. The use of telemedicine systems provides an opportunity to reduce labour-intensiveness and improve clinical outcomes for chronic diseases.[18] The aim of this study was to develop and fully evaluate a pilot system that integrated monitoring of clinical parameters or therapeutic outcomes, using portable POC testing devices, with electronic communication of the results from ACFs to GPs and electronic feedback from GPs to the ACFs, utilising national information communication technology (ICT) standards. We conducted a prospective before-and-after proof-of-concept study to compare the INR control achieved with POC INR monitoring and electronic communication to and from GPs with the control achieved in the 12 months immediately preceding the study using conventional management (laboratory INR with physician dose adjustment).

, 1968; Puhalla, 1968). By auxotrophic complementation experiments, Holliday (1974) has isolated solopathogenic strains of U. maydis that AG-014699 in vivo are diploid cells able to grow in axenic culture. Such strains are useful genetic tools, leading to the discovery that cell signalling transduction pathways involved in mating, virulence, dimorphism and cell cycle are intertwined processes (Banuett & Herskowitz, 1988, 1989; Kahmann &

Kamper, 2004). In spite of the genetic interest of the solopathogenic strains, their incidence in the biology of Ustilaginaceae is poorly documented. In the present study, we compare the ability of teliospores from three species of smut fungi to form solopathogenic yeasts: Sporisorium reilianum f.sp. zeae (Khün) Langdon & Fullerton, U. maydis and

Moesziomyces penicillariae (Bref.) Vánky. Sporisorium reilianum f.sp. zeae is the causal agent of maize head smut, infecting maize plantlets via the roots under field conditions (Matyac & Kommedahl, 1985; Martinez et al., 2000, 2002). Ustilago maydis, causing common smut of maize, is known to be infective on different aerial parts of corn (Agrios, 1993). Moesziomyces penicillariae is a pathogen of pearl millet, largely present in the subsahelian zone. It is an airborne pathogen spread by the wind but also by insects infecting young inflorescences (Baht, 1946; Wilson, 1995). We designed a protocol on S. reilianum INCB024360 price to isolate solopathogenic strains based on the isolation of stable fuzzy strains from germinated teliospores. Smoothened This approach was applied on the three Ustilaginaceae species to compare their frequency of formation of solopathogenic strains. Sori of S. reilianum f.sp. zeae (Kühn) Landon & Fullerton were collected from seven cornfields in France (Arçais, Deux Sèvres; Bischoffsheim, Bas Rhin; Buros, Pyrénées Atlantiques; Corbreuse, Essonne; Gourville, Charente; Montclar-Lauragais, Haute Garonne; Saint Ciers, Gironde, France). Two compatible

haploid yeast strains, SRZN and SRZM, were isolated from a sample collected in Saint Ciers (Gironde). Moesziomyces penicillariae (Bref.) Vánky sori were collected in pearl millet fields in 10 areas of Senegal (Doubalampor; Kaffrine; Keur Baka; Koumpentoum; Louga; Mountôgou; Mpack; Rao; Tambacounda; Ziguinchor) (Diagne-Lèye, 2005). Ustilago maydis (DC) Corda galls were collected in corn fields at Le Vernet, Muret (Haute Garonne, France), Pau (Hautes Pyrénées, France) and Gerona (Catalunya, Spain). The haploid, compatible strains SRZN and SRZM were inoculated in maize and the resulting teliospores were collected 6 weeks later. These teliospores were then sterilized by Chloramine T 3% for 15 min, rinsed twice with sterilized water and resuspended in water at a concentration of 500 cells mL−1. A volume of 100 μL of this suspension was spread on water–agar (3%) medium.

The genomic DNA fragment flanking the transposon was cloned into the pBluescript II SK (+) (pBS, Stratagene) vector at the BamHI site and sequenced

with primers zhang-O and zhang-I (Tian et al., 2010) localized at the two ends of the Tn5 transposon. Using primers hfqT3 and hfqT7 (Table S1), which were designed according to the Tn5-flanking sequence in the PMphlA23 mutant, a cosmid p5-2 was screened out by PCR from a genomic DNA library of strain 2P24 (Wei & Zhang, 2005). A 3.2-kb BamHI fragment from p5-2 was subcloned into pBS, giving rise to the plasmid pBS-hfq. The entire hfq gene was identified by sequencing of this fragment (Fig. 1; accession number FJ960506). The hfq gene in-frame deletion mutant was generated using a two-step homologous recombination strategy. The detailed protocol and PCR primers (Table S1) are given in the online Supporting Information. The hfq gene with Entinostat purchase an in-frame deletion was cloned into the suicide plasmid pHSG299 (TaKaRa) Selleck Dabrafenib to generate p299Δhfq (Table 1). Allelic exchange in the wild-type strain 2P24 using p299Δhfq resulted in the mutant PM107 (Δhfq), which was confirmed by PCR amplification (data not shown). For complementation of the strain PM107

(Δhfq), the full-length hfq gene was PCR amplified from P. fluorescens 2P24 with the primers hfq1 and hfq2 (Table S1) and cloned in the shuttle vector pRK415 to generate p415-hfq. For quantitative analysis of 2,4-DAPG production, Pseudomonas test strains were grown in KB liquid media at 30 °C for 30 h. The antibiotic 2,4-DAPG was extracted from the culture supernatant and assayed by HPLC using the method described by Shanahan et al. (1992). For extraction of AHL, P. fluorescens 2P24 and its derivatives were grown in LB liquid media at 30 °C for 30 h. The cell-free supernatants of culture samples (0.8 mL) were extracted with the same volume of ethyl acetate. The extracts were then dried and resuspended in 0.1 mL of methanol. For quantitative analysis of AHL, 3 μL of the samples (the equal volume of methanol as a control) were incubated with 0.2 mL of the AHL Selleckchem Depsipeptide biosensor A. tumefaciens

NTL4 (pZLR4) (OD600 nm=0.8). The reaction mixture was incubated at 30 °C for 3 h, and the β-galactosidase activity of the biosensor cells was assayed using the Miller method (Miller 1972). In vitro biofilm formation assays were performed as described previously (Wei & Zhang, 2006). Briefly, test strains were grown to saturation in LB media and then diluted 1 : 1000 in fresh LB media. The diluted culture (0.5 mL) was transferred to a polyvinyl chloride (PVC) plastic Eppendorf tube and incubated without shaking for 12, 24 and 36 h at 30 °C. The resulting biofilm was stained with 0.1% w/v crystal violet for 20 min, and then unattached cells and residual dye were removed. The dye was dissolved in 95% ethanol, and the A570 nm of the dissolved dye was determined.

Students’ knowledge about the use of contraception and emergency contraception were limited. Community pharmacists could be used to target young patients and provide further information about contraception. The majority of students in this study were uncomfortable talking to their parents about sex and over a third failed to recall sex education at school. The cost of condoms influenced students’ decision to use them. Pharmacists’ PLX3397 solubility dmso gender and ethnicity appear to influence female participants’

decision to request EC. These findings confirm there is clearly a need to offer young people additional tailored support and contraceptive services, as recently published by NICE_ENREF_1. The low response rate in this study is a limitation which may have influenced the results. 1. Ofsted. Department of Education. Not yet good enough: personal, social, health and economic education in schools Manchester2013 [cited 2014 May]. Available from: http://www.ofsted.gov.uk/resources/not-yet-good-enough-personal-social-health-and-economic-education-schools. 2. Dennison C. Teenage pregnancy: an overview of the research evidence. Yorkshire: Health Development Agency; 2004. N.-E. Salema, R. A. Elliott, C. Glazebrook The University of Nottingham, Nottingham, UK One barrier to the successful

management of long-term conditions in first-year undergraduate students is their underutilisation of community pharmacy services This study explored the role of community pharmacy in supporting first-year undergraduate students manage long-term conditions 3-MA cell line at university Better utilisation of existing community pharmacy services and a development of new targeted interventions is required to support and prepare young people to effectively manage Miconazole long-term conditions at university Community pharmacy (CP) in the United Kingdom (UK) is a readily accessible health care service.1 However, the need to improve the utilisation

of CP in the maintenance of health and management of illness is recognised.2 First-year undergraduate students have reported challenges with navigating CP as a barrier to successfully managing their long-term conditions (LTCs) at university. Moreover, the exact role CP has in supporting students with managing their LTC at university has not been widely explored. This study aimed to explore the current and potential contribution CP can make in this area of health care. A purposive sample comprising 18 university students with various LTCs, 19 CP staff and four general practice (GP) staff from Nottinghamshire were interviewed between October 2011 and December 2012. Strategies deployed to recruit interview participants included the use of GP staff and patient lists; electronic mail; poster displays; adverts on the intranet portal and professional networks; and personal contacts.