I think you will agree the quality of the papers published improves year on year, and the Journal at present has an acceptance rate of 10%. If accepted, a paper appears in ‘Early View’ and then in print approximately 6 months C59 wnt later. One trend I have noticed is the increase in papers examining oral health-related quality of life, an area of research I fully support. I understand the

need to validate these methodologies; however, it would be good to see these tools applied and reported in a way that provides information that would increase our understanding of the needs of children and the best treatment modalities. An issue I think the community of Paediatric Dentistry should address is pulpotomies: what agent should we be using and should we be doing them at all? Here in the UK, formocresol has not been taught as an acceptable pulpotomy agent since 2004 and I know this is the case elsewhere. There are effective alternative materials so should we still be using a material which has the potential

to harm our patients and, perhaps more importantly due to the repeated exposures, the dental team[1]. There now is substantial evidence that if caries is isolated from the biofilm on the Vincristine mouse surface, the lesion will arrest. Therefore, should we not just stop worrying about which material we use and instead seal the caries with an effective indirect pulp cap? I would like to thank all the reviewers who have supported the Journal in the past year and it is my pleasure to announce that Dr Ghanim Aghareed from the University of Melbourne is the Reviewer of the Year. Two members of the Editorial Board are retiring,

Magne Raadal and Satu Alaluusua. I would like to thank them Flavopiridol (Alvocidib) for their support of the Journal over the years. I am pleased to say that joining the Board are Ghassem Ansari, Shahid Behedhti Medical University, Iran and David Manton, Melbourne University, Australia. I will take this opportunity to thank the two Associate Editors, Professor Milton Houpt and Dr Paul Ashley, for all their help and advice, together with the team at Wiley, Jenifer Jimenez (Editorial Assistant) and Cheryl Chong (Production Editor) for their support and hard work. Thomas Trier-Mork (Journal Publishing Manager) has moved on to other roles in Wiley. Thomas has been very helpful and supportive of the Journal over many years and I wish him well. I welcome his successor Aske Munk-Jorgensen. My final thanks go to all the authors and readers of the Journal. I wish you all a successful 2014. “
“International Journal of Paediatric Dentistry 2011; 21: 200–209 Aim.  This study determined the prevalence of children’s dental behaviour management problems (BMP) in our clinic, investigated the influence of non-dental and dental background variables on BMP, and analysed the predictive power of these variables. Design.  The study group included 209 children aged 2–8 years who received dental treatment.

Two key outcome measures were collected to evaluate the success of the testing programme:

(i)  the proportion (%) of eligible patients offered an HIV test; The number of patients newly diagnosed with HIV infection and the proportion transferring to specialist care were secondary outcomes. The key outcome measures were derived from (1) the electronic patient database, which generated the total number of attendees, (2) an electronic prompt which ED staff completed to document the outcome of a test offered (accepted/declined/not Akt inhibitor offered), and (3) laboratory reports on the total number of HIV tests performed and the corresponding results. The ED and sexual health teams met weekly to evaluate the effectiveness of the testing service. Sustainability methodology, comprising

process mapping and plan-do-study-act (PDSA) cycles, was employed to identify ABC294640 chemical structure significant trends in the outcome measures, and to evaluate the impact of interventions to improve the model [9]. Interventions were manifold and included training exercises, identification of key staff (or ‘testing champions’), incentivization, information technology solutions, and changes to the testing pathway and methodology. Testing commenced in January 2011, and at the time of writing has continued for 30 months. The main outcome measures are shown graphically in Figure 1. There have been 44 582 attendances of eligible participants. The mean proportion offered an HIV test was 14%, varying from 6% to 54% per month over the testing period. The mean proportion accepting a test was 63% (range 33–100%), although for months 26 to 28 this is an inferred figure Tacrolimus (FK506) as the electronic prompt was unavailable. A total of 4327 HIV tests have been performed. There have been a total of 16 reactive results. Thirteen individuals (81%) have attended for confirmatory testing. Of the 13 individuals with confirmed HIV infection, all have transferred

to care. The prevalence of newly diagnosed HIV infection in the sample is 0.30% [95% confidence interval (CI) 0.18–0.51%]. The highest impact changes are shown in Figure 1. The changes with the biggest impacts were the switch to offer blood testing in addition to oral fluid-based testing (month 22) and the incorporation of nursing staff into the testing service (at month 24). Prior to these interventions, the average coverage was 11% over months 1–22, increasing significantly thereafter to 29% averaged over the last 8 months. Other interventions, such as the identification of testing champions among the ED staff and the regular provision of teaching and of newsletter updates had smaller (but probably cumulative) positive effects on the key outcome measures. This paper demonstrates that sustained routine HIV testing in an inner-city ED is feasible.

More than two/thirds of the eukaryotic proteins are predicted to be glycosylated (Apweiler et al., 1999), including many proteins of the

immune system. It has been shown that pathogenic and commensal Gram-positive bacteria produce enzymes that hydrolyze the glycans of glycoproteins, thus liberating nutrients supporting bacterial growth (Roberts et al., 2000, 2001; Collin & Fischetti, 2004; Sanchez et al., 2010; Ruiz et al., 2011). Glycan hydrolysis may also serve the purpose of modifying the functionality of specific host Roscovitine clinical trial proteins, e.g. in the immune system (Collin and Olsen, 2001, 2003). Enterococcus faecalis is known to have extracellular endo-β-N-acetylglucosaminidase activity that enables growth on RNaseB by releasing high-mannose type glycans from a single N-glycosylation site (Roberts, et al., 2000, 2001; Collin & Fischetti, 2004). There are three main types of N-linked glycans that are all build on a common core pentasaccharide (Man3-GlcNAc2) that is linked to the asparagine through one of two consecutive GlcNAc units (Supporting Information, Fig. S1): (1) the ‘high-mannose’

Selleckchem MG-132 type found in RNaseB, containing additional α-linked mannose residues, (2) the ‘complex’ type, which has no additional mannose residues but may have as many as five antennae containing a variety of additional sugar types, and (3) the ‘hybrid’ type, comprising a combination of high-mannose and complex-type branches. Hydrolysis of the N-linked glycans by endo-β-N-acetylglucosaminidases entails hydrolysis of the glycosidic bond between the two GlcNAc residues in the (Man3-GlcNAc2) core, which implies that the deglycosylated protein retains one GlcNAc (Morelle and Michalski, 2005, 2007). The ability of E. faecalis to release high-mannose type glycans from RNaseB has been ascribed to a protein called EndoE from E. faecalis SPTLC1 HER1044, corresponding to EF0114 of E. faecalis V583 (99% sequence identity; Collin & Fischetti, 2004). This is a two-domain protein consisting of a family 18 glycoside hydrolase (GH18) with the originally detected endo-β-N-acetylglucosaminidase activity and a GH20 domain that

hydrolyzes complex-type glycans of IgG. In addition to EF0114, the genome of E. faecalis V583 encodes two other GH18 proteins, EF0361 and EF2863 (Cantarel et al., 2009). EF0361 is a chitinase (Leisner et al., 2009) and its gene is followed by ef0362, encoding a CBM33 protein that belongs to a family of enzymes known to play a critical role in chitin degradation (Vaaje-Kolstad et al., 2010). EF2863 is predicted to be a secreted endo-β-N-acetylglucosaminidase that has not been investigated so far, despite its potential importance for the ability of E. faecalis V583 to exploit host glycoproteins. In this study, we have characterized the putative endo-β-N-acetylglucosaminidase, EF2863, from E. faecalis V583. The results confirm the predicted activity and provide information concerning the ability of this novel enzyme to hydrolyze different types of glycoproteins.

The internal EcoRV site present in pmtA was used for mutagenesis. A spectinomycin-resistance cassette obtained as a SmaI fragment from pHY109 was inserted into EcoRV-digested pDBM11, resulting in pDBM12. Finally, the 4-kb XhoI–XbaI fragment from pDBM12 was ligated into SalI/XbaI-digested pK18mobsacB, resulting in plasmid pDBM14. The pDBM14 construct contains the interrupted pmtA gene flanked on both sides by 1 kb of DNA from SEMIA 6144. Plasmid pDBM14 was introduced by biparental

mating into SEMIA 6144. After mating for 2 days at 28 °C, the bacterial mix was plated on YEM medium with nalidixic acid, spectinomycin and kanamycin to select against E. coli donor cells and for SEMIA 6144 recipient cells harbouring the suicide plasmid integrated into its chromosome. Resistant SEMIA 6144 colonies were grown in liquid YEM medium for 24 h before being streaked Temsirolimus in vitro out on YEM medium containing spectinomycin and 10% w/v saccharose to select for the loss of the vector backbone. Double-crossover events were confirmed by PCR and Southern blot. The Bradyrhizobium sp. SEMIA 6144 pmtA-deficient mutant was called DBM13. To complement the mutant, the HindIII fragment of pDBM01 was cloned into the broad-host-range vector pBBR1MCS-5 that had been digested with HindIII, resulting INCB018424 in vitro in pDBM07. The lipid

compositions of SEMIA 6144 wild type, DBM13, DBM13 complemented with pDBM07 and DBM13 harbouring the vector pBBR1MCS-5 were determined after labelling with 37 kBq mL−1 [1-14C]acetate sodium salt (New England Nuclear, 2.26 GBq mmol−1) for 72 h. Lipids were extracted according to Bligh and Dyer (1959). The chloroform MycoClean Mycoplasma Removal Kit phase was used for lipid analysis on thin layer chromatography (TLC) plates and the individual lipids were quantified as described previously (Medeot et al., 2007). Bacterial cultures in YEM medium were grown for 72 h until the mid-exponential phase was reached. Cells were observed with a Zeiss microscope (Axiophot Carl Zeiss) equipped with a Canon PC1089 Powershot G6 7.1-megapixel digital camera (Canon Inc.,

Japan). Photographs were processed and sizes were determined using software axiovision 4.1 (Carl Zeiss). The protocols were adapted from those of Dèziel et al. (2001). Swim plates (YEM medium with 0.3% agar) were point-inoculated with a toothpick and incubated for 48 h at 28 °C. Swimming was assessed qualitatively by examining the circular turbid zone formed by the bacterial cells migrating away from the point of inoculation. Seeds of A. hypogaea L. cv. Blanco Manfredi M68, obtained from INTA Manfredi (Córdoba, Argentina), were surface-sterilized, grown in sand and inoculated according to Dardanelli et al. (2009). Uninoculated plants did not develop nodules. For the competition assay, surface-sterilized seedlings were coinoculated with parental strain SEMIA 6144 and DBM13 in a 1 : 1 ratio. Bacteria were reisolated from surface-sterilized nodules and identified based on the spectinomycin resistance marker.

DNA fragments of 1–5 kb were recovered from an agarose gel and ligated into pUC118 BamH I/BAP (Takara). For amoxicillin-resistant fosmid clones, Peptide 17 cost the kanamycin-resistance vector pHSG298 (Takara) cut with BamH I (Takara) and treated with alkaline phosphatase (Takara) was used instead of pUC118, which cannot be used for amoxicillin-resistant screening because of bearing the ampicillin resistance marker ampr. Ligation products were transformed into E. coli DH5α (Invitrogen) and spread onto LB agar plates containing either 100 μg mL−1 ampicillin

for pUC118 or 50 μg mL−1 kanamycin for pHSG298 and another antibiotic as substrate: 8 μg mL−1 amoxicillin, 32 μg mL−1 kanamycin, 4 μg mL−1 tetracycline or Obeticholic Acid supplier 128 μg mL−1 d-cycloserine. After 24 h at 37 °C, a single resistant subclone from each plate was selected. Positive subclones were sequenced from two directions using M13 primers. Primers were designed from each read to close the insert sequence. Sequences were assembled with seqman software (DNAStar). Putative open reading frames (ORFs) were identified with ORF Finder (http://www.ncbi.nlm.nih.gov/projects/gorf/). All predicted ARGs were compared to exclude redundant ARGs (> 99% identity at nucleotide level), and the unique ARGs were analyzed as described previously (Sommer et al., 2009). Phylogenetic analysis was conducted with the neighbor-joining method using mega5 (Tamura et al., 2011).

Bootstrapping (1000 replicates) was used to estimate the reliability of phylogenetic reconstructions (Felsenstein,

1985). The kanamycin-resistance fused gene was amplified using the following primers: EcoRI-KM2-F, 5′-CCGGAATTCATGGAAAACAGGGCTGTG-3′ and XhoI-KM2-R, 5′-CGCTCGAGTTATTCTTCCT CCCCCGG-3′. The N-terminal domain of KM2 was amplified using primers EcoRI-KM2-F and XhoI-KM2-N-R, 5′-CCGCTCGAGTTACTTTCCTCCTAGTTTTTC-3′. The C-terminal domain of KM2 was amplified using primer XhoI-KM2-R with EcoRI-KM2-C-F, 5′-CCGGAATTCATGAATGACGTTAAGGCA-3′. see more The original fosmid DNA was used as the PCR template and products were cut with EcoRI and XhoI (Takara) and ligated into the expression vector pGEX-5X-3 (GE Healthcare) digested with EcoRI and XhoI and transferred into E. coli DH5α. The integrity of the cloned sequences in recombinant plasmids was confirmed by sequencing. Minimum inhibitory concentration (MICs) of kanamycin to the cloned whole length protein KM2 and its N-terminal and C-terminal domains were determined by broth microdilution according to Clinical & Laboratory Standards Institute (CLSI) (2010) guidelines. Escherichia coli DH5α carrying the vector pGEX-5X-3 was selected as negative control and E. coli ATCC 25922 was used as quality control strain. Sequence data from this work were deposited in GenBank with the following accession numbers: JN086157–JN086173. One metagenomic library from four human fecal samples was created, containing c. 415 000 clones. The average insert size was c. 30 kb for about 12.

MT Ivan: Exchange of E132, E147 or H168 in MT Ivan led to a complete loss of activity and zinc was not detected in the enzyme (see the asterisks in Fig. 2a). Hence, we screening assay believe that these amino acids are the zinc-binding partners. The exchange of all other amino acids tested did not result in a loss of zinc. Potential adjacent binding partners of E132, E147 or H168 were E133, H146 and H166. The activity of the enzymes mutated in these positions

was significantly reduced with vanillate as a substrate. MT Iver: Exchange of the amino acids D83, C111 or C151, respectively, led to a complete loss of the activity (see the asterisks in Fig. 2b); in all these mutants, the zinc content was <0.05 mol mol−1 enzyme, whereas the zinc content of the native enzyme was 1 mol mol−1. This result indicates that the

three amino acids involved in zinc binding of MT Iver are one aspartate and two cysteine residues. C151 is flanked by two potential BVD-523 zinc-binding amino acids: D150 and H152. To exclude that one of these amino acids rather than C151 is involved in zinc binding, D150 and H152 were also exchanged in separate experiments and the activity and the zinc content were determined. In these recombinant enzymes, the zinc content was between 0.96 and 1.03 mol mol−1 enzyme, indicating that none of these amino acids is involved in zinc binding. The activity of the latter mutants with veratrol as a substrate, however, was significantly reduced to <5% of the activity of the native enzyme. When C151 was exchanged for aspartate as a potential zinc-binding partner, the zinc content was reduced to about 0.07 mol mol−1 enzyme and no activity was detected. In separate experiments, H152 or D150 was exchanged for cysteine and simultaneously C151 for alanine to elucidate the impact of the position of the zinc-binding cysteine. In these mutants, neither zinc binding nor activity was detected.

These results reveal that not only the amino acid position but also the kind of amino acid is important. The exchange of single acidic amino acids close to the zinc-binding motif for alanine resulted in a significant loss of activity to ≤60% (Fig. 2b). The mutants obtained show partially Protein kinase N1 restricted substrate spectra (data not shown). All these mutants studied still contained approximately 1 mol zinc mol−1 protein. In the MT I, zinc is believed to have a catalytic rather than a structural function. This assumption is based on (1) the kind of amino acid as a binding partner for zinc, which should be cysteine for a structural function (Auld, 2001), (2) the comparison with methanogenic corrinoid-dependent methyltransferases (Hagemeier et al., 2006) and (3) the location of the assumed zinc-binding amino acids in MT I (Fig. 3).

5 m and at an angle of 45° to the right MAPK Inhibitor Library in vivo and left. The standard and deviant tones included the first two upper partials of the

fundamental frequency. Compared with the fundamental, the intensity of the second and third partials were −3 and −6 dB, respectively. The standard tones had a fundamental frequency of 500 Hz, were 200 ms in duration (including 10 ms rise and 20 ms fall times), and were presented at an intensity of 80 dB (sound pressure level) via both loudspeakers. Each deviant tone differed from the standard tones in frequency, intensity, duration, sound-source location, or by having a silent gap in the middle, but otherwise they were identical to the standard tones. The frequency deviants included large (f0: 750 or 333.3 Hz), Panobinostat cost medium (f0: 400 or 625 Hz) and small (f0: 454.5 or 550 Hz) frequency increments and decrements. The duration deviants included large, medium and small duration decrements, which were 100, 150, and 175 ms in duration, respectively. Only the responses to the largest frequency and duration deviants were included in the analysis because of their better signal-to-noise

ratio compared with the responses to the smaller deviants. The gap deviant had a 5 ms silent gap (5 ms fall and rise times) in the middle of the sound. The intensity deviants were either −6 or +6 dB compared with the standard. Finally, the sound-source location deviants were delivered through either only the left or right speaker (no intensity compensation was employed). The large frequency and

duration deviants were both presented 140 times and the intensity, sound-source location, and gap deviants, in turn, were presented 250 times each. In addition, repeating and varying novel sounds were included in the sequence. Similarly to the standard tones, the novel sounds were 200 ms in duration and their mean intensity was 80 dB. The varying novel sounds were machine sounds, animal calls, etc., whereas the repeating novel Amino acid sound was the word /nenä/ (‘nose’ in Finnish), spoken in a neutral female voice. The repeating and varying novel sounds were presented 216 and 72 times, respectively. Unlike the repeating novel sounds, each individual varying novel sound was presented no more than four times during the whole experiment. Furthermore, one-third of the varying novel sounds were presented via the right, one-third via the left, and one-third via both loudspeakers, whereas the repeating novel sounds were always presented through both loudspeakers. Because of these factors, the varying novel sounds are arguably more likely to trigger cognitive processes related to novelty detection and distraction than the repeating novel sounds. Consequently, only the responses to the varying novel sounds were included in the analysis of the current study.

The second group consisted of 26 fish isolates of GCSD, and one strain of pig GCSD that had PCR products above 1 kb, which was markedly larger than expected. The third group included two fish isolates (PF880 and PP1398) of GCSD that had PCR products above 2 kb, which was also larger than expected. On the basis of the nucleotide

sequences selleck chemicals llc of spegg genes extracted from fish and pig isolates, the size variation was confirmed to be due to the presence of IS in the spegg locus of fish isolates. The spegg locus obtained from GCSD fish strains (94414 and KNH07901) was 2059 bp long due to the presence of a 1224 bp IS. This IS was found to have 99% similarity to IS981SC of Streptococcus iniae (AY904444). The spegg locus sequence was interrupted 604 bp downstream from its start codon by IS981SC, resulting in a 3-bp (5′-ATA-3′) duplication at the insertion site. IS981SC contained two ORFs, designated ORF1 and ORF2, which

encode 86 and 279 amino acids, respectively. These ORFs were oriented in the direction opposite to that of the spegg (Fig. 2c). The spegg locus obtained from GCSD fish strain PP1398 was 3236 bp in length due HIF inhibitor to the presence of two IS: IS981SC and IS1161 (Fig. 3). The IS981SC sequence was interrupted after 50 bp from its noncodon part of the 3′ end by the IS1161-like element, resulting in a 13-bp (5′-ATTTTAATCTATT-3′) duplication at the insertion site. The IS1161-like element sequence has 98% similarity Axenfeld syndrome to IS1161 (NC_011375) of the S. pyogenes strain (NZ131). The IS1161-like element was 1164 bp in length. IS1161 has one ORF that encodes 342 amino acids, and this ORF was oriented in the direction opposite

to that of spegg, but in the same direction as that of the two ORFs in IS981SC (Fig. 2d). The hybrid IS981SC–IS1161-like element was found to be inserted into the same location as that of IS981SC in the spegg locus of fish strain KNH07901, resulting in an insertion mutation in ORF of spegg (Fig. 3). The spegg locus obtained from the pig GCSE (PAGU657) strain showed a five-nucleotide deletion mutation, from nucleotides 604 to nucleotides 608 (5′-AAGCT-3′), in the ORF of spegg (Fig. 2a). The spegg locus obtained from the pig strain of GCSE (PAGU656) yielded the expected product size and had 100% similarity to spegg variant 4 (AB105080), which has one ORF that encodes 234 amino acids (Fig. 2b). As expected from the sequence similarity results, phylogenetic analysis revealed that spegg of fish isolates (without IS) was related to that of β-hemolytic S. dysgalactiae ssp. equisimilis. Moreover, spegg of fish isolates could be distinguished from that of S. pyogenes (Fig. 4). The presence of the IS981SC–IS1161 hybrid IS-like element in various isolates of GCSD and GCSE was screened by PCR analysis using specific primers Seg8 and Seg9. All fish isolates of GCSD and one isolate of pig GCSD (dNo.

polymyxa CCM 7400. The resulting PCR fragments indicated the presence of amplicons corresponding to a

448-bp fragment from a putative small terminase gene and a 405-bp fragment from a putative holin gene. The specificity of chosen PCR products was confirmed by DNA sequencing of the amplicons. We identified the presence of both 448- and 405-bp amplicon on the chromosomes of all tested isolates of P. polymyxa CCM 7400. We confirmed the presence of ΦBP DNA on the chromosome of P. polymyxa using Southern blot hybridization. The results of Southern blot analysis are shown in Fig. 5. On blotted samples of genomic Sorafenib ic50 DNA from P. polymyxa CCM 7400, we detected signals corresponding to those on bacteriophage ΦBP DNA using each of the three probes. The positions of hybridization signals on both chromosomal DNA and phage DNA were identical, suggesting that the restriction patterns of ΦBP sequences on the chromosome of P. polymyxa CCM 7400 are the same as those of ΦBP DNA. Superinfection with ΦBP of the clones positive for prophage presence resulted in lytic development in all cases, suggesting that ΦBP might be a virulent mutant phage. The primary aim of this work was to find out whether the occasional lysis of the growing culture of P. polymyxa is the result of bacteriophage infection. After successful isolation of phage particles, we extracted the phage DNA. We decided to clone and sequence eight EcoRI fragments

within 0.9–2.5 kbp. The results of bioinformatic analysis suggested the presence of some typical phage genes. We identified regions similar to a small and a large subunit of phage terminase genes and regions similar to

phage lytic Selleckchem Rapamycin genes. Both terminase and lytic genes Tau-protein kinase (especially the holin one) are exclusively phage genes and their presence confirmed our suspicion of phage infection. The next step of our work was to find out whether the bacteriophage ΦBP can lysogenize P. polymyxa. Using PCR amplification and Southern blot hybridization, we confirmed the presence of phage DNA on the chromosome of P. polymyxa CCM 7400. In many bacterial genomes, the bacteriophage DNA is integrated into the bacterial chromosome, where it represents a significant part of the total bacterial DNA. However, prophages are not only passive genetic elements. They serve as the vectors for horizontal gene transfer, influence virulence or fitness of bacteria and account for interstrain genetic variability in bacterial species (Canchaya et al., 2003). Prophages are valuable tools for evaluation of the diversity and identification of bacterial strains. Such experiments were also performed on Paenibacillus species exploiting bacteriophages IPy1 (dos Santos et al., 2002) and PPL1c (Stahly et al., 1999). We decided to study another member of the group of bacteriophages from paenibacilli, the phage ΦBP, in more detail. Along with the search for phage genes, we performed a study of the ΦBP propagation, its host spectrum and its life cycle.

These can pose numerous challenges for the clinician. There is no published protocol on the management of double teeth. Aim.  To review the published literature and also patients managed at the Eastman Dental Hospital (EDH) and to develop a clinical protocol for the management of double teeth

in children and adolescents. Design.  Literature was searched (Medline and Embase) learn more and data collated. Patient notes of cases managed at the EDH were reviewed. Results.  Eighty-one teeth from 53 papers and 22 patients were included in the review. Success criteria were only reported in 32 papers and were variable. Twenty-three papers had no follow-up period. The main factor in determining the management of a double tooth was root and root canal system morphology. The treatment buy Dabrafenib of choice in teeth with separate roots was hemisection and in those with a single root was crown modification or extraction. Conclusion.  It was not possible to determine the best management strategies because of the variable reporting in the literature. The authors have proposed a protocol for management and a data collection sheet for essential information needed when reporting on double teeth cases. “
“International Journal of Paediatric Dentistry 2012; 22: 211–216 Objective.  The aim of this study was to evaluate

the knowledge of emergency medical physicians employed in hospital emergency rooms as to their potential role in the treatment for traumatic teeth

avulsion injuries (TTAI). Methods.  A 15-item questionnaire was distributed to the emergency rooms of one university and 10 public hospitals. The questionnaire gathered data on the respondents’ professional profiles and self-assessed perceived knowledge and actual knowledge of the emergency management of TTAIs. Results.  The study was implemented with 69 emergency physicians present at their workplaces during the time of data collection. Of these, 55 (79.7%) were employed at public hospitals and 14 (20.3%) at a university hospital. The professional profiles indicated Pembrolizumab mouse that 47 (68.1%) of the participants were general practitioners and the remaining 22 (31.9%) were distributed among various other medical specialties. Overall, 28 respondents (40.6%) assessed their knowledge regarding medical treatment for TTAI as insufficient, and the majority (78.3%) stated that they would like further education. Importantly, a large majority of practitioners could not provide correct answers to questions related to the emergency management of TTAI. Conclusion.  There is a need to improve the knowledge of emergency medical physicians regarding the emergency treatment for TTAI. “
“International Journal of Paediatric Dentistry 2012; 22: 280–285 Background.