The global burden of infectious diseases caused by mycobacteria highlights the importance of developing effective

tools for the diagnosis and prevention of mycobacterial infections (Wilson, 2008; First WHO Report on Neglected Tropical Diseases, 2010; WHO, 2012). The application Selleckchem Afatinib of molecular biological techniques provided a huge step forward in the identification of mycobacterial antigens for use in potential diagnostics and vaccines (Wilson, 2008; First WHO Report on Neglected Tropical Diseases, 2010). One of the first mycobacterial antigens to be identified using these techniques was the major 65-kDa antigen of M. tuberculosis (Young et al., 1987), which was initially discovered as an immunodominant antigen in both humoral and cell-mediated immune responses in TB and leprosy (Young et al., 1987, 1988). The subsequent demonstration that the 65-kDa antigen was homologous to

the heat shock protein GroEL of Escherichia coli led to its common nomenclature as Hsp65 in TB studies (Shinnick et al., 1988; Young et al., 1988) and numerous studies on the protein and encoding gene as potential diagnostics and vaccines (Silva, 1999). However, the demonstration of the function of E. coli GroEL as an essential molecular chaperone responsible for the correct folding of key housekeeping genes suggested that Hsp65 is a member of the family of protein chaperonins (Hemmingsen et al., Selleck FG-4592 1988). The chaperonins are a group of molecular chaperones related by homology to the GroEL proteins of E. coli (Hemmingsen et al., 1988; Hartl & Hayer-Hartl, 2002). They usually form oligomers of c. 800 kDa, made up of two heptameric rings of 60-kDa subunits, each with an apical, an intermediate and an equatorial domain that together enclose a central cavity in which client proteins fold (Hemmingsen et al., 1988; Hartl & Hayer-Hartl, 2002). Client proteins bind to the apical domains and chaperonin

function requires a heptameric cochaperonin (GroES in E. coli) which binds the same regions of the chaperonin as the client proteins and displaces these into the cavity, Amobarbital where they fold without interacting with other proteins with which they might aggregate (Hartl & Hayer-Hartl, 2002). The chaperonin folding cycle requires binding and hydrolysis of ATP, and networks of allosteric interactions within and between the two rings are needed to complete the cycle (Hartl & Hayer-Hartl, 2002). In E. coli, the groEL and groES genes form part of a single operon and homologous groEL/S operons have now been described as essential genes in all phyla and kingdoms; these genes have been ascribed the names cpn60 and cpn10 (Coates et al., 1993; Lund, 2001). However, c.

Forty-five participants were recruited to eight focus groups, run concurrently in Australia (23 participants in four

groups) and the UK (22 participants in four groups). Participants were provided with amended leaflets based on the medicine clopidogrel, containing textual and numerical benefit information presented BMS-354825 ic50 using numbers needed to treat (NNT). A topic guide which explored use of leaflets, preferences and opinions was used to direct discussion. Focus group discussions were recorded, transcribed verbatim and content analysed using adapted cross-case study analysis. The consensus was that the inclusion of benefit information was a positive factor. Many participants felt that textual benefit information offered an incentive to take a medicine, although some Australian participants had concerns that included benefit information could create anxiety. The presentation of numerical benefit information provoked strong feelings of disbelief and shock. Participants were surprised that so few people would click here benefit. Some participants struggled to understand and interpret the NNT and others found it difficult to comprehend the magnitude

of the benefit information, instead operating on initial and often crude assumptions of what the data meant. In both countries the provision of numerical benefit information appeared to shake participants’ faith in drug treatments. Participants were concerned about how this might affect the ‘less-informed’ patient. However, in the UK, participants stated that their adherence to treatment was also reinforced by their doctor’s stiripentol advice. Participants wanted to receive information about the benefits of their medicines. However, they may misinterpret the numerical information provided. “
“Objective  The purpose of this study was to describe antimicrobial utilization, consumption, indications and microbial resistance in a medical-surgical-trauma intensive care unit (ICU) of a teaching hospital

to identify potential targets for antimicrobial stewardship. Methods  This was a 30-day prospective observational study enrolling adults admitted to the ICU for at least 24 h and having received antimicrobial therapy. Primary endpoints included utilization as percentage use of antimicrobials by class and agent, consumption measured as days of therapy per 1000 patient days (DOT/1000PD), indications for use and prescriber. Secondary endpoints included reasons for modifications to therapy and microbial resistance. Key findings  Eighty-three patients were screened and 61 enrolled, receiving 133 courses of antimicrobial therapy, mainly intravenously and prescribed by ICU staff. The most frequently prescribed agents were piperacillin/tazobactam (20%), cefazolin (17%) and vancomycin (13%). The indications for therapy were empirical (50%), directed (27%) and prophylactic (23%). Overall consumption was 1368.

Complementation of the selleck kinase inhibitor sucB and ubiF mutants with the functional sucB and ubiF genes restored the wild-type level susceptibility to the antibiotics in both MIC and MBC tests, whereas the mutants transformed with vector control remained susceptible to the antibiotics like the mutants alone (Table 1). To determine the susceptibility of stationary phase cultures of the sucB and ubiF mutants to various antibiotics, the stationary phase cultures with log phase cultures as a control were exposed to ampicillin and gentamicin and the survival of the mutants at different

time points was assessed. Antibiotic exposure of the log phase and stationary phase cultures showed that both the sucB and ubiF mutants were more susceptible than the parent strain to ampicillin and gentamicin. For log phase cultures,

both sucB and ubiF mutants were completely killed after ampicillin (100 μg mL−1) or gentamicin (20 μg mL−1) exposure for 1 day, whereas a portion of the parent control strain BW25113 cells survived (Table 2). Complementation of the mutants restored the level of persisters to the wild-type level in the antibiotic exposure DAPT ic50 assays. For stationary phase cultures, both the sucB and ubiF mutants were initially killed to the same extent as the parent strain BW25113 during the first 3-day ampicillin (100 μg mL−1) or gentamicin (40 μg mL−1) exposure, but both mutants showed lower level of persisters than the parent strain after 6 days or longer (Table 3). Again, complementation of the sucB and ubiF mutants restored the level of persisters to that of the parent strain, whereas the mutants transformed with vector control behaved

like the mutants alone in having lower number of persisters (Table 3). It is worth noting that the sucB and ubiF mutants alone without antibiotics did not lose significant viability compared with those exposed to antibiotics in the exposure assay, Ribonucleotide reductase indicating that the decreased persister survival in the mutants is genuine and not due to a nonspecific loss of viability in the absence of antibiotics during the exposure time period (see Table 2). This has been found to be true in other experiments of this study. Overnight stationary phase cultures of the sucB and ubiF mutants and their complemented strains along with the parent strain BW25113 were exposed to H2O2 at 12.5, 25, 50 and 100 mM for 4 h and the number of persisters was assessed on LB plates. The sucB mutant was much more susceptible to peroxide than the ubiF mutant and the parent strain, as the sucB mutant was completely killed by H2O2 at 25 mM and above (not shown). The ubiF mutant was more sensitive to H2O2 than the parent strain at 100 mM, as the ubiF mutant had no surviving bacteria.

The temperature range for strain Sp-1 was 5–45 °C, with the optimum at 35 °C;

pH range was from 5.5 to 8, with the optimum at 6.2. The cells grew at NaCl concentrations from 0% to 2.5%. FeS, FeSO4 and FeCO3 were used as Fe(II) sources for lithotrophic growth. The strain was unable to use , , S0, and Fe(OH)3 as electron acceptors for anaerobic growth. H2 was not used as an electron donor in mineral media with nitrates. Strain Sp-1 used acetate, succinate, citrate, lactate, malate, fumarate, propionate, pyruvate, butyrate, propanol, glycerol, yeast extract and peptone for organotrophic growth. Weak growth occurred on amino acids alanine, histidine, aspartate and glutamate. Sugars, oxalate, formate, benzoate, ethanol, butanol, proline, leucine, asparagine, glutamine, phenylalanine, tryptophan and casein hydrolysate were not utilized. Ammonium salts, , N2O, urea, yeast extract and peptone were www.selleckchem.com/screening/mapk-library.html used as nitrogen sources. , histidine, aspartate and casein hydrolysate were not used. The major fatty acids in the cells of strain Sp-1 are as follows: 11-octadecenoic selleck kinase inhibitor (18 : 1ω7c), 31.1%; cyclopropane-nonadecanoic (19 : 0 cyc), 27%;

and hexadecanoic acids (16 : 0), 15.9%. Among the polar lipids of the cell membranes, phosphatidylethanolamine and two unidentified aminophospholipids were revealed. Ubiquinone Q–10 was the major respiratory lipoquinone. The strain was sensitive to amikacin, lincomycin, neomycin, polymyxin, streptomycin, rifampicin

and nalidixic acid. The strain was resistant to ampicillin, bacitracin, vancomycin, gentamycin, kanamycin, mycostatin, novobiocin, penicillin and tetracycline. Phylogenetic analysis based on 16S rRNA gene sequence comparison Fossariinae showed that novel isolate Sp-1 was closely related to members of two different orders Sneathiellales and Rhodospirillales within the class Alphaproteobacteria (Table 1). A neighbour-joining tree (Fig. 2) revealed that strain Sp-1 formed a separate branch within the order Sneathiellales, showing 80% of bootstrap value. Although strain Sp-1 could use O2 as an electron acceptor for Fe(II) oxidation under microaerobic conditions, the physiology and biochemistry of Fe(II) oxidation were investigated in anaerobic cultures to avoid the competition with the processes of rapid Fe(II) oxidation in the experiments. Biochemical analysis of the enzymes involved in the chain of reactions of nitrate reduction coupled to Fe(II) oxidation revealed significant differences in their activity. For example, the activity of nitrate reductase of strain Sp-1 was 46 nmol (min mg protein)−1, while the nitrite reductase activity was 30 times lower and did not exceed 1.4 nmol (min mg protein)−1. Unbalanced enzymatic activities in the chain of nitrate reduction reactions resulted in the accumulation of equimolar nitrite concentrations (up to 4.

1). The first set contained the isolate T10A1 (16). The second were the most virulent, and contained the isolates T8B1 (9), T1A2 (42), T24A1 (62) and T24H1 (64). The third set comprised the remaining isolates. Isolate T10A1 (pathotype 16), collected from the Touiref-Kef population, was identified as the most virulent pathotype, as all differentials were susceptible to it. In contrast, all except D3 (Athene) were resistant to isolate T17F1 (pathotype 26), sampled from the Nebeur region. The 79 R. secalis isolates were classified into 75 different pathotypes, indicating a broad and diverse pathogenicity spectrum for both Rihane and local landraces. Similar pathotypes were

paired as Compound C research buy follows: [T5A2 (4), T5G2 (5)], [T12B3 (19), T1F2 (45)], [T23A2 (33), T13C1 (69)] and [T23B2 (34), T24 F1 (63)]. No clearly predominant pathotype was discerned from the samples from the Rihane and local landraces. However, marked differences were noted in the susceptibility of differentials to the different pathotypes. Isolates sampled from Rihane were more virulent than those sampled from local landraces (Table 2). The most effective resistance gene in Tunisia appeared

to be BRR2, carried by the Astrix (D2) differential selleck chemical cultivar, as only 13.88% and 23.25% of the isolates collected from local landraces and Rihane, respectively, were shown to be significantly virulent to this cultivar (Table 2). Virulent isolates that could attack ‘Astrix’ were limited; among them, isolate T14A1 (6) was uniquely identified by the SSR

locus CA-SSR1 225 bp. The resistance gene BRR3 associated with the Athene cultivar was the least effective, because this cultivar was susceptible to R. secalis isolates sampled from either local MycoClean Mycoplasma Removal Kit landraces or Rihane host (Table 2). The 79 investigated R. secalis isolates were especially compared against differential cultivars with the same resistance genes (Table 1). Unexpectedly, although both Steudel and Jet cultivars possessed the resistance genes rh6 and rh7, they showed different reaction spectra to the 27 pathotypes. For instance, Steudel was resistant to 47 pathotypes, while Jet was resistant to only 35. Similarly, Kitchin and Abyssinian had the resistance gene Rh9 in common; they also had different reaction spectra to the 31 pathotypes, with Kitchin showing resistance to 39 and Abyssinian to 51 pathotypes. In all, 48 isolates caused different reaction spectra in the differentials (Table 1; see the gray squares). They constitute an isolate collection that will be useful in breeding program analysis. All microsatellite loci assayed for multi-locus genotypes were polymorphic. The number of alleles ranged from 3 to 11, with a total of 50, over seven loci (Table 3). The number of microsatellite alleles sampled from Rihane was 57, and that from local landraces was 38.

The diagnosis of enamel defects was performed using the Developmental Defects of Enamel (DDE) Index. Through interviews, information was collected on socio-demographic aspects, pregnancy, birthweight, prematurity, and breastfeeding. Statistical analysis was performed using the SPSS program for Windows and involved descriptive analysis, Fisher’s exact test, the chi-square test, and Poisson regression. Results:  The prevalence of developmental defects of enamel was 29.9%. learn more Demarcated opacity was the most frequent type of defect. Children with a history

of very low birthweight had a greater prevalence of enamels defects (PR, 2.7; 95% CI, 1.66–4.61). Prematurity and socio-demographic variables Ponatinib were not associated with enamel defects. Conclusion:  Children with a history of very low birthweight had a greater frequency of enamel defects in primary teeth. “
“Objective.  The aim of this study was to assess the influence of sucking habits and facial pattern measurements on the development of anterior open bite (AOB). Methods. 

A case–control study was carried out on 60 children aged 7 and 8 years attending municipal public schools in the city of Recife, Brazil. Data collection included interviews with guardians, oral examinations, and facial growth pattern analysis using cephalometric radiographs. The following cephalometric measurements were assessed: SN.Gn, SN.GoGn, FMA, and Facial Axis. Statistical analyses were performed using the Student’s t-test and Pearson’s chi-square test at a 5% level of significance. Results.  The percentage of children with sucking habits in the case group was much higher than in the control group (53.3%vs 16.7%) (P = 0.003). Children with sucking habits were six times more likely to develop AOB. Regarding the measurements assessed, no statistically significant differences

were observed between groups. Conclusion.  This study found no evidence that variations L-NAME HCl in cephalometric angles (SN.Gn, FMA, SN.GoGn, and facial axis) are risk factors for AOB. Only sucking habits demonstrated a positive correlation with an increased AOB. “
“Introduction.  It is well established that severe periodontitis clusters in families, but there are no data about the relationship between mothers with chronic periodontitis and their children’s periodontal status. Objective.  To evaluate a risk for periodontal diseases in children of periodontally diseased and healthy mothers. Methods.  Four study groups were included: (I) 20 female patients with untreated generalized severe chronic periodontitis, (II) their children (34), (III) 13 periodontally healthy mothers and (IV) their children (13). Material was collected from years 2004–2006. The clinical examination included registration of visible plaque index, modified gingival index and, bleeding sites on probing.

In this study, a soil-borne, glyphosate-resistant bacterium was selected and identified as Enterobacter. The EPSPS in this strain was found to have Alectinib in vitro been altered to a resistant one. A total of 42 differentially expressed genes (DEGs) in the glyphosate were screened using microarray techniques. Under treatment, argF, sdhA, ivbL, rrfA-H were downregulated, whereas the transcripts of speA, osmY, pflB, ahpC, fusA, deoA, uxaC, rpoD and a few ribosomal protein genes were upregulated. Data were verified by quantitative real-time PCR on selected

genes. All transcriptional changes appeared to protect the bacteria from glyphosate and associated osmotic, acidic and oxidative stresses. Many DEGs may have the potential to confer resistance to glyphosate alone, and some may be closely related to the shikimate pathway, reflecting the complex gene interaction network for glyphosate resistance. “
“Yersinia polynucleotide phosphorylase (PNPase), a 3’-5’ exoribonuclease, has been shown to affect growth during several stress responses. In E. coli, PNPase is one of the subunits of a multi-protein complex known as the degradosome, but also has degradosome-independent

functions. The carboxy–terminus of E. coli ribonuclease E (RNase E) serves as the scaffold upon which PNPase, enolase (a glycolytic enzyme), and RhlB helicase all have been shown to bind. In the yersiniae, only PNPase has thus far been shown to physically interact with RNase Z-VAD-FMK cost E. We show by bacterial two-hybrid and co-immunoprecipitation assays that RhlB and enolase also interact with RNase E. Interestingly, although PNPase is required for normal growth at cold temperatures, assembly of the yersiniae degradosome was not required. However, degradosome assembly was required for growth in the presence of reactive oxygen species. These data suggest that while the Y. pseudotuberculosis PNPase plays a role in the oxidative stress response through a degradosome-dependent mechanism, PNPase’s DCLK1 role during cold stress is degradosome-independent.

2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved “
“To examine why we failed in direct sequencing of rRNA gene internal transcribed spacer (ITS) in Pleurotus nebrodensis, we obtained monokaryons of P. nebrodensis (00489 and 00491) using a protoplast monokaryonization technique. PCR products of ITS amplifications were sequenced. There was a base pair insertion/deletion difference between the two nuclei of P. nebrodensis that led to failure in direct sequencing. Internal transcribed spacer regions (ITS1, ITS2, and 5.8S rRNA gene) of the nuclear ribosomal repeat are widely used in fungal systematics and phylogeny (Gardes & Bruns, 1993; Kårén et al., 1997; Cooke et al., 2000; Manter & Vivanco, 2007; Nilsson et al., 2009).

The first directs expression of the immediate upstream gene rpsO, and the second is positioned in the rpsO-pnp intergenic region (Portiers & Reginer, 1984). Irrespective of the transcriptional start site, the pnp mRNA is vulnerable to cleavage by endoribonuclease RNase III at positions

within 75 nucleotides upstream the pnp ORF, which in turn initiates degradation of the pnp mRNA by PNPase itself (Portier et al., 1987). Upon a cold shock, the pnp mRNA becomes stabilized allowing enhanced expression of PNPase (Beran & Simons, 2001). In enterobacteria, pnp is followed by nlpI (Blattner et al., 1997; McClelland et al., 2001; Nie et al., 2006). For E. coli, NlpI has been shown to be a lipoprotein (Ohara et al., 1999). We recently demonstrated that PNPase and NlpI posed opposing effect on biofilm formation in S. Typhimurium Selleck PLX4032 at decreased growth temperature (Rouf et al., 2011). Experiments that followed here demonstrate that mutational inactivation of pnp in S. Typhimurium results in an expected restricted growth at 15 °C. In addition, the experiments showed that pnp transcripts continued into nlpI and that nonpolar pnp mutations increased nlpI expression. Although S. Typhimurium pnp and nlpI are separated

buy CAL-101 by 109 base pairs, the promoter prediction software bprom (www.Softberry.com) failed to define any tentative nlpI promoter within this intergenic region (data not shown). Combined with the gene expression analysis, this strongly suggests that pnp and nlpI form an operon and implies that nlpI is subject to the same post-translational regulation of pnp. However, we cannot formally exclude potential nlpI promoters within pnp. The co-transcription of pnp and nlpI led us to detail whether, and to what extent, NlpI contributed to cold acclimatization. The data presented in this study demonstrate that nlpI does indeed functionally act as a cold shock gene in concert with, but independently of, pnp. Evidence to support includes the observation that two of Parvulin the three pnp mutants applied in this study had enhanced expression of nlpI, whilst the third had unaffected nlpI mRNA levels compared

to the wild type, yet all three mutants showed a very similar defect for growth at 15 °C. In addition, a pnp–nlpI double mutant had more restricted growth at 15 °C compared to either single mutant, whilst cloned pnp and nlpI enhanced the replication of all the respective mutants at 15 °C (Figs 4b and 5). The nlpI gene is adjacent to csdA/deaD in the genomes of enterobacteria (Blattner et al., 1997; McClelland et al., 2001; Nie et al., 2006). The csdA gene encodes for an alternative RNA helicase that in E. coli also contributes to cold acclimatization (Turner et al., 2007). In S. Typhimurium, the homologue for csdA is defined as deaD. Deleting deaD in S. Typhimurium resulted in a cold-sensitive growth phenotype. However, we could not trans-complement the cold-restricted growth of the deaD mutant phenotype with either pnp or nlpI.

, 2003), this value is, however, likely to be an underestimate. It is interesting to compare the kinetic behavior with that observed for the related DMS dehydrogenase of R. sulfidophilum. In this case, Creevey et al. (2008) investigated the interaction

between cytochrome c2 and DMS reductase and found a KM value of 21 μM (Creevey et al., 2008). The present observations with chlorate reductase are consistent with a KM value in this range. Moreover, Chang et al. (2010) investigated the electron transfer between the cbb3-type oxygen reductase and the soluble diheme cytochrome c4 in Vibrio cholerae. They conclude that a concentration of cytochrome c4 as high as 100 μM does not saturate the oxidase activity. In this case, it is suggested that

the activity is competitively inhibited by the oxidized product due to its similar affinity PI3K inhibitor to the redox partner (Chang et al., 2010). A high KM value can be the result of a fast off-rate for the substrate and thus a relatively low affinity, or of the reaction step subsequent to substrate binding being fast. Because this step would be an electron transfer from the reduced substrate to one of the redox centers in chlorate reductase, the latter alternative is a possible explanation. However, a more detailed Selleck PI3K Inhibitor Library kinetic characterization is required to understand the interaction between the enzyme and its electron donor substrate. In conclusion we have, using the purified reactants, demonstrated that the soluble 9-kDa cytochrome c-Id1 of I. dechloratans serves as an electron donor for its soluble periplasmic chlorate reductase. The route for electron transport in this case is thus more

similar to that observed with DMS dehydrogenase and selenate reductase than with electron transfer to (per)chlorate reductases in Dechloromonas species (Bender et al., 2005). This is consistent with the notion of I. dechloratans reductase being more closely related to DMS dehydrogenase and selenate reductase than to (per)chlorate reductase of Dechloromonas Flucloronide species. We thank Proteomics Core Facility at University of Gothenburg, especially Carina Sihlbom, for running the MS analysis. We also thank Dr Maria Rova for helpful comments and suggestions regarding the manuscript. “
“Vibrio cholerae, the causative agent of cholera and a natural inhabitant of aquatic environments, regulates numerous behaviors using a quorum-sensing (QS) system conserved among many members of the marine genus Vibrio. The Vibrio QS response is mediated by two extracellular autoinducer (AI) molecules: CAI-I, which is produced only by Vibrios, and AI-2, which is produced by many bacteria. In marine biofilms on chitinous surfaces, QS-proficient V. cholerae become naturally competent to take up extracellular DNA. Because the direct role of AIs in this environmental behavior had not been determined, we sought to define the contribution of CAI-1 and AI-2 in controlling transcription of the competence gene, comEA, and in DNA uptake.

The first case series of THA for INFH in HIV-positive patients was published in the early 21st Century and showed higher rates of subsequent infection and prosthesis complications than in the rest of the population. In 2003,

a study by Parvizi et al. was published of 21 HIV-infected patients who underwent total hip replacement surgery between 1979 and 1998; all the patients died within 10 years of follow-up, with 13 re-interventions and six cases of deep infection [22]. A very similar study, carried out by Christopher Lehman et al. in 29 HIV-positive patients who underwent surgery between 1983 buy Tofacitinib and 1995, also showed that this poor prognosis was even worse in patients with IDU antecedents [21]. More recent studies in the HAART era, however, have revealed lower infection rates in HIV-positive

patients, but none of them compared the results with those for non-HIV-infected patients [28-33]. In 2005, Craig Mahoney et al. reported their results for a group of 40 HIV-infected patients in whom acute infection rates in the immediate postoperative stage had been lower than expected [28]. Palbociclib mouse In 2008, Haberman et al. reported a series of 55 cases of THA in HIV-positive individuals; postoperative complications appeared mainly in patients with a difficult social background [29]. Also in 2008, Bahebeck et al. carried out a prospective study in the hospital of Yaoundé, Cameroon, in HIV-positive patients Florfenicol with CD4 counts >500 cells/μl without HAART and those with CD4 counts <500 cells/μl with HAART who underwent any traumatological intervention. In this study, postsurgical infection rates in HIV-infected patients were similar to those seen in non-HIV-infected patients, but HIV-infected patients need extended antibiotic prophylaxis [30]. INFH is a relatively infrequent THA indication [34]. According to the literature, 70% of all cases of necrosis of the femoral head are bilateral

[35] and some authors even claim that these are always bilateral, although not always symptomatic. In our study, 61% of patients in the HIV-positive group and 55% of patients in the control group had been diagnosed with bilateral necrosis. We did, however, find differences between the two groups in the involvement of other joints. HIV-infected patients had been more frequently diagnosed with osteonecrosis in areas other than the hip, such as the humeral head, femoral condyle or tibia and talus. Dudkiewicz et al. established that the aetiology of INFH did not affect initial THA results [36]. However, in cases in which INFH was induced by corticoid treatment, the longevity of the implant appeared more limited. In our study we found that there were no significant differences in the delay in INFH diagnosis, time spent in surgery, duration of hospitalitzation or the functional outcome of arthroplasty.