The external area of the pancreatic tissue involved by myofibroblastic cells of the IMT [Low power magnification - Hematoxylin and eosin stain (C)]. Discussion IMT is a histopathologic MI-503 mouse entity previously known as an inflammatory pseudotumor which was initially reported in 1990 in the pulmonary system [4]. Different names have been used to describe this entity, such as plasma cell granuloma, plasma

cell pseudotumor, inflammatory fibroxanthoma, inflammatory pseudotumor and histiocytoma [5]. The histological features vary slightly from site to site, which may, at least in part, be related to differences in the phase of the lesion’s development at the time of the detection. Representative features include the presence of a myofibroblastic proliferation Selleckchem CAL 101 and a varying degree of inflammatory infiltrates, mainly consisting of lymphocytes, histiocytes and plasma cells [6]. A number of the clinical and pathological features of IMT suggest the possibility that this lesion is more similar to a neoplasm than an inflammatory lesion [7]. Some investigators argue that IMT may be a true sarcoma and prefer the term inflammatory fibrosarcoma [7–9]. Whether IMT and inflammatory fibrosarcoma are actually the same tumor or different entities, it is remains controversial. Now, it is generally accepted that IMT is indeed

a true neoplasm with a wide spectrum of histopathological behavior, varying from benign lesions to rare aggressive tumors [7]. Recently, inflammatory fibrosarcoma has become included in the spectrum of inflammatory myofibroblastic proliferations [10]. Although IMT occurs more frequently in the pulmonary system

but it had been described in a wide variety of other organs [6]. In a clinicopathologic and immunohistochemical study of 84 cases of extrapulmonary IMT, the involved organs were intra-abdominal sites in 49 cases (58.4%), upper respiratory tract in 9 cases (10.7%), genitourinary tract in 8 cases (9.5%), trunk in 8 cases (9.5%), pelvis and retroperitoneum in 4 cases (4.8%), extremities in 3 cases (3.6%), Cediranib (AZD2171) and head and neck in 3 cases (3.6%) [11–13]. Furthermore, IMT has also been reported in the orbit [14], salivary glands [15], spleen [16–18], liver [19, 20], urinary bladder and soft tissues [20, 21], skin [22], kidneys [23], heart [24] and central nervous system [25]. IMT of the pancreas is rare. Only 27 cases of IMT located in the pancreas have been reported in English literature [5, 6, 26–43]. The age distribution of IMT of the pancreas resembled that of in pulmonary system ranging 2.5 to 70 years. IMT equally affects males and females. Commonly, the clinical presentation of IMT of the pancreas is a mass discovered incidentally by imaging investigations for other reasons. The presenting symptoms and signs of pancreatic IMT were abdominal pain (65.4%), unintentional weight loss (42.3%), jaundice (38.

A characteristic feature of all the HmuY homologues identified in this study is biofilm

formation. However, although we found several putative HmuY homologues in a broad range of bacteria, the similarity of the amino-acid sequences of HmuY from Porphyromonas and other species was low (5-47%) (see Additional file 1). Only between HmuY proteins encoded within Porphyromonas species was the similarity higher (24-100%) (see Additional file 1). In addition, only P. gingivalis strains possess both histidines engaged in heme coordination selleck kinase inhibitor [20, 21]. Here we also demonstrated that antibodies against purified HmuY raised in rabbits were highly specific and recognized only this antigen in P. gingivalis A7436 and W83 whole-cell lysates compared with a P. gingivalis hmuY deletion mutant strain (TO4) (figure 1), E. coli, or Bacteroides fragilis whole-cell lysates (data not shown). Figure 1 Analysis of HmuY protein in P. gingivalis cell. Detection of HmuY protein in whole-cell lysates of the wild-type W83 and A7436 strains and the hmuY deletion learn more mutant (TO4) strain was performed by SDS-PAGE and Coomassie Brilliant Blue G-250 staining (A) or Western blotting using rabbit anti-HmuY antibodies

and chemiluminescence staining (B). Hm, bacteria grown in basal medium supplemented with hemin; DIP, bacteria grown in basal medium supplemented with dipyridyl for the 1st, 2nd, and 3rd passages. HmuY is exposed on the surface of P. gingivalis cells The N terminus of HmuY shares characteristic features of classical lipoproteins, possessing a signal peptide sequence cleaved off by the signal peptidase II [19, 32]. After removal of the signal peptide, the α-amino group of the N-terminal cysteine is acylated, yielding

a mature lipoprotein. Although HmuY association with the outer membrane of the P. gingivalis cell was previously demonstrated [17, 19, 33], the orientation of the protein in the outer membrane was not examined. Bacterial lipoproteins may be located at the cell surface or directed into the periplasmic space. We hypothesized previously that HmuY functions as an external protein 4��8C [21]. To determine whether HmuY is surface exposed, the proteinase K accessibility assay was employed using the P. gingivalis A7436 and W83 wild-type strains. Upon incubation with proteinase K of intact cells grown under low-iron/heme conditions, most of the HmuY was not degraded (figure 2A). A similar effect was observed when P. gingivalis cells grown under high-iron/heme conditions and E. coli cells over-expressing membrane-associated HmuY were examined (data not shown). It is likely that HmuY may be partially protected by the cell wall, similar to other lipoproteins [34], or resistant to proteinase K digestion. The latter is highly possible since we previously demonstrated that HmuY is resistant to the proteolytic action of trypsin and gingipains [21].

Year Urine Blood Wound Pus Catheter tip Ascetic Fluid Eye Pleural Fluid Sputum Amiri (ADA) 9 2010                   2011           1       2012 8                 Ahamdi (KOC) 57 2010 38 5 2 2 2       1 2011 3                 2012 3     1           Yiaco-Adan (Y) 17 2010                   2011                   2012 13   2       1 1   PCR amplification and sequencing Table 3 shows the distribution of the bla genes among the 83 isolates of E. coli O25b-ST131. Four (4.8%) did not contain any of the β-lactamase

selleck inhibitor enzymes while the majority (95.2%) harboured at least one β-lactamase resistance gene. Two isolates harboured bla CTX-M-2 and bla CTX-M-56. bla NDM, bla IMP and bla VIM genes were not found. ISEcp1 was detected upstream region of 25 (33%) of the bla CTX-M-15 positive isolates. bla CMY-2 was only detected in four isolates (4.8%). IS elements were detected in 2 bla CMY-2 positive isolates, 1 contained class 1 integrons and 1 class II integrons. Table 3 Molecular characterization of bla genes among E. coli O25b-B2-ST131in Kuwait Profiles of the antibiotic resistance genes No.

of isolates (%) bla TEM-1 2 (2.4) bla SHV-12 1 (1.2) bla CTX-M-2 1 (1.2) bla CTX-M-15 32 (38.6) bla CTX-M-56 1 (1.2) bla TEM-1, bla SHV-12 1 (1.2) bla CTX-M-15, bla SHV-12 9 (10.8) bla CTX-M-15, bla TEM-1 21 (25.3) bla CTX-M-15, bla TEM-1, bla SHV-12 12 (14.5) Class 1 integrons were identified in 30 (36.1%) isolates

and only 5 (6%) LY3039478 datasheet contained class II integrons. None of the isolates contained both classes of integrons. Quinolone resistance determinants All but two isolates were resistant or had intermediate resistance to ciprofloxacin (MIC > 2 mg/l). Two sensitive isolates did not contain aac(6’)-Ib Ib-cr (isolates Y-116 and Y-159). We did not detect qnrA gene in any of the isolates tested. Three isolates harboured qnrB1 and 4 harboured qnrS1. qnrB1 and qnrS1 coexisted in only 2 isolates (Table 4). Table 4 Idoxuridine The profile of quinolone resistant E. coli O25b-B2-ST131isolates Profiles of the antibiotic resistance genes No. of Isolates bla CTX-M-56, bla cmy-2, qnrB1 1 bla CTX-M-15, aac(6’)-Ib-cr, bla TEM-1, qnrB1 1 bla CTX-M-15, aac(6’)-Ib-cr, bla OXA-1, bla TEM-1, qnrB1, ISEcp1 1 bla CTX-M-15, aac(6’)-Ib-cr, bla OXA-1,, bla TEM-1, qnrS1, ISEcp1 1 bla CTX-M-15, aac(6’)-Ib-cr, bla OXA-1,, qnrB1, qnrS1 2 bla CTX-M-15, aac(6’)-Ib-cr, bla OXA-1,, qnrS1, ISEcp1 2 bla CTX-M-15, qnrS1, bla OXA-1,, ISEcp1 1 Total 9 Fifty six (67.5%) isolates carried aac(6’)-Ib Ib-cr. Among the aac(6’)-Ib Ib-cr negative strains (27/83) 32.5%, 1 isolate carried qnrB1 and bla CTX-M-56 (KOC-10) and 1 isolate carried qnrS1 (ADA-234).

NN and MA were supported by the Swiss National Science Foundation grant 31003A_130735. Electronic supplementary material Additional file 1: File S1: Flow cytometry data. (XLS 137 KB) Additional SHP099 solubility dmso file 2: Figure S1: Variation in the expression of ptsG, mglB and rpsM reporters across different environments. The CV of log expression of PptsG-gfp (green), PmglB-gfp (blue) and PrpsM-gfp (red) was plotted against the mean log expression. Power regression was fitted to each dataset corresponding to the expression

of the same reporter across different environments. The individual curves of variation in the expression of ptsG and rpsM reporters showed negative associations between the mean expression and the

variation of expression across environments, whereas the mglB reporter showed a positive association. (TIFF 145 KB) Additional file 3: Text S1: Analysis of expression of fluorescent reporters in glucose-acetate mixtures. (PDF 57 KB) Additional file 4: Figure S2: Reporter expression in mixed-substrate environments. Expression of ptsG, mglB and acs reporters was measured in chemostats (D = 0.15 h-1) in mixed-substrate environments supplemented with 0.28 mM Glc and 0.28 mM Ac (green), or 2.8 mM Glc and 2.8 mM Ac (blue). The distributions were plotted together with the measurements of the reporter expression in the environments GDC-0449 mouse with only glucose in the feed (0.56 mM Glc – orange, and 5.6 mM

Glc – red). The fluorescence of the promoterless strain is presented in black. (TIFF 544 KB) Additional file 5: Figure S3: Expression of the pck reporter in different chemostat and batch conditions. Ppck-gfp fluorescence (indication of flux to gluconeogenesis) was measured in bacterial populations grown in chemostats (D = 0.15 h-1) and batch environments supplied with minimal media supplemented with only D-glucose, only sodium acetate or D-glucose plus sodium acetate. Again, background fluorescence is the fluorescence of the promoterless strain, depicted in black. The expression of the pck reporter was decreased in the exponential phase in glucose batch cultures in comparison PD184352 (CI-1040) to carbon-limited chemostats. (TIFF 757 KB) Additional file 6: Figure S4: Changes in gfp expression prior of reaching theoretical steady-state. Pacs-gfp fluorescence was measured for five independent replicates growing on different concentration of glucose in the feed. At time point of 0 hours, chemostat experiments were started at a minimal dilution rate of D = 0.14 h-1. After 24 hours, dilution rates were increased to D = 0.15 h-1. The fluorescence plots show gfp distribution in bacterial populations without gating, together with fluorescence of the promoterless strain depicted in black. All independent replicates showed reproducible measurements of GFP fluorescence after 3.6 volume turnovers at D = 0.15 h-1.

​tcdb.​org. a Transporter classes 6 and 7 have not been assigned in the TC system yet and therefore are

not listed here. b Auxiliary proteins facilitate transport via established transport systems and therefore are not counted as a separate system. Of the channel proteins, almost all are alpha-type channels (Subclass 1.A). A few outer membrane porins (Subclass 1.B) were identified, but these were not examined more closely because of the recent extensive studies of Bhat et al. [33]. No potential channel-forming toxins (Subclass 1.C) were detected. The secondary carriers include mostly symporters (importers) and antiporters selleck chemical (exporters), while almost all primary active transporters are ATP-dependent (Subclass 3.A). However, a smaller percentage may be oxidoreduction driven (Subclass 3.D) or decarboxylation driven (Subclass 3.B). Among the seven group translocation proteins, two belong to the phosphotransferase system (Subclass 4.A), while five may be acyl CoA ligase-coupled transport systems (Subclass 4.C). Of the ten proteins possibly functioning as transmembrane electron flow carriers, all ten are likely to carry an electron pair (Subclass 5.A). None is likely to be a single electron carrier (Subclass 5.B). Eight auxiliary transport proteins (Subclass 8.A)

and ten recognized transporters of unknown mechanism of action (Subclass 9.A) were also identified. Substrates transported by Mxa Table 5 and Figure 5 show numbers of transport proteins Pyruvate dehydrogenase in Sco organized according to substrate types. Transporters that utilize inorganic molecules as substrates make up a large portion of all click here transport proteins found in Mxa. Cation-specific transporters (23.7% — 84 total) are split evenly between primary and secondary carrier

systems (36 and 38 proteins, respectively) with only six recognized channels. There are markedly fewer inorganic anion transporters (5.1% — 18 total), including 6 primary carriers and 10 secondary carriers. In comparison, there are relatively few electron transport systems in Mxa. Table 5 Counts of Mxa transport proteins according to substrate type Substrate No. of proteins of indicated type acting on substrate type   Channels/Pores Primary carriers Secondary carriers Group translocators Transmembrane electron flow carriers Auxiliary proteins (Putative) Poorly characterized Total no. of systems I. Inorganic molecules                 A. Nonselective 3             3 B. Cations 6 36 38   1   3 84 C. Anions   6 10   2     18 D. Electrons   4     3     7 II. Carbon sources                 A. Sugars & polyols   4 2 2       8 B. Monocarboxylates               0 C. Di- & tricarboxylates     1         1 D. Organoanions (noncarboxylic)     2         2 E. Aromatic Compounds   4           4 III. Amino acids & their derivatives                 A. Amino acids & conjugates   6 14         20 B. Amines, amides, polyamines, & organocations 1             1 C.

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71. Saller MJ, Fusetti F, Driessen AJ: Bacillus subtilis SpoIIIJ and YqjG function in membrane protein biogenesis. J Bacteriol 2009,191(21):6749–6757.PubMedCentralPubMed 72. Otani M, Kozuka S, Xu C, Umezawa C, Sano K, Inouye S: Protein W, a spore-specific protein in Myxococcus xanthus, formation of a large electron-dense particle in a spore. Mol Microbiol 1998,30(1):57–66.PubMed 73. Kuner JM, Kaiser D: Fruiting body morphogenesis in submerged cultures of Myxococcus xanthus. J Bacteriol Sepantronium solubility dmso 1982,151(1):458–461.PubMedCentralPubMed 74. Kim YM, Kim JH: Formation and dispersion of mycelial pellets of Streptomyces coelicolor A3(2). J Microbiol 2004,42(1):64–67.PubMed 75. Elizarov SM, Danilenko VN: Multiple

phosphorylation of membrane-associated calcium-dependent protein serine/threonine kinase in Streptomyces fradiae. FEMS Microbiol Lett 2001,202(1):135–138.PubMed 76. Padan E, Bibi E, Ito M, Krulwich TA: Alkaline pH homeostasis in bacteria: new insights. Biochim Biophys Acta 2005,1717(2):67–88.PubMedCentralPubMed 77. Yen MR, Tseng YH, Nguyen EH, Wu LF, Saier MH Jr: Sequence and phylogenetic analyses of the twin-arginine targeting buy ICG-001 (Tat) protein export system. Arch Microbiol 2002,177(6):441–450.PubMed 78. Palmer T, Berks BC: The twin-arginine translocation (Tat) protein export pathway. Nat Rev Microbiol 2012,10(7):483–496.PubMed 79. Hvorup RN, Winnen B, Chang AB, Jiang Y, Zhou XF, Saier MH Jr: The multidrug/oligosaccharidyl-lipid/polysaccharide (MOP) exporter superfamily. Eur J Biochem 2003,270(5):799–813.PubMed Fossariinae 80. Ruiz N: Bioinformatics identification of MurJ (MviN) as the peptidoglycan lipid II flippase in Escherichia coli. Proc Natl Acad Sci U S A 2008,105(40):15553–15557.PubMedCentralPubMed

81. Vasudevan P, McElligott J, Attkisson C, Betteken M, Popham DL: Homologues of the Bacillus subtilis SpoVB protein are involved in cell wall metabolism. J Bacteriol 2009,191(19):6012–6019.PubMedCentralPubMed 82. Fay A, Dworkin J: Bacillus subtilis homologs of MviN (MurJ), the putative Escherichia coli lipid II flippase, are not essential for growth. J Bacteriol 2009,191(19):6020–6028.PubMedCentralPubMed 83. Mohammadi T, van Dam V, Sijbrandi R, Vernet T, Zapun A, Bouhss A, Diepeveen-de Bruin M, Nguyen-Disteche M, de Kruijff B, Breukink E: Identification of FtsW as a transporter of lipid-linked cell wall precursors across the membrane. Embo J 2011,30(8):1425–1432.PubMedCentralPubMed 84.

In addition three of the four tryptophans, which are present in all intimin subtypes [27], are also present in Ifp and invasin (Figure 1). Figure 1 Amino acid alignment of intimin, ifp and invasion. The C-terminal 280 residues of EPEC 2348/69 intimin (Int280) and the corresponding regions from Y. pseudotuberculosis IP32953 Ifp and invasin were aligned. Residues important in intimin function are shown: conserved cysteine residues are highlighted CRT0066101 mouse in light grey whilst tryptophan residues are highlighted in dark grey. Thermoregulated temporal expression of ifp and inv The expression of ifp (YPTB1572) and inv (YPTB1668) at 24°C, 28°C and 37°C, were monitored using lux-based promoter fusions

PI3K inhibitor 1572lux and 1668lux in Y. pseudotuberculosis IP32953,

with the resultant luminescence read in a Lucy1 combined photometer and luminometer (Figure 2). The expression was determined as relative light units/optical density (RLU/OD) therefore the growth phase could also be determined, based on these OD readings (Additional file 2). Inv was maximally expressed during log phase after 5 hours at 24°C and 28°C, but after only 2.5 hours at 37°C, suggesting that mammalian body temperature is important in the induction of inv and confirms the observation of Isberg et al. [38]. In contrast, ifp expression remains low at 24°C and 28°C throughout the time course, whereas at 37°C there was little expression in first 7.5 hours, after which expression increases to a peak at 13 hours (Figure 2). Figure 2 Temporal expression of ifp ( 1572lux ) and inv ( 1668lux ). Expression was determined by light emission from lux-reporter strains grown at (A) 24°C, (B) 28°C and Succinyl-CoA (C) 37°C. Three biological replicates are shown for each strain, with each biological replicate tested in triplicate. Ifp binds to localised foci on HEp-2 cells Invasin and intimin are able to bind directly to specific receptors on the surface of mammalian cells. We therefore investigated the ability of Ifp to bind directly to HEp-2 cells using a MBP tagged Ifp purified protein (MBP-Ifp). In addition, to determine if the terminal

cysteine was as important in Ifp functionality (as it is in invasin and intimin), a MBP-Ifp recombinant protein with the terminal cysteine mutated to a glycine (MBP-IfpC337G) was constructed and tested. Utilising flow cytometry, FACScan analysis showed a shift in the peak of fluorescence of HEp-2 cells which had been incubated with MBP-Ifp (Figure 3). This shift was not seen with cells incubated with MBP-IfpC337G or MBP alone, indicating not only that this is a specific binding of MBP-Ifp, but also that the terminal cysteine is important in the functional binding of Ifp to HEp-2 cells. However, MBP-Ifp only appears to bind to a subset of cells and to differing levels, as shown by the width of the shifted peak.

The histological changes in DEN-induced liver cancer in rats are similar to those seen in human HCC. We think the similar phenotype might be based on similar gene expression profiles. Affymetrix GeneChip Rat 230 2.0 arrays were used to analyze gene expression profiles of liver tissues from control and DEN-treated

rats during the process from cirrhosis to metastasis. This allowed us to obtain an almost complete picture of the early genetic alterations that are 4SC-202 directly or indirectly involved in the development of HCC. We supposed that the genes expression profiles deregulated during the process from liver cirrhosis to carcinoma and metastasis play key roles in the hepatocarcinogenesis. The data obtained from the gene expression profiles will allow us to acquire insights into the molecular mechanisms of hepatocarcinogenesis and identify specific genes (or gene products) that can be used for early

molecular diagnosis, risk analysis, prognosis prediction, and development of new therapies. Materials and methods Animals and treatments Male Wistar rats weighing 120–150 g at the beginning of the experiments were obtained from SLAC Laboratory Animal Co. Ltd. (Shanghai). The animals were PI3K inhibitor acclimatized to standard laboratory conditions (temperature 22–25°C, relative humidity 50–60%, and 12 hour photoperiods (lights on 07:00–19:00 h)) and were housed in stainless steel wire-mesh cages (five rats per cage). During the entire period of study, the rats were supplied with a semi-purified basal diet (Shanghai) and water ad lib. All experiments followed the Guide for the Care and Use of Laboratory Animals. Briefly, ninety Wistar rats were randomly divided into two groups: the control and DEN group (DEN, Sigma Chemical Co. St Louis, MO; CAS 56-23-5; purity > 98%). After one week on a basal diet, rats belonging to the DEN group underwent intragastric administration of 1% aqueous solution of DEN (70 mg/kg) once a week, consecutively for 14 weeks. Animals that belonged to the control group received distilled water. There were ten rats in the control group. Daily food and water intakes were noted

and the body weights of the animals from each group were recorded every second day. The rats were sacrificed Amino acid with 25% (g/ml) urethane anesthesia (6 ml/kg) by intraperitoneal injection and sacrificed at different time points. At the end of the 2nd, 4th and 6th week after DEN-treatment, 3, 3, and 4 rats were sacrificed respectively at these time periods. From the end of the 8th week until the end of the 20th week after DEN-treatment, ten rats were sacrificed respectively every two weeks. Meanwhile one age-matched control rat was sacrificed. All the age-matched rats from the control group and rats of treatment groups were sacrificed on the same day. Sample collection and histopathological analyses Animals were chosen sequentially for necropsy.

5 V, while for the point contacts in Figure 5c, the threshold voltage does not exceed 1 V. It is also noticed that there is a different response of the I-Vs in the two metal-dielectric-metal devices.

Figure 5 C -AFM measurements of a- TaN x . (a) Positive I-V curves (solid lines) of TaN x deposited on Au for four different points fitted by the space-charge-limited current (SCLC) model (dash lines). (b) Negative I-V curves (solid lines) of TaN x deposited on Au for the same points presented in (a) fitted by the SCLC selleck compound model (dash lines). (c) Positive I-V curves of TaN x deposited on Si for three different points. The conductive part of the I-Vs exhibits an CHIR-99021 almost parabolic to almost ohmic behavior (d) Negative I-V curves of TaN x deposited on Si for the points presented

in (b). In all I-Vs, the leakage current is quite high, displaying also a very noisy profile. In general, the total current flowing through a semiconductor can be written as I tot = I b + I s, where I b is the current from the bulk part of the film and I s includes the electronic conduction through the surface states and through the space charge layer beneath the surface. Taking into account the amorphous nature of the semiconducting film, the main conduction mechanism from the bulk is expected to be the Poole-Frenkel effect [43]. Usually in amorphous materials, the predominant

conduction mechanism is the Poole-Frenkel effect, i.e., the thermal emission of electrons from charged vacancies, attributed to impurities and defects that are present in large numbers inside the bulk of the amorphous matrix [43, 44]. In the present samples, charged nitrogen vacancies act like Coulombic traps that promote the injection of electrons from the Au or Ag bottom electrode as the electric field increases during forward bias direction and from Pt/Ir tip during the reverse bias direction. For Poole-Frenkel emission, the current density is given by [45]: (1) where C and β are material dependent constants, E is the induced electric field, q is the electron charge, T is the temperature, k is the Boltzmann HSP90 constant, and φ is the ionization potential in V. The constant C is related to charge carrier mobility and trap’s density, while β is related to the dielectric constant ε 0 ε r via (2) Other possible charge carrier transport mechanisms from the bulk of the film could be thermionic emission of charge carriers across the metal-dielectric interface or field emission by electron tunneling from the metal or charge traps to the quasi-conduction band of the amorphous semiconductor [46]. These mechanisms have also exponential like I-V behavior.

To assess for differences between outcomes in the intervention and control groups, multi-level hierarchical modelling using the General Estimating Equation (GEE) approach was used to account for clustering to estimate the treatment effect as an odds ratio and test for significance [33, 34]. First-order interaction terms (specifically: sex by intervention status) were evaluated. The 95% confidence intervals and p values were calculated using the sandwich estimator of variance.

The analysis was carried out using R: A Language and Environment for Statistical Computing version 2.10.1 [35, 36]. The GEE models were fit using the R package geepack selleck kinase inhibitor version 1.0-17. Results Study flow Of the 54 eligible hospitals, 36 agreed to participate and

were randomly assigned to intervention or control group (18 in each group). We obtained 801 records for fracture patients within 3 months of their admission to the ED; 139 were received 3 months after fracture. Of these, 443 were excluded: 298 were unable to reach, 51 had died or were in long-term care, 43 lived outside of the hospital catchment area, 21 refused, 18 had previously been screened by a fracture clinic coordinator and 12 had significant cognitive or hearing impairment, resulting in 358 enrolled subjects (Fig. 1). Fig. 1 Flow of patients through the trial Cluster size was comparable between the groups with ten (range, 3–16) Unoprostone learn more in the intervention and ten (range, 4–18) in the control hospitals. Of those randomized, 52 from the intervention hospitals and 39 from the control hospitals were lost to follow-up

leaving a total of 267 subjects with complete data for analysis. The primary analysis is a ‘complete case’ and includes only those whose outcome is known [37]. A secondary analysis was the strict intention to treat analysis in which all randomized subjects were included. Baseline characteristics The mean age of the study participants was 66.0 years in the intervention and 65.4 in the control group; about two thirds were female and married. Twenty-seven percent had a history of a previous fracture since the age of 40 years, 20% were current smokers and 23% had fallen in the previous 12 months. Thirty-one percent had a BMD test in the previous 12 months, 25% self-reported a diagnosis of osteoporosis and 19% were currently taking osteoporosis medications. The most common fracture type was wrist (34%), followed by ankle (16%), rib (12%), shoulder (12%) and hip (8%). There was no significant difference in demographic and clinical characteristics among patients in the intervention and control groups (Table 1).