Int J Food Microbiol 2006, 108:178–181 CrossRef 61 Joint Committ

Int J Food Microbiol 2006, 108:178–181.CrossRef 61. Joint Committee on Powder Diffraction Standards: Powder Diffraction File Card 04–0783. Swathmore, AR-13324 order PA: International Center for Diffraction Data; 1987. Competing interests The authors declare that they have no competing interests. Authors’ contributions ERL, RIP, and

REN carried out the experiments. ERL, RIP, REN, JT, RHU, and AM analyzed the data. CIP conducted the plate count experiments. ERL, RIP, JT, and AM developed the conceptual framework, and AM supervised the whole work. ERL, RIP, and AM drafted the paper. All authors read and approved the final manuscript.”
“Background GSK2118436 Carbon nanotube (CNT) arrays for field emission (FE) applications have been extensively studied experimentally and theoretically [1–5]. Various improvements to fabricate well-aligned CNT arrays have been achieved, but non-uniformities are always present. To build precise arrays is expensive and difficult in extending to large areas. Simulation of CNT arrays is cost effective; however, check details simulation of these structures including non-uniformity is rare in the literature. To model non-uniformities in FE, it is necessary to understand their effects on the emission current. The simulation of FE in large domains is notoriously difficult especially in three dimensions, which is necessary in this analysis. The difficulties include long simulation times, large computer memory requirements,

and computational instability. The first analysis of this kind is the recent work of Shimoi and Tanaka [6]. They managed to perform three-dimensional (3D) simulations based on boundary elements that avoided meshing the volume of the 3D domain. They simulated carbon nanofibers

with random position and height to match the emission pattern that they obtained experimentally. In this work, we perform simulations of non-uniform CNTs with dispersions in selleck chemical height, radius, and position in limited ranges and with small CNT aspect ratios aiming to correlate the current from non-uniform arrays with the current expected from perfect arrays. We restrict our analysis to a hemisphere-on-a-post model [4, 6–8], in which the CNTs are regarded as perfect conductors, with a smooth surface and oriented normal to the substrate. In this report, we shall refer to these idealized tubes as CNTs. Methods The CNTs are positioned in a 3 × 3 square array, as shown in Figure 1. We shall explain hereafter that a 3 × 3 square array is an efficient way to perform the simulations. The ith CNT height H i , radius R i , and coordinates (X i ,Y i ) are stochastic variables with expected values (or averages), respectively, equal to h = 10 a.u., r = 1 a.u., and (x i ,y i ) being the center of the ith unit cell in the array. Thus, the default aspect ratio is 10, which is quite small. However, larger aspect ratios cause simulation difficulties that will be discussed later.

Most of the Bochdalek hernias are diagnosed

Most of the Bochdalek hernias are diagnosed LY3023414 mw in children who present with pulmonary symptoms [6, 7, 11]. Since Bochdalek hernia in an adult is an asymptomatic condition,

it is usually an incidental finding which makes its incidence difficult to be estimated. These can sometimes present with vague chest and gastrointestinal symptoms [6, 11]. The predominance of the left side in symptomatic cases both in neonates and adults may be due to narrowing of the right pleuroperitoneal canal by the caudate lobe of the liver [12]. Another reason may be that the right pleuroperitoneal canal closes earlier. According to a recent report in 2002, there are only seven symptomatic cases involving the right hemidiaphragm in the literature [13]. The hernial size varies and the content of the hernial sac may differ from each selleck products other in every age group. Hernias on the left side may contain intestinal loops, spleen, liver, pancreas, kidney or fat. Colon in a Bochdalek hernia is a rare learn more condition and usually found in the left-sided hernias as was also

the case in our patient [7, 14]. A medline search for cases of colon in a BH revealed about 32 cases (Table 1) [15–39]. A coexisting hernial sac has also been reported in 10–38% of the cases according to large series [7]. Some authors believe that long-term survival may be due to the persistence of a pleuroperitoneal sac (hernial sac) and that the rupture of the sac in adult life may trigger the characteristic

symptoms [40]. There was no hernial sac in our patient. Drugs such as thalidomide or antiepileptics administered during pregnancy i.e. before the closure of the pleuroperitoneal canal before 9th to 10th weeks’ gestation along with the genetic predisposition have been incriminated as the etiological factors. A congenital diaphragmatic hernia can be accompanied by other congenital anomalies in 25–57% and by chromosomal disorders in 10–20% of cases [10]. Our patient did not have any obvious congenital anomaly. Bochdalek hernias may show up on chest X-rays as air and fluid-filled viscera in the hemithorax, as in our case. Associated mechanical obstruction may be Celastrol obvious on plain X-ray imaging. Contrast-enhanced computed tomography (CT) has been an increasingly important investigation method in assessment of acute presentation which was not used in our case. The rare finding of a dilated bowel above the hemidiaphragm makes the diagnosis obvious. Other investigations including upper gastrointestinal contrast studies can exclude malrotation [41]. Gastrointestinal contrast studies could not be done since our case was an emergency situation. A delayed or missed diagnosis of diaphragmatic hernia can lead to significant morbidity and mortality [42].

However, the deposition of thicker buffer layer is limited becaus

However, the deposition of thicker buffer layer is limited because of the poor adhesion of the lanthanum nitrate buffer layer with the underlying PVP organic film. The X-ray diffraction (XRD) measurements indicate that the films are crystallized into a pure perovskite phase, with a tetragonal geometry. It is evident from Figure 1b that no diffraction peaks are observed for the samples (buffer layer thickness 8.9 nm) annealed at 600°C, whereas it shows well-defined peaks for films annealed at 700°C. The films annealed at 600°C do not show any learn more diffraction

peaks of fresnoite or BTO, indicating the amorphous nature of the film. The peak observed around 26° correspond to La2O3. The absence of the fresnoite silicate phases also indicates that no reaction happened at the BTO/buffer layer interface due to the interdiffusion of Si. Figure 1c shows the XRD patterns of BTO thin films (annealed at 700°C) deposited on 8.9-nm-thick buffer layers that are heat-treated at 450°C or 600°C. It is obvious from the measurements that crystallization of the BTO films is influenced by the heat treatment of the buffer layer. Since the LaO(NO3) intermediate phase is only present up to 570°C, after which an non-stoichiometric unstable La(O)1.5(NO3)0.5 phase appears, it is clear that the LaO(NO3) phase exhibits

superior properties as an intermediate layer. The heat treatment influences the nucleation mechanism of the BTO film selleck inhibitor and results selleckchem in different diffraction peaks in the XRD spectrum. Crystal orientation of BTO thin film The dielectric, piezoelectric, and electro-optical properties of the thin films depend strongly on the crystal orientation. Highly c-axis-oriented BTO thin films reported before are grown on either a single-crystalline oxide substrate or with a preferentially oriented thick (>100 nm) conductive or dielectric intermediate buffer layer [13, 15]. The use of a thick buffer layer limits the performance of the ferroelectric films for certain applications (e.g., electro-optical devices). The results shown in Figure 2 indicate that we can grow highly c-axis SB-715992 price textured BTO films with LaO(NO3)

buffer layers (keeping the buffer layer thickness as 8.9 nm) by adding the number of annealing steps. Figure 2 XRD patterns obtained for BTO thin films. The films were deposited on a buffer layer with a thickness of 8.9 nm and a BTO seed layer of 30 nm (a) annealing after each 30-nm BTO layer deposition at different temperatures and (b) annealing at 700°C after each 30-nm BTO layer deposition or after four 30-nm BTO depositions (120 nm). Figure 2 shows the XRD pattern of BTO films grown on a BTO seed layer. The seed layer is prepared by depositing a thin layer (30 nm) of BTO film on the buffer layer (8.9 nm), followed by pyrolysis (350°C) and annealing (700°C). After the seed layer, either the normal procedure is followed (annealing after 120 nm of BTO is deposited) or layer-by-layer annealing is used (after each 30-nm deposition).

The three

The three rescued viruses were named FMDV-RDD, FMDV-RGD, and FMDV-RSD, respectively. To increase the virus titers, all rescued viruses were subjected to serial passage in BHK-21 cells, after which the VP1 sequence was analyzed to confirm that the recovered viruses had maintained the cDNA-encoded receptor binding motifs (Table 2). When the growth characteristics of the rescued viruses were compared with the parental see more virus

Asia1/JSp1c8 by one-step growth kinetics assays, rescued viruses showed similar growth properties to the parental virus (Figure 2a). In addition, the buy MRT67307 plaque sizes of the parental virus and the rescued viruses were also similar (Figure 2b). These results suggest that single amino acid substitutions in the receptor

binding site of Asia1/JSp1c8 virus do not affect virus viability. Figure 2 Growth characteristics of three rescued viruses in cell culture compared with parental virus. (a), One-step growth curves of the parental and three cloned viruses. (b), Morphology of plaques formed in BHK-21 cell monolayers by the parental and three cloned viruses. The pathogenicity of the rescued viruses in cattle and MM-102 research buy swine To investigate the pathogenicity of the non-RGD viruses in the natural host, we performed direct inoculation of parental virus Asia1/JSp1c8 and recombinant viruses (FMDV-RSD and FMDV-RDD) in cattle and pigs. After inoculation, a number of disease parameters were analyzed, including fever, clinical score, and viremia. The animals, except for the FMDV-RSD-inoculated animals, showed fever and extensive tissue damage at the inoculation sites by day 1 and achieved the maximal score of lesions on day 2-4. Some FMDV-RSD-inoculated animals developed Epothilone B (EPO906, Patupilone) fever and tissue damage by day 2 and achieved the maximal score of lesions on day 3-5. Two animals (infected with FMDV-RSD) had no evidence of tissue damage, except for occasional depression and anorexia when their body temperatures

rose. The Asia1/JSp1c8 and FMDV-RDD viruses produced more extensive tissue damage at the injected sites and induced fever and vesicles a day earlier than in the FMDV-RSD-inoculated animals. There were significant differences in lesion scores between RDD viruses (Asia1/JSp1c8 and FMDV-RDD) and RSD virus (P < 0.05, P < 0.05), however, no significant differences in lesion scores between cattle and pigs (P > 0.05). The lesion scores for the inoculated animals are summarized in table 3 and figure 3 shows the rectal temperature of all of the inoculated animals. The disease was characterized by viremia in all inoculated animals, including the animals that did not generate vesicular lesions. The level of viremia increased following inoculation, typically reaching a peak level after two or three days then decreasing to zero by day 8.

Growth was followed by OD600 measured in a Secomah spectrophotome

Growth was followed by OD600 measured in a Secomah spectrophotometer. As 30 μM

CuSO4 may be added to the culture, we monitored its global effect on L. sakei growth. In static or anaerobic growth conditions, 30 μM CuSO4 had no effect on growth. In aeration conditions, 30 μM CuSO4 had a Bioactive Compound Library slight effect on growth (2-10% lower OD600 at the end of growth), and slightly extended viability. Meat juice was obtained from beef meat homogenized with half volume of sterile water in a Stomacher for 2 cycles of 3 min each. The supernatant obtained after centrifugation (10,000g for 15 min) was filter sterilized and stocked at -20°C (M.-C. Champomier Vergès, unpublished). Escherichia coli (DH5αF’ or TGI) was cultured aerobically in LB at 37°C. Selective pressure for plasmids was maintained in E. coli with ampicillin 100 mg.l-1, and in L. sakei, with erythromycin 5 mg.l-1. DNA techniques Standard procedures were used for DNA manipulation. Classical PCR reactions were performed with Taq polymerase (Fermentas) or Pfu

polymerase (Promega) for cloning purpose, and run in MJ research PTC-200 thermocycler. Extraction of plasmids and chromosomal DNA as well as electroporation of L. sakei and L. casei BL23 was carried out as described check details [52]. Primers are listed in additional file 4. Diversity of sigH in L. sakei L. sakei strains (18, 21, 23 K, 64, 112, 160 K, 300, 332, JG3, MF2091, MF2092, ATCC15521, CIP105422, SF771, LTH677, LTH2070) were from our collection or different sources as described [20]. PCR amplification of the sigH locus was carried out with two pairs of primers (AML31/AML32 and AML50/AML58). Sequence of the 561 nt fragment corresponding to entire CDS and the 77 nucleotides of the upstream intergenic region was performed on PCR-amplified genomic DNA using each of the four primers.

Pairwise distances were calculated by MEGA 4 [53] using a Kimura 2-parameter substitution model. Construction of sigH mutant and sigH Amine dehydrogenase expression strains SigH production and sigH mutant strains were constructed from RV2002, a derivative of L. sakei 23 K that had undergone a deletion of the lacLM gene encoding β-galactosidase [23]. Their construction used plasmids pRV610 and pRV613 [27] which contain two replication origins, one functional in E. coli (pBluescript) and one for Gram-positive bacteria (pRV500). The L. sakei σH overproducer strain sigH(hy)* was obtained by introducing plasmid pRV619 into RV2002. pRV619 was constructed from pRV613 which bears the PatkY copper-inducible promoter cassette of L. sakei fused to the E. coli lacZ reporter gene [27]. lacZ was replaced by sigH Lsa in pRV619 as follows. The sigH Lsa coding region was PCR-amplified from L. sakei strain 23 K chromosomal DNA with primers AML31 and AML32 and the BamHI/XbaI fragment was cloned into pRV613 digested by the same enzymes, using Lactobacillus casei BL23 as a host, since neither L. sakei nor E.

Moreover, a multiple regression model showed that C2 was not sign

Moreover, a multiple regression model showed that C2 was not significantly related to other variants as above. ROC curves were drawn to detect the optimum cut-off level of the average C2 or C0 for CR (Fig. 5). Using all data of the cases treated for 48 weeks in groups 1 and 2 (N = 37), the area under ROC curves were 0.731 ± 0.089 (95 % CI 0.557–0.905, p = 0.022)

for C2 and 0.373 ± 0.109 (95 % CI 0.156–0.587, not significant) for C0. From these results, the optimum cut-off point for C2 was determined to be 615 ng/mL (sensitivity 75.0 %, specificity 76.9 %); however, C0 was inappropriate eFT-508 cost to predict remission. Using the data of group 2 alone (N = 19), similar results were obtained. Namely, the AUCs were BI 10773 cell line 0.802 ± 0.101 (95 % CI 0.604–1.000, p = 0.025) for C2 and 0.444 ± 0.158 (95 % CI 0.135–0.754, not significant) for C0, and the cut-off point for C2 was determined to be 598 ng/mL (sensitivity 66.7 %, specificity 100 %). When the data of C2 were limited to the cases <340 mg/dL of total cholesterol

(N = 25), the AUCs were greater (0.868 ± 0.072, 95 % CI 0.712–1.000, p = 0.003) and the cut-off point 598 ng/mL was more accurately provided (sensitivity 81.3 %, specificity 88.9 %). Fig. 5 Receiver operator characteristic (ROC) curves for serum CyA concentration. The optimal cut-off level of C2 for CR was determined to be 615 ng/mL (sensitivity 75.6 %, specificity 76.9 %) and 598 ng/mL (sensitivity 81.3 %, specificity 88.9 %) (arrows), using the ROC curve drawn from the average C2 of all cases and the cases <340 mg/dL of total cholesterol treated for 48 weeks in groups 1 and 2, respectively Relationship between blood CyA concentration and treatment responses Patients in groups 1 and 2 were further divided into subgroups A (C2 ≥600 ng/mL) and B (C2 <600 ng/mL) because the ROC showed that the optimal cut-off point of C2 was approximately 600 ng/mL. The number of patients in groups 1A, 1B, 2A, and 2B was Buspirone HCl 19, 4, 10, and 13, respectively (Fig. 6). Most of the patients in groups 1A and 2A achieved CR. Among these 4 groups, groups 1A and 2A showed

significantly higher cumulative CR ratios than group 2B for 48 weeks; group 1B was excluded because of the statistically insufficient number of patients (Fig. 7). Meanwhile, there was no significant difference between groups 1A and 2A. Groups 1A and 2A, consisting of all patients with C2 ≥ 600 ng/mL, also showed a significantly higher cumulative ratio of not only CR (p = 0.0028, Fig. 8a) but also CR + ICRI (p = 0.0069, Fig. 8b) than groups 1B and 2B (C2 <600 ng/mL). Fig. 6 Remission and withdrawal rates of groups 1A, 1B, 2A, and 2B at 48 weeks. Patients were divided into groups 1 and 2 according to administration frequency and then subdivided into subgroups A (C2 ≥600 ng/mL) and B (C2 <600 ng/mL). There was a significant difference in CR between groups A and B (p = 0.018, per-protocol analysis) Fig.

These results indicate that parthenolide induced amastigote cell

These results indicate that parthenolide induced amastigote cell death by autophagy, but other mechanisms of cell death cannot be dismissed, such as apoptosis and necrosis. Considering the limited repertoire of existing antileishmanial compounds, continuously developing new leishmanicidal compounds is essential. In the ongoing search for the best antileishmanial compounds, products derived from plants are gaining ground. The isolation and purification of the active components of medicinal

plants has been one the greatest advances. Additionally, delineation of the biochemical mechanisms involved in mediating effect of these compounds would help develop new chemotherapeutic approaches. Methods Drugs selleck chemicals Parthenolide (minimum 90%) was purchased from Sigma-Aldrich (Steinheim, Germany). Amphotericin B (Cristália, Produtos Químicos Farmacêuticos Ltda, Itapira, SP, Brazil) was used as a positive control. In all of the tests, 0.05% dimethyl sulfoxide (DMSO; Sigma, St. Louis, MO, USA) was used to dissolve the highest dose of the compounds and had no effect on the parasites’ proliferation or morphology.

Axenic amastigotes Promastigotes of the Leishmania species differentiate to amastigotes with the combination of low pH and high temperature [46]. The WHOM/BR/75/Josefa strain of Leishmania amazonensis, isolated by C.A. Cuba-Cuba (University of Brasília, Brasília, Distrito Federal, Brazil) from a human case of diffuse cutaneous leishmaniasis, was used in the present study. Axenic amastigote cultures were obtained by the in vitro differentiation of promastigotes from the stationary phase in 25 cm2 tissue culture flasks by progressive temperature increase and pH decrease [47]. The cultures were maintained at 32°C in Schneider’s insect medium (Sigma, St. Louis, MO, USA), pH 4.6,

with 20% fetal bovine serum PARP inhibitor through weekly serial sub-culturing for further studies. Antiproliferative effect For the parasite growth inhibition assays, L. amazonensis axenic amastigotes were harvested during the exponential phase of growth, and 106 cells were added to each well of a 24-well plate and treated with different concentrations of parthenolide aminophylline and amphotericin B. Medium alone and 0.05% DMSO were used as negative controls. For each treatment, the parasites were observed and counted daily using a Neubauer chamber with an optical microscope. Each experiment was performed in duplicate and twice on different occasions. The antiproliferative effect (percentage of growth inhibition) was evaluated with 5 day treatment, and the data are expressed as the mean ± standard error of the mean (Microsoft Excel). The corresponding 50% and 90% inhibitory concentrations (IC50 and IC90) were determined from the concentration-response curves (Excel software).

The 6-TG inhibited Mpn growth with MIC value of 0 20 μg ml-1, whi

The 6-TG inhibited Mpn growth with MIC value of 0.20 μg ml-1, which is equivalent to tetracycline (MIC = 0.1 μg ml-1). However, 6-MP, a 6-TG analog did not inhibit Mpn growth. Neither theophylline, 7-(2, 3-dihydroxypropyl) theophylline, allopurinol, nor caffeine inhibited Mpn growth. 6-TG strongly inhibited uptake and incorporation of Nutlin-3a supplier nucleotides derived from Hx and Gua into DNA and RNA, indicating that the observed inhibition by 6-TG was both at the level of transport and metabolism. It is noteworthy that the uptake/metabolism of Hx and Gua was inhibited by all the analogs used. Thiopurines, especially Crenolanib concentration mercaptopurines, are the first line drugs for the treatment of acute

leukemia since the 1950s. They are also used in the treatment of inflammatory bowel disease [43]. The 6-TG and 6-MP exert their cytotoxicity through incorporation into DNA as deoxy-6-thioguanosine. These thiopurines are metabolized to deoxy-6-thioguanosine triphosphate via the purine salvage pathway initiated by HPRT (Figure 4). Thiopurine methyl transferase is a key enzyme in converting mercaptopurine to its cytotoxic metabolites, which can either inhibit purine nucleotide biosynthesis

or incorporate into DNA or RNA, causing DNA damage and cell death [37]. Mpn does not possess the essential enzymes, inosine monophosphate dehydrogenase and thiopurine methyl transferase, to convert mercaptopurine to the cytotoxic thioguanine

nucleotides, the respective methyl thiopurine nucleotides. This may explain why 6-MP did not inhibit Mpn growth. To further investigate the selleck chemicals mechanism by which 6-TG inhibited Mpn growth, Mpn HPRT was expressed, purified, and characterized. Both Hx and Gua are good substrates for the enzyme and the Vmax values for these substrates are in the same order of magnitude as the human enzyme [44]. In humans, the plasma concentrations of Hx and Gua are approximately 172 μM and 97 μM [45], which is close to the Km and S0.5 values of Mpn HPRT with Hx and Gua. These results almost suggest that Mpn HPRT is capable of efficiently salvaging both Hx and Gua. In addition, Mpn HPRT showed positive cooperativity with Gua, indicating that at higher Gua concentration the enzyme utilizes Gua better. 6-TG and 6-MP are structural analogs. The observed significant differences in their inhibitory effects with Mpn and human HPRT suggest that there are structural differences in binding of these two compounds to the respective HPRTs in their active sites. These differences could be used in future design of Mycoplasma specific inhibitors. HPRT has been suggested as a target for anti-parasite drug development and new compounds have been developed [46]. Halogenated pyrimidine analogs such as 5FdU inhibited Mpn and Ureaplasma growth, as reported in our earlier studies [30, 35].

0)[26] grade 2 from previous anti-cancer therapy Alanine aminotra

0)[26] grade 2 from previous anti-cancer therapy Alanine aminotransferase (ALT), aspartate aminotransferase (AST), or alkaline phosphatase (ALP) >5× Upper Limit of Normal (ULN), serum

bilirubin >1.5× ULN or serum creatinine >185 µmol/L Leukocytes <4.0 10 9/l and/or platelet count <150 10 9/l Significant cardiac event (e.g. myocardial Navitoclax infarction, superior vena cava (SVC) syndrome, New York Heart Association (NYHA) classification of heart disease ≥2 within 3 months before entry, or presence of cardiac disease that, in the opinion of the investigator, increases the risk of ventricular arrhythmia Pregnancy or breast feeding Comorbidity with a grave prognosis (estimated survival <3 months) and/or worse than the basic disease for which the patients will be included in the study Abnormalities of the bile ducts (such as stents) with an increased chance of infection Diseases with an increased chance of liver toxicity, such as primary biliary cirrhosis or xeroderma pigmentosum Patients who are declared

incompetent or have a psychiatric disorder that makes a comprehensive judgement impossible, such as psychosis, hallucinations and/or depression Previous enrolment in the present study or previous treatment with radioembolization Treatment with an investigational click here agent within 42 days prior to enrolment Female patients who are not using an acceptable method of contraception or are less than 1 year postmenopausal or surgically sterile during their participation in this study (from the time the consent form is signed) to prevent pregnancy Male patients who are not surgically sterile or do not use an acceptable

method of contraception during their participation in this study to prevent pregnancy in a partner Evidence of portal hypertension, splenomegaly or ascites Body weight >150 kg Active hepatitis (B and/or Thiamine-diphosphate kinase C) Liver weight >3 kg (determined by software using CT data) Allergy for intravenous contrast agent used (Visipaque ®) General MRI contra-indications (severe claustrophobia, metal implants, implanted pacemaker and/or neurostimulators) Patients who have arterial variations that will not allow whole liver treatment by a single administration via the hepatic artery Acknowledgements The authors thank Ms. Tjitske Bosma (clinical research coordinator, University Medical find more Center Utrecht) for her contribution to the study design and coordination, and Mr. Remmert de Roos for his assistance in the preparation of the microspheres. This study was financially supported by the Dutch Cancer Society (KWF Kankerbestrijding), under grant UU2009-4346. References 1. Choti MA, Bulkley GB: Management of hepatic metastases. Liver Transpl Surg 1999, 5:65–80.PubMedCrossRef 2. Russell AH, Tong D, Dawson LE, Wisbeck W: Adenocarcinoma of the proximal colon. Sites of initial dissemination and patterns of recurrence following surgery alone.

9 5,802 25 9 0 1,897 24 9 1,897 24 9

0 85–89 5,775 25 8 5

9 5,802 25.9 0 1,897 24.9 1,897 24.9

0 85–89 5,775 25.8 5,775 25.8 0 1,685 22.1 1,685 22.1 0 90+ 4,515 20.1 4,515 20.1 0 982 12.9 982 12.9 0 Fiscal year 04/05 5,786 25.8 5,786 25.8 Selleck NVP-BSK805 0 1,856 24.4 1,856 24.4 0 05/06 5,481 24.4 5,481 24.4 0 1,871 24.6 1,871 24.6 0 06/07 5,539 24.7 5,539 24.7 0 1,919 25.2 1,919 25.2 0 07/08 5,612 25.0 5,612 25.0 0 1,965 25.8 1,965 25.8 0 RIOa Mean ± STD, 0 (most urban) to 100 (most rural) 16.7 ± 18.9   16.1 ± 18.7   0.03 17.3 ± 19.6   17.1 ± 20.1   0.01 LTCa   4,797 21.4 4,797 21.4 0 1,352 17.8 1,352 17.8 0 Income quintilea 1 (low) 5,218 23.3 5,315 23.7 0.01 1,739 22.8 1,649 21.7 0.03 2 4,536 20.2 4,563 20.4 0 1,569 20.6 1,625 21.4 0.02 3 4,361 19.5 4,377 19.5 0 1,419 18.6 1,417 19.3 0.02 4 4,216 18.8 4,119 18.4 0.01 1,421 18.7 1,396 18.3 0.01 5 (high)

4,087 18.2 4,044 18.0 0 1,463 18.0 1,470 19.3 0 Number of CADGsb 0–3 8,079 36 8,032 35.8 0 2,502 32.9 2,360 31 0.04 4–7 13,567 60.5 13,670 61 0.01 4,816 63.3 4,987 65.5 0.05 8–12 772 3.4 716 3.2 0.01 293 3.8 264 3.5 0.02 Osteoporosis diagnosisb   2,050 9.1 1,785 8.0 0.04 271 3.6 180 2.4 0.07 DXA testb   2,346 10.5 2,707 12.1 0.05 337 4.4 296 3.9 0.03 Osteoporosis treatmentb   7,145 31.9 6,178 27.6 0.1c 753 9.9 448 5.9 0.15c Prior fractureb  Humerus/radius/ulna   948 4.2 464 2.1 0.12c 183 2.4 58 0.8 0.13c  Vertebral   329 1.5 110 0.5 0.1c 87 1.1 36 0.5 0.07  Otherd   2,863 12.8 493 2.2 0.41c 903 11.9 134 1.8 0.41c CADG collapsed ambulatory diagnostic group, DXA dual-energy X-ray absorptiometry, IQR interquartile range, LTC long-term care, RIO rurality index for Ontario, SD standardized difference, STD standard deviation aBased on postal code and census data at time of index bMedical and pharmacy claims identified within 365 days prior to index cSD >0.1 indicates unbalance between ZD1839 mouse cohorts [23] dOther = femur, pelvis, lumbar spine, ribs, shoulder and upper arm, shoulder girdle, pathological or stress fracture Outcomes and resource utilization With the exception of same day surgery,

more individuals in the fracture cohort than the non-hip fracture cohort utilized health-care resources (Table 2). Of patients residing in the check details community at the time of hip fracture, 19 % (men) to 24 % (women) entered a LTC facility within a year of hip fracture.