Occup Environ Med 59:777–784CrossRef Kuper H, check details Marmot M, Kuper H, Marmot M (2003) Job strain, job demands, decision latitude,

and risk of coronary heart disease within the Whitehall II study. J Epidemiol Commun Health 57:147–153CrossRef Kuper H, Adami HO, Theorell T, Weiderpass E (2006) Psychosocial determinants of coronary heart disease in middle-aged women: a prospective study in Sweden. Am J Epidemiol 164:349–357CrossRef Lee S, Colditz G, Berkman L, Kawachi I (2002) A prospective study of job strain and coronary heart disease in US women. Int J Epidemiol 31:1147–1153CrossRef Lynch J, Krause N, Kaplan GA, Tuomilehto J, Salonen JT (1997) Workplace conditions, socioeconomic Etomoxir supplier status, and the risk of mortality and acute myocardial

infarction: the Kuopio ischemic heart disease risk factor study. Am J Public Health 87:617–622CrossRef Markovitz JH, Matthews KA, Whooley M, Lewis CE, Greenlund KJ (2004) Increases in job strain are associated with incident hypertension in the CARDIA study. Ann Behav Med 28:4–9CrossRef Matthews KA, Gump BB (2002) Chronic work stress and marital dissolution increase risk of posttrial mortality in men from the multiple risk factor intervention trial. Arch Intern Med 162:309–315CrossRef Mosterd A, Hoes AW, Grobbee DE (1998) Epidemiology of heart failure: contours of an impending epidemic? Amylase EPZ015666 Neth J Med 53:235–244CrossRef Netterstrøm B, Juel K (1988) Impact of work-related and psychosocial factors on the development of ischemic heart disease among urban bus drivers in Denmark. Scand J Work Environ Health 14:231–238CrossRef Netterstrøm B, Kristensen TS (2005) Psykisk arbejdbelastning og iskaemik hjertesygdom. Ugeskr Laeger 167(46):4348–4355 Netterstrøm B, Kristensen

TS, Sjøl A (2006) Psychological job demands increase the risk of ischaemic heart disease: a 14-year cohort study of employed Danish men. Eur J Cardiovasc Prev Rehabil 13:414–420CrossRef O’Connell JB (2000) The economic burden of heart failure. Clin Cardiol 23:III6–III10CrossRef Orth-Gomer K, Wamala SP, Horsten M, Schenck-Gustafsson K, Schneiderman N, Mittleman MA (2000) Marital stress worsens prognosis in women with coronary heart disease: The Stockholm female coronary risk study. JAMA 284:3008–3014CrossRef Orth-Gomer K, Albus C, Bages N, DeBacker G, Deter HC, Hermann-Lingen C, Oldenburg B, Sans S, Williams RB, Schneiderman N (2005) Psychosocial considerations in the European guidelines for prevention of cardiovascular diseases in clinical practice: Third Joint Task Force.

The TiO2 films were sintered at 450°C for 30 min. The thickness of the TiO2 films was about 10 μm, and the active area of the TiO2 electrode was 0.25 cm2. The obtained TiO2 film was immersed in 0.5 mmol ethanol solution of N719 dye (Solaronix, Aubonne, Switzerland) for 24 h to adsorb the dye molecules. A Pt check details counter electrode was fabricated by squeeze printing of the Pt-Sol (Solaronix) on an FTO substrate. The sandwich-type solar cell was assembled by placing a Pt counter electrode on the dye-sensitized TiO2 electrode. The redox electrolyte (Dyesol) was injected between the electrodes.

Characterization An AM 1.5 solar simulator (white light from a 150-W Xenon lamp, McScience, Suwon-si, South Korea) was used as the light source. The incident light intensity was calibrated with a standard Si solar cell (Japan Quality Assurance JNJ-26481585 Organization, Tokyo, Japan). Electrochemical impedance spectroscopy (EIS) was conducted using Iviumstat (Ivium Technologies B.V., Eindhoven, the Netherlands) at an open-circuit potential selleck chemicals at frequencies ranging from 10−1 to 105 Hz with an AC amplitude of 10 mV. The diffusion coefficients and electron lifetime of the electrons in the TiO2 films were determined

using ModuLight-module under a red LED (λ = 625 nm) as light source (Ivium Technologies). The values of the diffusion coefficient and electron lifetime were obtained under 0.55-, 0.7-, 0.85-, and 1-V light intensity. Results and discussion TEM images and XRD data of the TiO2 nanorods sintered at various temperatures are shown in Figure 1. The phase transition of the TiO2 was observed depending on the sintering temperatures. With increasing sintering temperature, the amorphous TiO2 underwent phase transition to anatase and rutile structures. The crystallinity increased and the crystal size in the nanorods grew with increasing temperature. Comparison with the XRD peaks of P25, which contains both anatase and rutile phases, confirmed that the sintered nanorods at 750°C, 850°C, and 1,000°C had rutile peaks. During the high-temperature

thermal treatment, the average ADP ribosylation factor crystal size increased, reducing the grain boundaries and crystal defects. The decreased number of trap sites on the nanorods reduced the number of obstacles on the fast electron moving paths. These effects influenced the charge trap conditions and consequently increased the electron diffusion speed [20]. Among the nanorods sintered at various temperatures, those sintered at 850°C had the highest energy conversion efficiency in DSSCs. The photoelectrodes using a homemade paste with P25 TiO2 and 3 wt.% nanorod sintered at 450°C, 650°C, 750°C, 850°C, and 1,000°C exhibited efficiencies of 3.32%, 3.12%, 3.16%, 3.47%, and 3.41%, respectively. Figure 1 TEM images and XRD data of TiO 2 nanorods after sintering at various temperatures.

1 Specify whether the publications are open access (free access on Internet)   yes [] no [] – If yes: Enter the website address________________________________________________   8. Does your Institution agree to make its own scientific production freely accessible online on the open archive DSpace ISS http://​dspace.​iss.​it/​dspace set up by the Istituto Superiore di Sanità? yes [] no []   9. Please leave here any comments or notes if needed to clarify the answers given (by specifying the number of the related answer): Name and signature of the chief librarian or the person in charge at managing the publications

produced by your Institution Name_______________________________________________________________________ Signature____________________________________________________________________ Tel._________________________________________________________________________ check details E-mail_______________________________________________________________________ Date________________________________________________________________________ Print the

questionnaire and send it to_____________________fax number_______________ within_____________________________ Thank you   PRIVACY POLICY Notice provided according to the terms of art. 13 of Italian Legislative Decree no. 196 of 30 June 2003 for the protection of personal data The data AR-13324 chemical structure provided in the Questionnaire will be processed by means of automated equipment, only to fulfill the following tasks: to build up a unique reference access point to scientific information produced by the institutions surveyed through the digital archive DSpace ISS http://​dspace.​iss.​it/​dspace/​. Does the user grant her/his permission to processing their personal data according to the above mentioned tasks? Yes [] No [] Acknowledgements The authors wish to thank the colleagues tuclazepam from the Italian institutions surveyed who actively collaborated by providing data through the questionnaire administered: Barbara Matrascia, Pellegrino Musto, Antonio Rosato, William Russell-Edu, Alessandra Trocino. Special thanks to Roberto Ricci

for his expert support in implementing data export procedures to DSpace ISS XML schema and to Roberto Rizzo for revising the manuscript and bibliography according to the Instructions. The authors are also very grateful to Norah May and Tania Merlino who revised the English text. References 1. Law D: Making science count: Open Access and its impact on the visibility of science. In Proceedings of the Conference Institutional archives for research: experiences and projects in Open Access. Istituto Superiore di Sanità. Rome, 30 November-1 December 2006. XAV-939 ic50 Edited by: De Castro P, Poltronieri E. Roma: Istituto Superiore di Sanità; 2007:6–14. (Rapporti ISTISAN 07/12) 2. Di Diodoro D: EBM ed editoria scientifica. In Etica conoscenza e sanità: Evidence-Based medicine fra ragione e passione. Edited by: Liberati A.

ovis     63/290 (ATCC 25840; BCCN R17) Sheep Africa A A A F A B NA NA A C       Reo 198 (BCCN R22) Sheep United States A A A F A B NA NA A C       BCCN 76–250 Sheep France A A A F A B NA NA A C B. canis     RM6/66 (ATCC 23365; BCCN R18) Dog United States A A A D D C A A A A       D519 (BCCN C1) Dog Madagascar A A A D D C A A A A       BCCN 87.65 Dog Canada A A A D D C A A A A B. neotomae   A 5K33 (ATCC 23459; BCCN R16) Desert rat United States A B A D GS-4997 A A A A A A Marine mammal: B. pinnipedialis   A B2/94 Common seal Scotland A A A G A A A A A A B. ceti   A B1/94 Porpoise Scotland

A A A G A A A A A A aATCC, American Type Culture Collection; BCCN, Brucella Culture Collection, Nouzilly, France. NA: Not Amplified Figure 2 Restriction maps of the core- and O-polysaccharide genes with the restriction enzymes used. For each gene, restriction map A corresponds to that deduced from the nucleotide sequence of B. melitensis 16 M. Only differences compared to the nucleotide GSK2399872A research buy sequences of B. melitensis 16 M are indicated in restriction maps B, C, D, E, F and G. The

restriction patterns Pexidartinib mouse A, B, C, D, E, F and G are further indicated in Table 1 for each gene and for each Brucella strain studied. Additional sites and their most probable location according to restriction patterns are indicated by the restriction name (e.g. Hf) and by the position name and an asterisk. Figure 3 PCR-RFLP analysis

of Brucella LPS genes manA O-Ag , manB O-Ag , wbkD , wbkF , wboA and wa**. melitensis 16 M uncut; Fludarabine 3, manA O – Ag from B. melitensis 16 M cut by Alu I; 7, wbkF from B. melitensis bv2 cut by Alu I; 8, wbkF from B. abortus bv2 cut by Alu I; 9, wbkF 2* from B. melitensis 16 M uncut; 10, wbkF 2* from B. canis uncut; 11, wbkF 2* from B. melitensis 16 M cut by EcoR V; 12, wbkF 2* from B. canis cut by EcoR V; 13, wboA from B. melitensis 16 M uncut; 14, wboA from B. melitensis 16 M cut by Alu I; 15, wboA from B. abortus cut by Alu I; 16, wa** from B. melitensis 16 M uncut; 17, wa** from B. melitensis 16 M cut by Ava II; 18, wa** from B. suis bv2 cut by Ava II; 19, wa** from B. melitensis 16 M cut by Hinf I; 20, wa** from B. ovis cut by Hinf I. Panel B. Lanes: 1, molecular size markers; 2, manB O – Ag from B. melitensis 16 M uncut; 3, manB O – Ag from B. pinnipedialis uncut; 4, manB O – Ag from B. melitensis 16 M cut by Sau 3A; 5, manB O – Ag from B. melitensis bv2 cut by Sau 3A; 6, manB O – Ag from B. abortus cut by Sau 3A; 7, manB O – Ag from B. suis cut by Sau 3A; 8, manB O – Ag from B.

SAD, PB and WK performed cluster analysis and checked the dataset for errors. KN, PB, SAD and HN designed the Brucella specific Micronaut™ microtiter plate. SAD wrote the report. KN, HN and WK helped to draft the manuscript. All authors read, commented and approved the final article.”
“Background Mycobacterium avium subsp. paratuberculosis (MAP), the causative agent of Johne’s disease (JD) of ruminants, often selleck screening library requires eight to sixteen weeks to see colonies in culture – a major hurdle in the diagnosis and therefore in implementation of optimal control measures. Unlike other mycobacteria, which mobilize iron via mycobactins, MAP is unable to produce

detectable IWP-2 mycobactin in vitro or in vivo [1–3]. Although the reasons for the in vitro mycobactin dependency of MAP are currently unknown, we selleckchem have recently shown that the mycobactin (mbt) operon promoter is active and that the mycobactin genes are transcribed by MAP inside macrophages [4] and in tissues of naturally infected animals (accepted for publication in BMC Genomics). Pathogenic mycobacteria encounter a wide variety of stressors inside the host cells and their ability to overcome iron deprivation and iron toxicity represents a major virulence determinant [5]. Transcript and protein profiling of MTB and other pathogens in response

to in vitro iron stress is well documented [6–9]. While MAP transcriptome or proteome profiles in response to heat shock, pH, oxidative stress, hypoxia, and nutrient starvation have been demonstrated [10–12], stress responses to iron supplementation or starvation are lacking. Iron dependent regulator (IdeR) has been very well studied as a global regulator involved in maintaining iron homeostasis in Mycobacterium tuberculosis (MTB) [13]. Recently we have demonstrated that IdeR of MAP in the presence of iron recognizes a consensus sequence on the promoter called “”iron box”" and regulates expression of genes involved in iron acquisition (mbt) and storage (bfrA). Astemizole More interestingly, we demonstrated

that polymorphisms in the promoter of iron storage gene (bfrA) in S MAP strains relative to C MAP strains results in a differential gene regulation [4]. IdeR dependent repression of bfrA in the presence of iron suggests variations in iron storage mechanisms and/or iron requirements in cattle and sheep MAP strains. Comparative genomic hybridizations, short sequence repeat analysis and single nucleotide polymorphisms of MAP isolates obtained from diverse host species have established and indexed genomic differences between C and S strains of MAP [14–19]. Phylogenetic analysis of sequences has identified C and S strains as separate pathogenic clones that share a common ancestor [20–23]. Furthermore, cellular infection studies show distinctive phenotypes between the two MAP strain types [24, 25].

The identity of the bands has been confirmed previously [5]. The glycolipids marked with an asterisk have not been analyzed. Figure 3 Role of bgsB in biofilm formation and bacterial adherence to Caco-2 cells. A Biofilm formation on polystyrene. Microtiter plates were incubated with bacteria for 18 h, non-adherent bacteria removed by washing with PBS, and biofilms stained with crystal violet. Data represent the means ± SEM. *** P < Tukey's multiple

comparison test. B Development of biofilm on polystyrene of E. faecalis 12030 wt, 12030ΔbgsB, and 12030ΔbgsA over time. After incubation periods of ≥ 4 h, E. faecalis 12030 wt elaborated significantly more biofilm than the deletion mutants (P < 0.001, Tukey's multiple comparison test). Bars represent FK228 means ± SEM. C Bacterial adherence to Caco-2 cells. Caco-2 cells were incubated at a multiple of infection of 100:1 for 2 h with the respective strain grown to mid-log

selleck phase. Data represent the means ± SEM. *** P < 0.001, Dunn's multiple comparison test. Deletion of bgsB leads to a complete loss of glycolipids from the cell membrane and to expression of LTA with increased chain length We hypothesized that, because it is located immediately downstream from bgsA and has high homology to ALmgs in Acholeplasma laidlawii, the gene product of bgsB glycosylates diacylglycerol to yield MGlcDAG. To test this hypothesis, we extracted the total lipids of the cell membrane, separated them by thin layer chromatography (TLC), and stained glycolipids with α-naphthol (Figure 2). As shown previously, inactivation of bgsA resulted in accumulation of else MGlcDAG in the cell membrane (Figure 2). In contrast, no glycolipids were visualized in 12030ΔbgsB extracts, suggesting that bgsB encodes for a glycosyltransferase that glycosylates DAG to form MGlcDAG. MGlcDAG is the substrate of BgsA, which adds a second glucose to yield DGlcDAG (Figure 1). Since BgsA does not accept DAG as a substrate, inactivation of BgsB results in the loss of all glycolipids from the cell membrane (Figure 2). We recently showed

that inactivation of bgsA also affects LTA synthesis, increasing the chain length of the Anlotinib in vivo glycerol-phosphate polymer [5]. Inactivation of bgsB has a similar effect on the LTA chain length (Figure 4). To estimate the chain length of the glycerol-phosphate chain by 1H-NMR analysis, we used the fatty acid signals of the molecule as an internal reference and compared the integration values of H1 of glucose and -CH3 of alanine to the -CH3 and -CH2- signals (δ 1.26-1.29, and 0.88) of the fatty acids [5]. The integral ratios yielded higher amounts of glucose and alanine incorporated into the LTA of 12030ΔbgsB and 12030ΔbgsA compared to the wild type, suggesting an increased length of the glycerol-phosphate polymer (Figure 4). These results are supported by quantification of LTA from butanol extracts by ELISA (Figure 5).

The aim of the study presented here was to analyze which MCF7 signaling pathways were affected by the placenta. Methods: MCF7-eGFP cells cultured on matrigel with or without placental explants were separated from the placenta

by cell sorting and their mRNA was subjected to microarray analysis. ERa/STAT3/mTOR expression and phosphorylation levels were analyzed in these cells. Results: Trophoblast cells differentiate into extravillous trophoblast cells (EVT) which migrate into the matrigel. The effects (apoptosis/proliferation/detachment) were mainly observed in MCF7 cells that were located near the EVT cells. Microarray results have demonstrated significant changes in genes related to cell adhesion, glycan, breast carcinoma estrogen and JAK-STAT pathways.

Decreased ERa and elevated pmTOR and ABT-888 cost STAT3 proteins detected by immunobloting confirmed our findings at the transcript level. Moreover, promoter analysis of significantly affected genes in this array demonstrated an enrichment of motifs located at the transcription start site that match annotation for ISRE (interferon-stimulated response element), suggesting the activation of interferon (INF) signaling. Conclusion: Our results suggest that the placenta attenuates MCF7 growth in its vicinity by modulating INF/STAT and inducing detachment/migration and apoptosis. Published data demonstrated that the above pathways may THZ1 indeed stimulate these processes. The involvement of these signaling pathways in MGCD0103 clinical trial cell migration/apoptosis and the fate of the detached MCF7 cells will be further studied. Poster No. 113 Identification of Secretory Stromal Gene Signature of the Ovarian

17-DMAG (Alvespimycin) HCl Tumor Microenvironment and Implications for Ovarian Cancer Progression Melissa Thompson 1 , Lina Albitar2, Kwong-Kwok Wong1, Michael Birrer3, Samuel Mok1 1 Department of Gynecologic Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, USA, 2 Department of Obstetrics, Gynecology, and Reproductive Biology, Brigham and Women’s Hospital, Boston, MA, USA, 3 Department of Medicine, Massachusetts General Hospital, Boston, MA, USA The stromal microenvironment provides structural support and myriad signaling cues, which can significantly affect cell growth and development. The tumor-associated stromal microenvironment has been shown to play a key role in many cancers by influencing tumor initiation, invasion and metastasis. Our objective was to identify specific genes that are differentially regulated in the stromal component of high-grade late-stage serous ovarian cancer that may contribute to ovarian cancer progression.

DAPI stained CA4P nuclei (blue). Figure 6 Quantification of marked cells was done by learn more flow cytometry of HepG2 cells. Annexin V staining (Green Fluor-Log-Y) and PI staining (Red Fluor-Log-X) of HepG2 (B) and Huh7 (C) cells are shown. Values are shown on quadrants as means and standard errors of the mean SEM). Figure 7 Quantification of marked cells was done by flow cytometry of Huh7 cells. Annexin V staining (Green Fluor-Log-Y) and PI staining (Red Fluor-Log-X) of HepG2 (B) and Huh7 (C) cells are shown. Values are shown on quadrants as means and standard errors of the mean SEM). NAC increases IFN-a antitumoural responses mediated by NF-kB Pathway inhibition We then explored the role of the NF-kB pathway on NAC and IFN-α toxicity using siRNA-mediated p65 knockdown (KD cells). At 24 h post-transfection, a greater reduction of 95% of p65 expression levels was observed both through fluorescence microscopy (data not shown) and real-time PCR (Figure 8). Figure 8 Knock down of p65 subunit shown by real-time PCR. Relative quantification of p65 normalised by the expression of GAPDH in HepG2 and Huh7 cells 24 hours after transfection. Values are shown as means and standard errors of the mean (SEM). a- siRNAp65x COsiRNA p<0.01-HepG2. b- siRNAp65x COsiRNA p<0.01-Huh7.

The combined treatment with p65 siRNA with IFN-α for 24 h showed a decrease in cell viability that was comparable to that observed in NAC plus IFN-α treatment. On CHIR-99021 order the other hand, suppression of p65 did not sensitise cells to NAC, suggesting that the

mechanism of action of NAC primarily involves reduction of NF-kB (Figures 9 and 10). Figure 9 Effects of IFN and NAC on cell viability of HepG2 cells with p65 knock down. HepG2 cells were treated 24 h after siRNA duplexes transfection with IFN 2.5×104 U/mL and/or NAC 10 mM, and cell viability was determined after 24 hours of treatment. Values are shown as means and standard error of media (SEM). a- COsiRNA+NAC x COsiRNA x siRNAp65 p<0.01. b- siRNAp65 x COsiRNA x siRNAp65+IFN p<0.05. c- siRNAp65+IFN x COsiRNA x COsiRNA +NAC x siRNAp65 x siRNAp65+NAC 3-mercaptopyruvate sulfurtransferase (10 and 20 mM) p<0.05. Figure 10 Effects of IFN and NAC on cell viability of Huh7 cells with p65 knock down. Huh7 cells were treated 24 h after siRNA duplexes transfection with IFN 2.5×104 U/mL and/or NAC 10 mM, and cell viability was determined after 24 hours of treatment. Values are shown as means and standard error of media (SEM). a- COsiRNA+NAC x COsiRNA x siRNAp65 p<0.01. b- siRNAp65 x COsiRNA x siRNAp65+IFN p<0.05. c- siRNAp65+IFN x COsiRNA x COsiRNA +NAC x siRNAp65 x siRNAp65+NAC (10 and 20 mM) p<0.05. Discussion Given that the efficiency of IFN-α is only marginal in treating HCC, our study aimed to evaluate the effect of NAC on IFN-α toxicity, and how the co-treatment of NAC and IFN-α modulates cell death and growth inhibition in HCC human cell lines.

All media and serum were purchased from Gibcol. Normal human astrocytes (NHA) were obtained and maintained in specific growth medium AGM bullet kit

from Clonetics-BioWhittaker (Walkersville, MD, USA). U251 cells (2 × 105) in serum-free DMEM were infected with Ad-bFGF-siRNA at 100 MOI or an adenovirus vector expressing green fluorescent protein (Ad-GFP) or null (Ad-null) as mock controls at 100 MOI. Cells treated with DMSO were used as the controls. 8 h later, the virus-containing medium was removed and replaced with fresh DMEM containing 10% FBS. Cells were further incubated for 24, 48, or 72 h, respectively. Cells were then lysed and total protein was extracted. 2.2 Western Blot Western blot analysis was performed as previously described [8, 9]. Briefly, the treated and untreated U251 cells were lysed in M-PER Reagent (Thermo Co, Ltd) containing the halt protease and phosphatase inhibitor MEK162 in vivo cocktail. Protein (30 μg/lane), quantified with the BCA protein assay kit (Pierce, Fisher Scientific), was separated by 8-12% SDS-PAGE and transferred to PVDF membranes. The membranes were blocked with 5% non-fat dry milk in TBST (for non-phosphorylated proteins) or 5% BSA in TBST (for phosphorylated proteins) for 1 h and then incubated with primary Angiogenesis inhibitor antibodies overnight at 4°C. After washing, the membranes

were incubated with secondary antibodies conjugated to horseradish peroxidase (1:5000) for 1 h at room temperature and developed by an ECL kit (Thermo Co., Ltd.) 2.3 Antibodies and regents The primary antibodies

were obtained from Santa Cruz (Beijing China) (bFGF, pJAK2 (Tyr1007/1008), STAT3, pSTAT3 (Ser727), CyclinD1, Caspase3, Cytochrome C, Bcl-xl, Bax, and Beta-actin). Other antibodies were form CP673451 nmr Genemapping (Tianjin China) (JAK2, pSTAT3 (Tyr705), anti-Src, anti-pSrc (Tyr419), anti-ERK1/2, anti-pERK1/2 (Thr202/Tyr204)). Human recombinant IL-6 was purchased from Sigma (Beijing China). 2.4 ELISA Analysis of IL-6 Release The U251 cells were infected as above and collected from 0-24, 24-48, or 48-72 h periods IL-6 secretion was determined using Loperamide a human IL-6 ELISA kit (4A Biotech, Beijing, China). The results were read using a microplate reader at 450 nm. A standard curve prepared from recombinant IL-6 was used to calculate the IL-6 production of the samples. 2.5 Measurement of mitochondrial transmembrane potential (ΔΨm) Mitochondrial transmembrane potential (ΔΨm) was measured with the mitochondrial membrane potential assay kit with JC-1 (Beyotime, Shanghai, China). Cells were infected with Ad-bFGF-siRNA at 100 MOI for 8 h in 6-well plates, incubated in fresh DMEM for 72 h, and collected and resuspended in fresh medium. Cells were then incubated at 37°C for 20 min with 0.5 mL of JC-1 working solution.

Garver P, Muriana M:

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