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Palm, Eleonor
Publications (10 of 13) Show all publications
Ljunggren, S., Bengtsson, T., Karlsson, H., Johansson Starkhammar, C., Palm, E., Nayeri, F., . . . Lönn, J. (2019). Modified lipoproteins in periodontitis: a link to cardiovascular disease?. Bioscience Reports, 39(3), Article ID BSR20181665.
Open this publication in new window or tab >>Modified lipoproteins in periodontitis: a link to cardiovascular disease?
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2019 (English)In: Bioscience Reports, ISSN 0144-8463, E-ISSN 1573-4935, Vol. 39, no 3, article id BSR20181665Article in journal (Refereed) Published
Abstract [en]

There is a strong association between periodontal disease and atherosclerotic cardiovascular disorders. A key event in the development of atherosclerosis is accumulation of modified lipoproteins within the arterial wall. We hypothesize that patients with periodontitis have an altered lipoprotein profile towards an atherogenic form. Therefore, this study aims at identifying modifications of plasma lipoproteins in periodontitis. Lipoproteins from ten female patients with periodontitis and gender- and age-matched healthy controls were isolated by density-gradient-ultracentrifugation. Proteins were separated by two-dimensional gel-electrophoresis and identified by map-matching or by nano-liquid chromatography followed by mass spectrometry. ApoA-I methionine oxidation, Oxyblot, total antioxidant capacity and a multiplex of 71 inflammation-related plasma proteins were assessed.Reduced levels of apoJ, phospholipid transfer protein, apoF, complement C3, paraoxonase 3 and increased levels of alpha-1-antichymotrypsin, apoA-II, apoC-III were found in HDL from the patients. In LDL/VLDL, the levels of apoL-1 and platelet-activating factor acetylhydrolase as well as apo-B fragments were increased. Methionine oxidation of apoA-I was increased in HDL and showed a relationship with periodontal parameters. Alpha-1 antitrypsin and alpha-2-HS glycoprotein were oxidised in LDL/VLDL and antioxidant capacity was increased in the patient group. 17 inflammation-related proteins were important for group separation with the highest discriminating proteins identified as IL-21, Fractalkine, IL-17F, IL-7, IL-1RA and IL-2.Patients with periodontitis have an altered plasma lipoprotein profile, defined by altered protein levels as well as posttranslational and other structural modifications towards an atherogenic form, which supports a role of modified plasma lipoproteins as central in the link between periodontal and cardiovascular disease (CVD).

Place, publisher, year, edition, pages
Portland Press, 2019
Keywords
Lipoproteins, nLC-MS/MS, periodontal microbiota, periodontitis, two-dimensional gel electrophoresis
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:oru:diva-73198 (URN)10.1042/BSR20181665 (DOI)000465453700016 ()30842338 (PubMedID)2-s2.0-85063936955 (Scopus ID)
Funder
Knowledge Foundation, Dnr20150037Magnus Bergvall Foundation
Note

Funding Agency:

Foundation Längmanska Kulturfonden

Available from: 2019-03-19 Created: 2019-03-19 Last updated: 2019-06-19Bibliographically approved
Fürsatz, M., Skog, M., Sivlér, P., Palm, E., Aronsson, C., Skallberg, A., . . . Aili, D. (2018). Functionalization of bacterial cellulose wound dressings with the antimicrobial peptide ε-poly-L-Lysine. Biomedical Materials, 13, Article ID 025014.
Open this publication in new window or tab >>Functionalization of bacterial cellulose wound dressings with the antimicrobial peptide ε-poly-L-Lysine
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2018 (English)In: Biomedical Materials, ISSN 1748-6041, E-ISSN 1748-605X, Vol. 13, article id 025014Article in journal (Refereed) Published
Abstract [en]

Wound dressings based on bacterial cellulose (BC) can form a soft and conformable protective layer that can stimulate wound healing while preventing bacteria from entering the wound. Bacteria already present in the wound can, however, thrive in the moist environment created by the BC dressing which can aggravate the healing process. Possibilities to render the BC antimicrobial without affecting the beneficial structural and mechanical properties of the material would hence be highly attractive. Here we present methods for functionalization of BC with ε-Poly-L-Lysine (ε-PLL), a non-toxic biopolymer with broad-spectrum antimicrobial activity. Low molecular weight ε-PLL was cross-linked in pristine BC membranes and to carboxymethyl cellulose (CMC) functionalized BC using carbodiimide chemistry. The functionalization of BC with ε-PLL inhibited growth of S. epidermidis on the membranes but did not affect the cytocompatibility to cultured human fibroblasts as compared to native BC. The functionalization had no significant effects on the nanofibrous structure and mechanical properties of the BC. The possibility to functionalize BC with ε-PLL is a promising, green and versatile approach to improve the performance of BC in wound care and other biomedical applications.

Place, publisher, year, edition, pages
Institute of Physics Publishing (IOPP), 2018
Keywords
bacterial cellulose; antimicrobial; carboxymethyl cellulose; epsilon-poly-L-Lysine
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy) Biomaterials Science Textile, Rubber and Polymeric Materials
Identifiers
urn:nbn:se:oru:diva-62415 (URN)10.1088/1748-605X/aa9486 (DOI)000423860700006 ()29047451 (PubMedID)
Funder
Carl Tryggers foundation Knowledge Foundation
Note

Funding Agencies:

Linkoping University  2009 00971 

Swedish Government Strategic Research Area in Materials Science on Functional Materials at Linkoping University  2009 00971 

Available from: 2017-12-11 Created: 2017-12-11 Last updated: 2018-08-16Bibliographically approved
Bengtsson, T., Lönn, J., Khalaf, H. & Palm, E. (2018). The lantibiotic gallidermin acts bactericidal against Staphylococcus epidermidis and Staphylococcus aureus and antagonizes the bacteria-induced proinflammatory responses in dermal fibroblasts. MicrobiologyOpen, 7(6), Article ID e606.
Open this publication in new window or tab >>The lantibiotic gallidermin acts bactericidal against Staphylococcus epidermidis and Staphylococcus aureus and antagonizes the bacteria-induced proinflammatory responses in dermal fibroblasts
2018 (English)In: MicrobiologyOpen, ISSN 2045-8827, E-ISSN 2045-8827, Vol. 7, no 6, article id e606Article in journal (Refereed) Published
Abstract [en]

Antimicrobial resistance needs to be tackled from new angles, and antimicrobial peptides could be future candidates for combating bacterial infections. This study aims to investigate in vitro the bactericidal effects of the lantibiotic gallidermin on Staphylococcus epidermidis and Staphylococcus aureus, possible cytotoxic effects and its impact on host-microbe interactions. Minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) of gallidermin were determined, and cytotoxicity and proinflammatory effects of gallidermin on fibroblasts, red blood cells (RBCs) and in whole blood were investigated. Both MIC and MBC for all four tested strains of S. epidermidis was 6.25 μg/ml. Both MIC and MBC for methicillin-sensitive S. aureus was 12.5 μg/ml and for methicillin-resistant S. aureus (MRSA) 1.56 μg/ml. Gallidermin displayed no cytotoxic effects on fibroblasts, only a high dose of gallidermin induced low levels of CXCL8 and interleukin-6. Gallidermin hemolyzed less than 1% of human RBCs, and did not induce reactive oxygen species production or cell aggregation in whole blood. In cell culture, gallidermin inhibited the cytotoxic effects of the bacteria and totally suppressed the bacteria-induced release of CXCL8 and interleukin-6 from fibroblasts. We demonstrate that gallidermin, expressing low cell cytotoxicity, is a promising candidate for treating bacterial infections caused by S. epidermidis and S. aureus, especially MRSA.

Place, publisher, year, edition, pages
John Wiley & Sons, 2018
Keywords
Streptococcus, antimicrobial resistance, bacteriocin, cytokines, fibroblasts, gallidermin
National Category
Immunology Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-65822 (URN)10.1002/mbo3.606 (DOI)000453616500003 ()29536668 (PubMedID)2-s2.0-85043709207 (Scopus ID)
Funder
Knowledge Foundation, 20150244
Available from: 2018-03-15 Created: 2018-03-15 Last updated: 2019-01-08Bibliographically approved
Khalaf, H., Palm, E. & Bengtsson, T. (2017). Cellular Response Mechanisms in Porphyromonas gingivalis Infection. In: Pachiappan Arjunan (Ed.), Periodontitis: A Useful Reference (pp. 45-68). InTech
Open this publication in new window or tab >>Cellular Response Mechanisms in Porphyromonas gingivalis Infection
2017 (English)In: Periodontitis: A Useful Reference / [ed] Pachiappan Arjunan, InTech, 2017, p. 45-68Chapter in book (Refereed)
Abstract [en]

The pathogenicity of the periodontal biofilm is highly dependent on a few key species, of which Porphyromonas gingivalis is considered to be one of the most important pathogens. P. gingivalis expresses a broad range of virulence factors, of these cysteine proteases (gingipains) are of special importance both for the bacterial survival/proliferation and for the pathological outcome. Several cell types, for example, epithelial cells, endothelial cells, dendritic cells, osteoblasts, and fibroblasts, reside in the periodontium and are part of the innate host response, as well as platelets, neutrophils, lymphocytes, and monocytes/macrophages. These cells recognize and respond to P. gingivalis and its components through pattern recognition receptors (PRRs), for example, Toll-like receptors and protease-activated receptors. Ligation of PRRs induces downstream-signaling pathways modifying the activity of transcription factors that regulates the expression of genes linked to inflammation. This is followed by the release of inflammatory mediators, for example, cytokines and reactive oxygen species. Periodontal disease is today considered to play a significant role in various systemic conditions such as cardiovascular disease (CVD). The mechanisms by which P. gingivalis and its virulence factors interact with host immune cells and contribute to the pathogenesis of periodontitis and CVD are far from completely understood.

Abstract [en]

Periodontitis - A Useful Reference is a comprehensive book compiled by a team of experts with the objective of providing an overview of the basic pathology of "periodontitis" and its implication on oral health and general systemic health. Periodontitis has become a global health burden in recent days. It is noteworthy that oral health is being considered as the mirror of general health and the study of oral-systemic health connections has advanced among scientists, clinicians, and the public as well. We wish the array of chapters that highlights the importance and impact of periodontal health could be a useful guide for the community of public, students, and clinicians.

Place, publisher, year, edition, pages
InTech, 2017
Keywords
Host-microbe interaction, immune cells, pathogen recognition receptors, intracellular signaling, inflammatory responses, Porphyromonas gingivalis, gingipains, LPS, cardiovascular disease, treatment
National Category
Medical and Health Sciences Medical Bioscience
Research subject
Medicine; Biomedicine
Identifiers
urn:nbn:se:oru:diva-63388 (URN)978-953-51-3606-4 (ISBN)978-953-51-3605-7 (ISBN)
Available from: 2017-12-15 Created: 2017-12-15 Last updated: 2018-02-07Bibliographically approved
Palm, E. (2015). Inflammatory responses of gingival fibroblasts in the interaction with the periodontal pathogen Porphyromonas gingivalis. (Doctoral dissertation). Örebro: Örebro university
Open this publication in new window or tab >>Inflammatory responses of gingival fibroblasts in the interaction with the periodontal pathogen Porphyromonas gingivalis
2015 (English)Doctoral thesis, comprehensive summary (Other academic)
Place, publisher, year, edition, pages
Örebro: Örebro university, 2015. p. 70
Series
Örebro Studies in Medicine, ISSN 1652-4063 ; 113
Keywords
Porphyromonas gingivalis, fibroblasts, CXCL8, TGF-β1, IL-6, SLPI, IDO, c-JUN, PKC, p38, periodontitis
National Category
Medical and Health Sciences Biomedical Laboratory Science/Technology
Research subject
Biomedicine
Identifiers
urn:nbn:se:oru:diva-38660 (URN)978-91-7529-056-0 (ISBN)
Public defence
2015-02-06, Universitetssjukhuset, Bomanssonsalen, Södra Grev Rosengatan, Örebro, 09:00 (Swedish)
Opponent
Supervisors
Available from: 2014-11-17 Created: 2014-11-17 Last updated: 2017-10-17Bibliographically approved
Palm, E., Khalaf, H. & Bengtsson, T. (2015). Suppression of inflammatory responses of human gingival fibroblasts by gingipains from Porphyromonas gingivalis. Molecular Oral Microbiology, 30(1), 74-85
Open this publication in new window or tab >>Suppression of inflammatory responses of human gingival fibroblasts by gingipains from Porphyromonas gingivalis
2015 (English)In: Molecular Oral Microbiology, ISSN 2041-1006, E-ISSN 2041-1014, Vol. 30, no 1, p. 74-85Article in journal (Refereed) Published
Abstract [en]

The interaction between human gingival fibroblasts (HGFs) and Porphyromonas gingivalis plays an important role in the development and progression of periodontitis. Porphyromonas gingivalis possesses several virulence factors, including cysteine proteases, the arginine-specific (Rgp) and lysine-specific (Kgp) gingipains. Studying the mechanisms that P.gingivalis, and its derived virulence, use to propagate and interact with host cells will increase the understanding of the development and progression of periodontitis. In this study, we aimed to elucidate how P.gingivalis influences the inflammatory events in HGFs regarding transforming growth factor-(1) (TGF-(1)), CXCL8, secretory leucocyte protease inhibitor (SLPI), c-Jun and indoleamine 2,3-dioxygenase (IDO). HGFs were inoculated for 6 and 24h with the wild-type strains ATCC 33277 and W50, two gingipain-mutants of W50 and heat-killed ATCC 33277. The P.gingivalis regulated CXCL8 and TGF-(1) in HGFs, and the kgp mutant gave significantly higher immune response with increased CXCL8 (P<0.001) and low levels of TGF-(1). We show that HGFs express and secrete SLPI, which was significantly suppressed by P.gingivalis (P<0.05). This suggests that by antagonizing SLPI, P.gingivalis contributes to the tissue destruction associated with periodontitis. Furthermore, we found that P.gingivalis inhibits the expression of the antimicrobial IDO, as well as upregulating c-Jun (P<0.05). In conclusion, P.gingivalis both triggers and suppresses the immune response in HGFs. Consequently, we suggest that the pathogenic effects of P.gingivalis, and especially the activity of the gingipains on the inflammatory and immune response of HGFs, are crucial in periodontitis.

Keywords
CXCL8, gingipain, indoleamine 2, 3-dioxygenase, periodontitis, secretory leucocyte protease inhibitor, transforming growth factor-β
National Category
Microbiology in the medical area Medical and Health Sciences
Research subject
Microbiology; Medicine
Identifiers
urn:nbn:se:oru:diva-42617 (URN)10.1111/omi.12073 (DOI)000347897100007 ()25055828 (PubMedID)2-s2.0-84920913980 (Scopus ID)
Funder
Swedish Research CouncilSwedish Heart Lung Foundation
Note

Funding Agencies:

Foundation of Olle Engkvist

Knowledge Foundation

Available from: 2015-02-13 Created: 2015-02-13 Last updated: 2018-01-11Bibliographically approved
Palm, E., Demirel, I., Bengtsson, T. & Khalaf, H. (2015). The role of toll-like and protease-activated receptors in the expression of cytokines by gingival fibroblasts stimulated with the periodontal pathogen Porphyromonas gingivalis. Cytokine, 76(2), 424-432
Open this publication in new window or tab >>The role of toll-like and protease-activated receptors in the expression of cytokines by gingival fibroblasts stimulated with the periodontal pathogen Porphyromonas gingivalis
2015 (English)In: Cytokine, ISSN 1043-4666, E-ISSN 1096-0023, Vol. 76, no 2, p. 424-432Article in journal (Refereed) Published
Abstract [en]

Porphyromonas gingivalis is a periodontitis-associated pathogen and interactions between the bacterium and gingival fibroblasts play an important role in development and progression of periodontitis, an inflammatory disease leading to degeneration of tooth-supporting structures. Gingival fibroblasts, which expresses protease activated receptors (PARs) as well as toll-like receptors (TLRs), produces inflammatory mediators upon bacterial challenges. In this study, we elucidated the importance of PAR1, PAR2, TLR2 and TLR4 for the expression and secretion of CXCL8, interleukin-6 (IL-6), transforming growth factor-beta 1 (TGF-beta 1) and secretory leukocyte inhibitor (SLPI). Human gingival fibroblasts were transfected with small-interfering RNA against the target genes, and then stimulated with P. gingivalis wild-type W50 and W50-derived double rgp mutant E8 and kgp mutant K1A. TLR2-silencing reduced P. gingivalis-induced CXCL8 and IL-6. IL-6 was also reduced after PAR1-silencing. No effects were observed for TGF-beta 1. SLPI was suppressed by P. gingivalis and silencing of PAR1 as well as TLR2, gave additional suppression at the mRNA level. TLR4 was not involved in the regulation of the investigated mediators. CXCL8 and IL-6 are important for progression and development of periodontitis, leading to a chronic inflammation that may contribute to the tissue destruction that follows an exacerbated host response. Therefore, regulating the expression of TLR2 and subsequent release of CXCL8 and IL-6 in periodontitis could attenuate the tissue destruction seen in periodontitis.

Place, publisher, year, edition, pages
Academic Press, 2015
Keywords
Fibroblasts, Porphyromonas gingivalis, CXCL8, Interleukin-6, Secretory leukocyte protease inhibitor
National Category
Microbiology in the medical area Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy) Immunology in the medical area
Research subject
Biomedicine; Immunology
Identifiers
urn:nbn:se:oru:diva-47006 (URN)10.1016/j.cyto.2015.08.263 (DOI)000364244400041 ()26318255 (PubMedID)2-s2.0-84943819518 (Scopus ID)
Funder
Swedish Research CouncilSwedish Heart Lung FoundationKnowledge Foundation
Note

Funding Agencies:

Mats Kleberg Foundation

Foundation of Olle Engkvist

Available from: 2015-12-09 Created: 2015-12-09 Last updated: 2018-07-02Bibliographically approved
Lönn, J., Johansson, C. S., Nakka, S., Palm, E., Bengtsson, T., Nayeri, F. & Ravald, N. (2014). High Concentration but Low Activity of Hepatocyte Growth Factor in Periodontitis. Journal of Periodontology, 85(1), 113-122
Open this publication in new window or tab >>High Concentration but Low Activity of Hepatocyte Growth Factor in Periodontitis
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2014 (English)In: Journal of Periodontology, ISSN 0022-3492, E-ISSN 1943-3670, Vol. 85, no 1, p. 113-122Article in journal (Refereed) Published
Abstract [en]

Background: High levels of hepatocyte growth factor (HGF), a healing factor with regenerative and cytoprotective effects, are associated with inflammatory diseases, including periodontitis. HGF biological activity requires binding to its receptors, the proto-oncogene c-Met (c-Met) and heparan sulphate proteoglycan (HSPG). Here we investigated HGF expression and its relationship to subgingival microbiota in medically healthy individuals with and without periodontitis.

Methods: Saliva, gingival crevicular fluid (GCF), and blood samples from 30 patients with severe periodontitis and 30 healthy controls were analyzed for HGF concentration using enzyme-linked immunosorbent assay (ELISA), and binding affinity for HSPG and c-Met using surface plasmon resonance (SPR). The regenerative effects of saliva from three patients and controls were analyzed in an in vitro model of cell injury. Subgingival plaques were analyzed for the presence of 18 bacterial species.

Results: Patients with periodontitis showed higher HGF concentrations in saliva, GCF, and serum (P < 0.001); however, the binding affinities for HSPG and c-Met were reduced in GCF and saliva (P < 0.002). In contrast to the controls, saliva from patients showed no significant regenerative effect over time on gingival epithelial cells. Compared to controls, patients had a higher prevalence of periodontal-related bacteria.

Conclusion: Higher circulatory HGF levels indicate a systemic effect of periodontitis. However, the HGF biological activity at local inflammation sites was reduced, and this effect was associated with the amount of periodontal bacteria. Loss of function of healing factors may be an important mechanism in degenerative processes in periodontally susceptible individuals.

Place, publisher, year, edition, pages
Chicago, USA: American Academy of Periodontology, 2014
Keywords
Hepatocyte growth factor, porphyromonas gingivalis, periodontitis, systemic inflammation, coronary artery disease, chronic renal failure, lipoxin
National Category
Medical and Health Sciences Dentistry
Research subject
Biomedicine
Identifiers
urn:nbn:se:oru:diva-29141 (URN)10.1902/jop.2013.130003 (DOI)000331139400016 ()23594192 (PubMedID)2-s2.0-84890190195 (Scopus ID)
Funder
Swedish Heart Lung FoundationSwedish Research Council
Note

Funding Agencies:

Public Dental Service in Ostergotland County, Sweden

Foundation of Olle Engkvist

Available from: 2013-05-23 Created: 2013-05-23 Last updated: 2018-09-12Bibliographically approved
Palm, E., Khalaf, H. & Bengtsson, T. (2013). Porphyromonas gingivalis downregulates the immune response of fibroblasts. BMC Microbiology, 13, 155
Open this publication in new window or tab >>Porphyromonas gingivalis downregulates the immune response of fibroblasts
2013 (English)In: BMC Microbiology, ISSN 1471-2180, E-ISSN 1471-2180, Vol. 13, p. 155-Article in journal (Refereed) Published
Abstract [en]

Background: Porphyromonas gingivalis is a key pathogen in periodontitis, an inflammatory disease leading to destruction of bone and tooth-supporting tissue. P. gingivalis possesses a number of pathogenic properties to enhance growth and survival, including proteolytic gingipains. Accumulating data shows that gingipains are involved in the regulation of host inflammatory responses. The aim of this study was to determine if P. gingivalis infection modulates the inflammatory response of fibroblasts, including the release of chemokines and cytokines. Human gingival fibroblasts or primary dermal fibroblasts were pre-stimulated with tumor-necrosis factor-alpha (TNF-alpha) and cocultured with P. gingivalis. Gingipain inhibitors were used to explore the effect of gingipains. CXCL8 levels were determined with ELISA and the relative levels of various inflammatory mediators were determined by a cytokine assay.

Results: TNF-alpha-triggered CXCL8 levels were completely abolished by viable P. gingivalis, whereas heat-killed P. gingivalis did not suppress CXCL8. Accumulation of CXCL8 was partially restored by an arginine-gingipain inhibitor. Furthermore, fibroblasts produced several inflammatory mediators, notably chemokines, all of which were suppressed by viable P. gingivalis.

Conclusion: These findings provide evidence that fibroblast-derived inflammatory signals are modulated by heat-instable gingipains, whereby the bacteria can escape killing by the host immune system and promote its own growth and establishment. In addition, we show that fibroblasts are important mediators of inflammation in response to infection and thereby play a crucial role in determining the nature and magnitude of the invasion of immune cells.

Keywords
Porphyromonas gingivalis, Fibroblasts, Chemokines, Cytokines
National Category
Microbiology in the medical area
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-30310 (URN)10.1186/1471-2180-13-155 (DOI)000322041700001 ()2-s2.0-84880027349 (Scopus ID)
Funder
Swedish Research CouncilSwedish Heart Lung Foundation
Note

Funding Agency: Foundation of Olle Engkvist; Mats Kleberg Foundation

Available from: 2013-08-23 Created: 2013-08-23 Last updated: 2018-01-11Bibliographically approved
Nakka, S. S., Palm, E., Bengtsson, T. & Khalaf, H.Bacteriocin plantaricin NC8 αβ antagonizes Porphyromonas gingivalis infection and induces proliferation of gingival epithelial cells.
Open this publication in new window or tab >>Bacteriocin plantaricin NC8 αβ antagonizes Porphyromonas gingivalis infection and induces proliferation of gingival epithelial cells
(English)Manuscript (preprint) (Other academic)
National Category
Other Basic Medicine
Research subject
Biomedicine
Identifiers
urn:nbn:se:oru:diva-52858 (URN)
Available from: 2016-10-06 Created: 2016-10-06 Last updated: 2018-01-14Bibliographically approved
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