Viral targets for antisense oligonucleotides: a mini review
Identifieur interne : 000E86 ( Istex/Corpus ); précédent : 000E85; suivant : 000E87Viral targets for antisense oligonucleotides: a mini review
Auteurs : A. Kirk FieldSource :
- Antiviral Research [ 0166-3542 ] ; 1998.
English descriptors
- Teeft :
- Adsorption, Agents chemother, Akata cells, Anti6iral, Antisense, Antisense activity, Antisense mechanism, Antisense oligodeoxynucleotides, Antisense oligonucleotide, Antisense oligonucleotides, Antiviral, Antiviral activities, Antiviral activity, Antiviral agents, Assay, Aurelian, Cell transformation, Gene expression, Gene target, Herpes, Herpes simplex virus type, Human cytomegalovirus, Human virus type, Hybridization, Inhibition, Inhibitor, Kilkuskie, Kirk, Kirk field anti6iral research, Kulka, Mrna, Nucleic acids, Nucleotide, Oligodeoxynucleotides, Oligonucleotide, Oligonucleotide libraries, Oligonucleotides, Open reading frames, Pari, Phosphodiester, Phosphorothioate, Polymerase, Replication, Rnase, Secondary structure, Selectivity, Simplex, Splice, Target sequences, Viral, Virus adsorption, Virus replication.
Url:
DOI: 10.1016/S0166-3542(97)00060-0
Links to Exploration step
ISTEX:3666B469CB5E0173605EBE31F911261398C075C0Le document en format XML
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Replacement</json:string><json:string>Roberts</json:string><json:string>Recent</json:string><json:string>Anazodo</json:string><json:string>Aurelian</json:string></persName><placeName><json:string>Hydrophilicity</json:string><json:string>Wales</json:string><json:string>MA</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Ojwang et al., 1995</json:string><json:string>Fennewald et al., 1995</json:string><json:string>Krieg et al. (1995)</json:string><json:string>Kulka and Aurelian, 1995</json:string><json:string>Pari and Anders, 1993</json:string><json:string>Cowsert et al. (1993)</json:string><json:string>Shah and Howley, 1996</json:string><json:string>Bordier et al., 1992</json:string><json:string>Pagano et al., 1992</json:string><json:string>Gao et al., 1989</json:string><json:string>Stein et al., 1993</json:string><json:string>Ho et al. (1996)</json:string><json:string>Daibata et al. (1996)</json:string><json:string>Agrawal and Temsamani, 1996</json:string><json:string>Pari et al., 1995</json:string><json:string>Townsend et al., 1995</json:string><json:string>Jeffries and De Clercq, 1995</json:string><json:string>Jairath et al., 1997</json:string><json:string>Offensperger et al. (1993)</json:string><json:string>Korba and Gerin (1995)</json:string><json:string>Kulka et al., 1989, 1993, 1994</json:string><json:string>Han et al., 1994</json:string><json:string>Roth et al., 1994</json:string><json:string>Lewis et al., 1997</json:string><json:string>Peyman et al., 1995</json:string><json:string>Austermann et al., 1992</json:string><json:string>Wyatt et al., 1994</json:string><json:string>Field and Goodchild, 1995</json:string><json:string>Hatta et al., 1993</json:string><json:string>Poddevin et al., 1994</json:string><json:string>Smith and Pari, 1995</json:string><json:string>Roberts et al., 1997</json:string><json:string>Zelphati et al., 1994</json:string><json:string>Daibata et al., 1996</json:string><json:string>Galasso et al., 1990</json:string><json:string>Chen et al., 1996</json:string><json:string>Frank et al., 1993</json:string><json:string>Kilkuskie and Field, 1997</json:string><json:string>Anazodo et al. 1995</json:string><json:string>Stein and Krieg, 1994</json:string><json:string>Stull et al., 1992</json:string><json:string>Stephenson and Zamecnik, 1978</json:string><json:string>Martin et al., 1997</json:string><json:string>Kean et al., 1995</json:string><json:string>Crooke and Bennett, 1996</json:string><json:string>Bishop et al., 1996</json:string><json:string>Crooke et al., 1996</json:string><json:string>Pagano, 1995</json:string><json:string>Huang, 1991</json:string><json:string>Azad et al., 1993</json:string><json:string>Anazodo et al., 1995</json:string><json:string>Frank and Goodchild, 1996</json:string><json:string>Zamecnik and Stephenson, 1978</json:string><json:string>Sczakiel et al., 1993</json:string><json:string>Kawamura et al. (1991)</json:string><json:string>Temsamani and Agrawal, 1996</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-28BSMRZ4-5</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string><json:string>2 - pharmacology & pharmacy</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Pharmacology, Toxicology and Pharmaceutics</json:string><json:string>3 - Pharmacology</json:string></scopus></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1016/S0166-3542(97)00060-0</json:string></doi><id>3666B469CB5E0173605EBE31F911261398C075C0</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-28BSMRZ4-5/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-28BSMRZ4-5/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-28BSMRZ4-5/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Viral targets for antisense oligonucleotides: a mini review</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©1998 Elsevier Science B.V.</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>1998</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Section title: Mini-review</note><note type="content">Fig. 1: Antisense oligonucleotides may bind to target viral precursor mRNA, processed mRNA, or genomic RNA, preventing protein synthesis by translation arrest. In addition, DNA/RNA heteroduplexes formed by oligodeoxynucleotide binding to RNA may be recognized by cellular RNase H, cleaving the target RNA, and potentially freeing the antisense oligonucleotide for binding to another RNA target.</note><note type="content">Fig. 2: mRNA transcription, processing, and translation are all potential targets for antisense oligonucleotide intervention. The arrows indicate potentially vulnerable antisense inhibition sites.</note><note type="content">Fig. 3: Antisense oligonucleotide selection. Oligonucleotide libraries (thin lines) are incubated with 5′ end-labeled RNA (thick line), then treated with RNase H. RNA regions with bound oligonucleotide are digested, producing families of shorter labeled RNAs, which are separated on polyacrylamide gels. Discrete families of RNAs are detected on gels (lane RH) and compared to molecular weight markers (lane Mu) to identify regions of maximum oligonucleotide binding.</note><note type="content">Fig. 4: Structure of oligonucleotides. B=any of the heterocyclic bases found in DNA or in RNA. The terminal hydroxyl groups are distinguished as being at either the 5′ or 3′ ends. Some substitutions at the non-bridging oxygens (X,Y) of the phosphodiester linkage, or at the 2′ position on the sugar moiety (Z) are shown in the accompanying table.</note><note type="content">Fig. 5: UL36ANTI base-pair mismatches and their effect on inhibition of HCMV DNA replication are depicted by Southern analysis. Relative band intensities were calculated by scanning analysis. Positive control samples are assigned a value of one, with all other band intensities reported as a decimal fraction. UL36ANTI and various other oligonucleotides are shown below, with underlined bases indicating the substitutions. Relative differences in Tm values are shown at the right of the oligonucleotide sequences (Pari et al., 1995).</note><note type="content">Fig. 6: Selective inhibition of UL36 mRNA. (A; UL 36 and IE 1) Northern analysis of infected total cellular RNA, harvested 6 h post infection from samples treated at the indicated concentrations with oligonucleotides, shows that UL36ANTI specifically decreases the steady-state level of UL36 RNA, using a UL 36-specific probe. The blot was also hybridized with a probe specific for IE1 mRNA, indicating that the steady-state level of IE1 RNA is unaffected by either UL36ANTI or nonspecific (NS) PS oligonucleotides. (B; UL 36 and IE 2) Northern analysis of immediate-early RNA in the presence of specific and nonspecific oligonucleotides. An autoradiogram of a Northern blot hybridized with a probe specific for IE2 mRNA indicates that the steady-state level of IE2 is unaffected in the absence of UL36 mRNA and in presence of UL36ANTI or nonspecific PS oligonucleotides (Smith and Pari, 1995).</note><note type="content">Fig. 7: Inhibition of HIV p24 production. B4.14 cells, stably transfected to express HIV-1p24, were treated with an antisense oligonucleotide (GP12A) spanning bases 1189–1208 of HIV. Two control oligonucleotides containing either two mutations (2.mutations) or the sense sequence were also tested. p24 production, measured by immunoprecipitation using a rabbit polyclonal antibody, was decreased only in cells treated with the antisense oligonucleotide. Control and 2.mutation oligonucleotides did not alter p24 levels. Cells that were not transfected (W.T.) did not express p24 (Anazodo et al., 1995).</note><note type="content">Fig. 8: Evaluation of genomic RSV RNA by reverse transcriptase polymerase chain reaction (RT–PCR). RT–PCR scheme (A) and results (B) are shown. RSV RNA was reverse transcribed using primer BC1. PCR was then conducted using OD1 and BC2 or OD1 and BC6. (B) shows the 410-base pair product generated from OD1 and BC2 in all samples; the 940-base pair product was generated from OD1 and BC6 and was missing from the antisense (v590) treated cells, but not from those treated with the reverse sequence oligonucleotide (590s) or a random oligonucleotide (r20) (Jairath et al., 1997).</note><note type="content">Fig. 9: Human Papillomavirus scheme showing the open reading frames (orfs), their suggested functions, and the relative locations on the HPV-6b genome.</note><note type="content">Table 1: Some properties of oligonucleotide modification</note><note type="content">Table 2: Antiviral activities of oligonucleotidesa</note><note type="content">Table 3: Suggested criteria for antisense activity</note><note type="content">Table 4: Inhibition of productive EBV replication by anti-BZLF1 antisense oligonucleotides in anti-IgG-stimulated Akata cells (Daibata et al., 1996)</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Viral targets for antisense oligonucleotides: a mini review</title><author xml:id="author-0000"><persName><forename type="first">A.</forename><surname>Kirk Field</surname></persName><note type="biography">Present address: 376 Meadowbrook Rd. North Wales, PA 19454, USA; Tel. +1 215 6995563; Fax: +1 215 6997976.</note><affiliation>Present address: 376 Meadowbrook Rd. North Wales, PA 19454, USA; Tel. +1 215 6995563; Fax: +1 215 6997976.</affiliation><affiliation>Hybridon, Inc., Cambridge, MA, 02139, USA</affiliation></author><idno type="istex">3666B469CB5E0173605EBE31F911261398C075C0</idno><idno type="ark">ark:/67375/6H6-28BSMRZ4-5</idno><idno type="DOI">10.1016/S0166-3542(97)00060-0</idno><idno type="PII">S0166-3542(97)00060-0</idno></analytic><monogr><title level="j">Antiviral Research</title><title level="j" type="abbrev">AVR</title><idno type="pISSN">0166-3542</idno><idno type="PII">S0166-3542(00)X0036-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998"></date><biblScope unit="volume">37</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="67">67</biblScope><biblScope unit="page" to="81">81</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Antisense</term></item><item><term>Oligonucleotides</term></item><item><term>Design selective inhibitors</term></item><item><term>Selective inhibitors</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-28BSMRZ4-5/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="gr3"></istex:entity><istex:entity SYSTEM="gr4" NDATA="IMAGE" name="gr4"></istex:entity><istex:entity SYSTEM="gr5" NDATA="IMAGE" name="gr5"></istex:entity><istex:entity SYSTEM="gr6" NDATA="IMAGE" name="gr6"></istex:entity><istex:entity SYSTEM="gr7" NDATA="IMAGE" name="gr7"></istex:entity><istex:entity SYSTEM="gr8" NDATA="IMAGE" name="gr8"></istex:entity><istex:entity SYSTEM="gr9" NDATA="IMAGE" name="gr9"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>AVR</jid><aid>1088</aid><ce:pii>S0166-3542(97)00060-0</ce:pii><ce:doi>10.1016/S0166-3542(97)00060-0</ce:doi><ce:copyright year="1998" type="full-transfer">Elsevier Science B.V.</ce:copyright></item-info><head><ce:dochead><ce:textfn>Mini-review</ce:textfn></ce:dochead><ce:title>Viral targets for antisense oligonucleotides: a mini review</ce:title><ce:author-group><ce:author><ce:given-name>A.</ce:given-name><ce:surname>Kirk Field</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="AFF2">b</ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Hybridon, Inc., Cambridge, MA, 02139, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Pharmacology and Molecular Toxicology, University of Massachusetts Medical Center, Worcester, MA, USA</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Present address: 376 Meadowbrook Rd. North Wales, PA 19454, USA; Tel. +1 215 6995563; Fax: +1 215 6997976.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="28" month="7" year="1997"></ce:date-received><ce:date-accepted day="3" month="10" year="1997"></ce:date-accepted><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Antisense</ce:text></ce:keyword><ce:keyword><ce:text>Oligonucleotides</ce:text></ce:keyword><ce:keyword><ce:text>Design selective inhibitors</ce:text></ce:keyword><ce:keyword><ce:text>Selective inhibitors</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Viral targets for antisense oligonucleotides: a mini review</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Viral targets for antisense oligonucleotides: a mini review</title></titleInfo><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Kirk Field</namePart><affiliation>Hybridon, Inc., Cambridge, MA, 02139, USA</affiliation><description>Present address: 376 Meadowbrook Rd. North Wales, PA 19454, USA; Tel. +1 215 6995563; Fax: +1 215 6997976.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1998</dateIssued><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><note type="content">Section title: Mini-review</note><note type="content">Fig. 1: Antisense oligonucleotides may bind to target viral precursor mRNA, processed mRNA, or genomic RNA, preventing protein synthesis by translation arrest. In addition, DNA/RNA heteroduplexes formed by oligodeoxynucleotide binding to RNA may be recognized by cellular RNase H, cleaving the target RNA, and potentially freeing the antisense oligonucleotide for binding to another RNA target.</note><note type="content">Fig. 2: mRNA transcription, processing, and translation are all potential targets for antisense oligonucleotide intervention. The arrows indicate potentially vulnerable antisense inhibition sites.</note><note type="content">Fig. 3: Antisense oligonucleotide selection. Oligonucleotide libraries (thin lines) are incubated with 5′ end-labeled RNA (thick line), then treated with RNase H. RNA regions with bound oligonucleotide are digested, producing families of shorter labeled RNAs, which are separated on polyacrylamide gels. Discrete families of RNAs are detected on gels (lane RH) and compared to molecular weight markers (lane Mu) to identify regions of maximum oligonucleotide binding.</note><note type="content">Fig. 4: Structure of oligonucleotides. B=any of the heterocyclic bases found in DNA or in RNA. The terminal hydroxyl groups are distinguished as being at either the 5′ or 3′ ends. Some substitutions at the non-bridging oxygens (X,Y) of the phosphodiester linkage, or at the 2′ position on the sugar moiety (Z) are shown in the accompanying table.</note><note type="content">Fig. 5: UL36ANTI base-pair mismatches and their effect on inhibition of HCMV DNA replication are depicted by Southern analysis. Relative band intensities were calculated by scanning analysis. Positive control samples are assigned a value of one, with all other band intensities reported as a decimal fraction. UL36ANTI and various other oligonucleotides are shown below, with underlined bases indicating the substitutions. Relative differences in Tm values are shown at the right of the oligonucleotide sequences (Pari et al., 1995).</note><note type="content">Fig. 6: Selective inhibition of UL36 mRNA. (A; UL 36 and IE 1) Northern analysis of infected total cellular RNA, harvested 6 h post infection from samples treated at the indicated concentrations with oligonucleotides, shows that UL36ANTI specifically decreases the steady-state level of UL36 RNA, using a UL 36-specific probe. The blot was also hybridized with a probe specific for IE1 mRNA, indicating that the steady-state level of IE1 RNA is unaffected by either UL36ANTI or nonspecific (NS) PS oligonucleotides. (B; UL 36 and IE 2) Northern analysis of immediate-early RNA in the presence of specific and nonspecific oligonucleotides. An autoradiogram of a Northern blot hybridized with a probe specific for IE2 mRNA indicates that the steady-state level of IE2 is unaffected in the absence of UL36 mRNA and in presence of UL36ANTI or nonspecific PS oligonucleotides (Smith and Pari, 1995).</note><note type="content">Fig. 7: Inhibition of HIV p24 production. B4.14 cells, stably transfected to express HIV-1p24, were treated with an antisense oligonucleotide (GP12A) spanning bases 1189–1208 of HIV. Two control oligonucleotides containing either two mutations (2.mutations) or the sense sequence were also tested. p24 production, measured by immunoprecipitation using a rabbit polyclonal antibody, was decreased only in cells treated with the antisense oligonucleotide. Control and 2.mutation oligonucleotides did not alter p24 levels. Cells that were not transfected (W.T.) did not express p24 (Anazodo et al., 1995).</note><note type="content">Fig. 8: Evaluation of genomic RSV RNA by reverse transcriptase polymerase chain reaction (RT–PCR). RT–PCR scheme (A) and results (B) are shown. RSV RNA was reverse transcribed using primer BC1. PCR was then conducted using OD1 and BC2 or OD1 and BC6. (B) shows the 410-base pair product generated from OD1 and BC2 in all samples; the 940-base pair product was generated from OD1 and BC6 and was missing from the antisense (v590) treated cells, but not from those treated with the reverse sequence oligonucleotide (590s) or a random oligonucleotide (r20) (Jairath et al., 1997).</note><note type="content">Fig. 9: Human Papillomavirus scheme showing the open reading frames (orfs), their suggested functions, and the relative locations on the HPV-6b genome.</note><note type="content">Table 1: Some properties of oligonucleotide modification</note><note type="content">Table 2: Antiviral activities of oligonucleotidesa</note><note type="content">Table 3: Suggested criteria for antisense activity</note><note type="content">Table 4: Inhibition of productive EBV replication by anti-BZLF1 antisense oligonucleotides in anti-IgG-stimulated Akata cells (Daibata et al., 1996)</note><subject><genre>Keywords</genre><topic>Antisense</topic><topic>Oligonucleotides</topic><topic>Design selective inhibitors</topic><topic>Selective inhibitors</topic></subject><relatedItem type="host"><titleInfo><title>Antiviral Research</title></titleInfo><titleInfo type="abbreviated"><title>AVR</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1998</dateIssued></originInfo><identifier type="ISSN">0166-3542</identifier><identifier type="PII">S0166-3542(00)X0036-8</identifier><part><date>1998</date><detail type="volume"><number>37</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>67</start><end>140</end></extent><extent unit="pages"><start>67</start><end>81</end></extent></part></relatedItem><identifier type="istex">3666B469CB5E0173605EBE31F911261398C075C0</identifier><identifier type="ark">ark:/67375/6H6-28BSMRZ4-5</identifier><identifier type="DOI">10.1016/S0166-3542(97)00060-0</identifier><identifier type="PII">S0166-3542(97)00060-0</identifier><accessCondition type="use and reproduction" contentType="copyright">©1998 Elsevier Science B.V.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Elsevier Science B.V., ©1998</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-28BSMRZ4-5/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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