The Developing Mouse Dentition
Identifieur interne : 003874 ( Istex/Corpus ); précédent : 003873; suivant : 003875The Developing Mouse Dentition
Auteurs : Renata Peterková ; Miroslav Peterka ; Hervé LesotSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2003-12.
English descriptors
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- Teeft :
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Abstract
Abstract: Developing limb or differentiating neural and blood cells are traditional models used to study programmed cell death in mammals. The developing mouse dentition can also be an attractive model for studying apoptosis regulation. Apoptosis is most extant during early odontogenesis in mice. The embryonic tooth pattern is comprised not only of anlagen of functional teeth (incisor, molars), but also of vestiges of ancestral tooth primordia that must be suppressed. Apoptosis is involved in (a) the elimination of vestigial tooth primordia in the prospective toothless gap (diastema) between the incisor and molars and (b) the shaping of germs in functional teeth. This type of apoptosis occurs in the dental epithelium according to a characteristic temporo‐spatial pattern. Where apoptosis concentrates, specific signaling is also found. We proposed a hypothesis to explain the stimulation of apoptosis in the dental epithelium by integrating two concepts: (1) The regulation of epithelial budding by positional information generated from interactions between growth‐activating and growth‐inhibiting signals, and (2) apoptosis stimulation by the failure of death‐suppressing signals. During the budding of the dental epithelium, local excess in growth inhibitors (e.g., Bmps) might lead to the epithelial cells' failure to receive adequate growth‐activating (apoptosis‐suppressing) signals (e.g., Fgfs). The resulting signal imbalance leads to cell “suicide” by apoptosis. Understanding of apoptosis regulation in the vestigial tooth primordia can help to elucidate the mechanism of their suppression during evolution and to identify factors essential for tooth survival. The latter knowledge will be important for developing a technology of tooth engineering.
Url:
DOI: 10.1196/annals.1299.083
Links to Exploration step
ISTEX:72ABA95C209A7699FF4B59400E223E1692227799Le document en format XML
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study programmed cell death in mammals. The developing mouse dentition can also be an attractive model for studying apoptosis regulation. Apoptosis is most extant during early odontogenesis in mice. The embryonic tooth pattern is comprised not only of anlagen of functional teeth (incisor, molars), but also of vestiges of ancestral tooth primordia that must be suppressed. Apoptosis is involved in (a) the elimination of vestigial tooth primordia in the prospective toothless gap (diastema) between the incisor and molars and (b) the shaping of germs in functional teeth. This type of apoptosis occurs in the dental epithelium according to a characteristic temporo‐spatial pattern. Where apoptosis concentrates, specific signaling is also found. We proposed a hypothesis to explain the stimulation of apoptosis in the dental epithelium by integrating two concepts: (1) The regulation of epithelial budding by positional information generated from interactions between growth‐activating and growth‐inhibiting signals, and (2) apoptosis stimulation by the failure of death‐suppressing signals. During the budding of the dental epithelium, local excess in growth inhibitors (e.g., Bmps) might lead to the epithelial cells' failure to receive adequate growth‐activating (apoptosis‐suppressing) signals (e.g., Fgfs). The resulting signal imbalance leads to cell “suicide” by apoptosis. Understanding of apoptosis regulation in the vestigial tooth primordia can help to elucidate the mechanism of their suppression during evolution and to identify factors essential for tooth survival. The latter knowledge will be important for developing a technology of tooth 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olplw</json:string><json:string>jurzwk lqklelwruv</json:string><json:string>plwrfkrqguldo sdwkzd</json:string><json:string>wrrwk sdwwhuq</json:string><json:string>hqdpho nqrw</json:string><json:string>hslwkholdo exgglqj</json:string><json:string>3urjudpphg fhoo ghdwk</json:string><json:string>fdghplf 3uhvv</json:string><json:string>wkuhh glphqvlrqdo uhfrqvwuxfwlrq</json:string><json:string>hslwkholdo fhoov</json:string></teeft></keywords><author><json:item><name>RENATA PETERKOVÁ</name><affiliations><json:string>Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic</json:string><json:string>E-mail: repete@biomed.cas.cz</json:string></affiliations></json:item><json:item><name>MIROSLAV PETERKA</name><affiliations><json:string>Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic</json:string></affiliations></json:item><json:item><name>HERVÉ LESOT</name><affiliations><json:string>INSERM U‐595, 11, rue Humann, 67085 Strasbourg, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>apoptosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tooth</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>development</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>model</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>regulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>growth factor</value></json:item></subject><articleId><json:string>NYAS453</json:string></articleId><arkIstex>ark:/67375/WNG-ZQPWMSNS-9</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Abstract: Developing limb or differentiating neural and blood cells are traditional models used to study programmed cell death in mammals. The developing mouse dentition can also be an attractive model for studying apoptosis regulation. Apoptosis is most extant during early odontogenesis in mice. The embryonic tooth pattern is comprised not only of anlagen of functional teeth (incisor, molars), but also of vestiges of ancestral tooth primordia that must be suppressed. Apoptosis is involved in (a) the elimination of vestigial tooth primordia in the prospective toothless gap (diastema) between the incisor and molars and (b) the shaping of germs in functional teeth. This type of apoptosis occurs in the dental epithelium according to a characteristic temporo‐spatial pattern. Where apoptosis concentrates, specific signaling is also found. We proposed a hypothesis to explain the stimulation of apoptosis in the dental epithelium by integrating two concepts: (1) The regulation of epithelial budding by positional information generated from interactions between growth‐activating and growth‐inhibiting signals, and (2) apoptosis stimulation by the failure of death‐suppressing signals. During the budding of the dental epithelium, local excess in growth inhibitors (e.g., Bmps) might lead to the epithelial cells' failure to receive adequate growth‐activating (apoptosis‐suppressing) signals (e.g., Fgfs). The resulting signal imbalance leads to cell “suicide” by apoptosis. Understanding of apoptosis regulation in the vestigial tooth primordia can help to elucidate the mechanism of their suppression during evolution and to identify factors essential for tooth survival. The latter knowledge will be important for developing a technology of tooth engineering.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>249</abstractWordCount><abstractCharCount>1768</abstractCharCount><keywordCount>6</keywordCount><score>9.988</score><pdfWordCount>5590</pdfWordCount><pdfCharCount>34646</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>14</pdfPageCount><pdfPageSize>612 x 792 pts (letter)</pdfPageSize></qualityIndicators><title>The Developing Mouse Dentition</title><pmid><json:string>15033770</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Annals of the New York Academy of Sciences</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1749-6632</json:string></doi><issn><json:string>0077-8923</json:string></issn><eissn><json:string>1749-6632</json:string></eissn><publisherId><json:string>NYAS</json:string></publisherId><volume>1010</volume><issue>1</issue><pages><first>453</first><last>466</last><total>14</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2003</json:string></date><geogName></geogName><orgName></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName></persName><placeName></placeName><ref_url></ref_url><ref_bibl></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-ZQPWMSNS-9</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - multidisciplinary sciences</json:string></wos><scienceMetrix><json:string>1 - general</json:string><json:string>2 - general science & technology</json:string><json:string>3 - general science & technology</json:string></scienceMetrix><scopus><json:string>1 - Social Sciences</json:string><json:string>2 - Arts and Humanities</json:string><json:string>3 - History and Philosophy of Science</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - General Biochemistry, Genetics and Molecular Biology</json:string></scopus></categories><publicationDate>2003</publicationDate><copyrightDate>2003</copyrightDate><doi><json:string>10.1196/annals.1299.083</json:string></doi><id>72ABA95C209A7699FF4B59400E223E1692227799</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/72ABA95C209A7699FF4B59400E223E1692227799/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/72ABA95C209A7699FF4B59400E223E1692227799/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/72ABA95C209A7699FF4B59400E223E1692227799/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">The Developing Mouse Dentition</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-12"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">The Developing Mouse Dentition</title><title level="a" type="sub">A New Tool for Apoptosis Study</title><author xml:id="author-0000" role="corresp"><persName><forename type="first">RENATA</forename><surname>PETERKOVÁ</surname></persName><affiliation>Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic<address><country key="CZ"></country></address></affiliation><affiliation>Address for correspondence: R. Peterková, Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic. Voice: +420‐241‐062‐232; fax: +420‐241‐062‐604. repete@biomed.cas.cz</affiliation></author><author xml:id="author-0001"><persName><forename type="first">MIROSLAV</forename><surname>PETERKA</surname></persName><affiliation>Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic<address><country key="CZ"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">HERVÉ</forename><surname>LESOT</surname></persName><affiliation>INSERM U‐595, 11, rue Humann, 67085 Strasbourg, France<address><country key="FR"></country></address></affiliation></author><idno type="istex">72ABA95C209A7699FF4B59400E223E1692227799</idno><idno type="ark">ark:/67375/WNG-ZQPWMSNS-9</idno><idno type="DOI">10.1196/annals.1299.083</idno><idno type="unit">NYAS453</idno><idno type="toTypesetVersion">file:NYAS.NYAS453.pdf</idno></analytic><monogr><title level="j" type="main">Annals of the New York Academy of Sciences</title><title level="j" type="alt">ANNALS OF NEW YORK ACADEMY SCIENCES</title><idno type="pISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><idno type="book-DOI">10.1111/(ISSN)1749-6632</idno><idno type="book-part-DOI">10.1111/nyas.2003.1010.issue-1</idno><idno type="product">NYAS</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">1010</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="453">453</biblScope><biblScope unit="page" to="466">466</biblScope><biblScope unit="page-count">14</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-12"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">A<hi rend="smallCaps">bstract</hi>: </hi> Developing limb or differentiating neural and blood cells are traditional models used to study programmed cell death in mammals. The developing mouse dentition can also be an attractive model for studying apoptosis regulation. Apoptosis is most extant during early odontogenesis in mice. The embryonic tooth pattern is comprised not only of anlagen of functional teeth (incisor, molars), but also of vestiges of ancestral tooth primordia that must be suppressed. Apoptosis is involved in (a) the elimination of vestigial tooth primordia in the prospective toothless gap (diastema) between the incisor and molars and (b) the shaping of germs in functional teeth. This type of apoptosis occurs in the dental epithelium according to a characteristic temporo‐spatial pattern. Where apoptosis concentrates, specific signaling is also found. We proposed a hypothesis to explain the stimulation of apoptosis in the dental epithelium by integrating two concepts: (1) The regulation of epithelial budding by positional information generated from interactions between growth‐activating and growth‐inhibiting signals, and (2) apoptosis stimulation by the failure of death‐suppressing signals. During the budding of the dental epithelium, local excess in growth inhibitors (e.g., Bmps) might lead to the epithelial cells' failure to receive adequate growth‐activating (apoptosis‐suppressing) signals (e.g., Fgfs). The resulting signal imbalance leads to cell “suicide” by apoptosis. Understanding of apoptosis regulation in the vestigial tooth primordia can help to elucidate the mechanism of their suppression during evolution and to identify factors essential for tooth survival. The latter knowledge will be important for developing a technology of tooth engineering.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">apoptosis</term><term xml:id="k2">tooth</term><term xml:id="k3">development</term><term xml:id="k4">model</term><term xml:id="k5">regulation</term><term xml:id="k6">growth factor</term></keywords><keywords rend="tocHeading1"><term>Apoptosis from Signaling Pathways to Therapeutic Tools: Part X. 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Voice: +420‐241‐062‐232; fax: +420‐241‐062‐604. <email>repete@biomed.cas.cz</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS453.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="87"></count><count type="linksCrossRef" number="148"></count></countGroup><titleGroup><title type="main">The Developing Mouse Dentition</title><title type="subtitle">A New Tool for Apoptosis Study</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>RENATA</givenNames><familyName>PETERKOVÁ</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>MIROSLAV</givenNames><familyName>PETERKA</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>HERVÉ</givenNames><familyName>LESOT</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CZ"><unparsedAffiliation>Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>INSERM U‐595, 11, rue Humann, 67085 Strasbourg, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">apoptosis</keyword><keyword xml:id="k2">tooth</keyword><keyword xml:id="k3">development</keyword><keyword xml:id="k4">model</keyword><keyword xml:id="k5">regulation</keyword><keyword xml:id="k6">growth factor</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>A<sc>bstract</sc>: </b> Developing limb or differentiating neural and blood cells are traditional models used to study programmed cell death in mammals. The developing mouse dentition can also be an attractive model for studying apoptosis regulation. Apoptosis is most extant during early odontogenesis in mice. The embryonic tooth pattern is comprised not only of anlagen of functional teeth (incisor, molars), but also of vestiges of ancestral tooth primordia that must be suppressed. Apoptosis is involved in (a) the elimination of vestigial tooth primordia in the prospective toothless gap (diastema) between the incisor and molars and (b) the shaping of germs in functional teeth. This type of apoptosis occurs in the dental epithelium according to a characteristic temporo‐spatial pattern. Where apoptosis concentrates, specific signaling is also found. We proposed a hypothesis to explain the stimulation of apoptosis in the dental epithelium by integrating two concepts: (1) The regulation of epithelial budding by positional information generated from interactions between growth‐activating and growth‐inhibiting signals, and (2) apoptosis stimulation by the failure of death‐suppressing signals. During the budding of the dental epithelium, local excess in growth inhibitors (e.g., Bmps) might lead to the epithelial cells' failure to receive adequate growth‐activating (apoptosis‐suppressing) signals (e.g., Fgfs). The resulting signal imbalance leads to cell “suicide” by apoptosis. Understanding of apoptosis regulation in the vestigial tooth primordia can help to elucidate the mechanism of their suppression during evolution and to identify factors essential for tooth survival. The latter knowledge will be important for developing a technology of tooth engineering.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Positional information specifies cells in a coordinate system.<link href="#b81">81</link> Reaction‐diffusion processes generate spatial variation depending on interactions between activator and inhibitor substances.<link href="#b63 #b82">63,82</link></p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The Developing Mouse Dentition</title><subTitle>A New Tool for Apoptosis Study</subTitle></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The Developing Mouse Dentition</title></titleInfo><name type="personal"><namePart type="given">RENATA</namePart><namePart type="family">PETERKOVÁ</namePart><affiliation>Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic</affiliation><affiliation>E-mail: repete@biomed.cas.cz</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MIROSLAV</namePart><namePart type="family">PETERKA</namePart><affiliation>Institute of Experimental Medicine, Academy of Sciences CR, Videnska 1083, 142 20 Prague 4, Czech Republic</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HERVÉ</namePart><namePart type="family">LESOT</namePart><affiliation>INSERM U‐595, 11, rue Humann, 67085 Strasbourg, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2003-12</dateIssued><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">4</extent><extent unit="tables">0</extent><extent unit="formulas">0</extent><extent unit="references">87</extent><extent unit="linksCrossRef">148</extent></physicalDescription><abstract>Abstract: Developing limb or differentiating neural and blood cells are traditional models used to study programmed cell death in mammals. The developing mouse dentition can also be an attractive model for studying apoptosis regulation. Apoptosis is most extant during early odontogenesis in mice. The embryonic tooth pattern is comprised not only of anlagen of functional teeth (incisor, molars), but also of vestiges of ancestral tooth primordia that must be suppressed. Apoptosis is involved in (a) the elimination of vestigial tooth primordia in the prospective toothless gap (diastema) between the incisor and molars and (b) the shaping of germs in functional teeth. This type of apoptosis occurs in the dental epithelium according to a characteristic temporo‐spatial pattern. Where apoptosis concentrates, specific signaling is also found. We proposed a hypothesis to explain the stimulation of apoptosis in the dental epithelium by integrating two concepts: (1) The regulation of epithelial budding by positional information generated from interactions between growth‐activating and growth‐inhibiting signals, and (2) apoptosis stimulation by the failure of death‐suppressing signals. During the budding of the dental epithelium, local excess in growth inhibitors (e.g., Bmps) might lead to the epithelial cells' failure to receive adequate growth‐activating (apoptosis‐suppressing) signals (e.g., Fgfs). The resulting signal imbalance leads to cell “suicide” by apoptosis. Understanding of apoptosis regulation in the vestigial tooth primordia can help to elucidate the mechanism of their suppression during evolution and to identify factors essential for tooth survival. The latter knowledge will be important for developing a technology of tooth engineering.</abstract><subject lang="en"><genre>keywords</genre><topic>apoptosis</topic><topic>tooth</topic><topic>development</topic><topic>model</topic><topic>regulation</topic><topic>growth factor</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of Sciences</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><identifier type="ISSN">0077-8923</identifier><identifier type="eISSN">1749-6632</identifier><identifier type="DOI">10.1111/(ISSN)1749-6632</identifier><identifier type="PublisherID">NYAS</identifier><part><date>2003</date><detail type="title"><title>Apoptosis from Signaling Pathways to Therapeutic Tools</title></detail><detail type="volume"><caption>vol.</caption><number>1010</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>453</start><end>466</end><total>14</total></extent></part></relatedItem><identifier type="istex">72ABA95C209A7699FF4B59400E223E1692227799</identifier><identifier type="ark">ark:/67375/WNG-ZQPWMSNS-9</identifier><identifier type="DOI">10.1196/annals.1299.083</identifier><identifier type="ArticleID">NYAS453</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/72ABA95C209A7699FF4B59400E223E1692227799/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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