Mouse diaphragm assay for detection of antibodies against botulinum toxin type B
Identifieur interne : 002942 ( Istex/Corpus ); précédent : 002941; suivant : 002943Mouse diaphragm assay for detection of antibodies against botulinum toxin type B
Auteurs : Dirk Dressler ; M. Lange ; Hans BigalkeSource :
- Movement Disorders [ 0885-3185 ] ; 2005-12.
English descriptors
Abstract
With the advent of a commercial preparation of botulinum toxin type B (BT‐B) for treatment of cervical dystonia detection of antibodies against BT‐B (BT‐B‐AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT‐B 3 ng/ml the time to half‐maximal twitch force reduction (paralysis time [PT]) was 69 ± 4 min (n = 25). Addition of sera from patients with antibodies against BT‐A produced a PT of 68 ± 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 ± 6 min (n = 30). When defined amounts of BT‐B‐AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT‐B‐AB added, thus producing a calibration curve. The threshold for BT‐B‐AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 ± 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 ± 2.9) and complete secondary failure of BT‐B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 ± 2,601 MU/injection series, 1.86 ± 0.69 injection series before complete secondary therapy failure; 100.4 ± 15.8 days between injection series with normal therapeutic effect) were tested, BT‐B‐AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT‐B‐AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT‐B‐AB titers in partial BT‐B therapy failure. © 2005 Movement Disorder Society
Url:
DOI: 10.1002/mds.20625
Links to Exploration step
ISTEX:9024A63E77257377126A0FC967D49F0520D10BA8Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mouse diaphragm assay for detection of antibodies against botulinum toxin type B</title><author><name sortKey="Dressler, Dirk" sort="Dressler, Dirk" uniqKey="Dressler D" first="Dirk" last="Dressler">Dirk Dressler</name><affiliation><mods:affiliation>Department of Neurology, Rostock University, Rostock, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lange, M" sort="Lange, M" uniqKey="Lange M" first="M." last="Lange">M. Lange</name><affiliation><mods:affiliation>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Bigalke, Hans" sort="Bigalke, Hans" uniqKey="Bigalke H" first="Hans" last="Bigalke">Hans Bigalke</name><affiliation><mods:affiliation>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9024A63E77257377126A0FC967D49F0520D10BA8</idno><date when="2005" year="2005">2005</date><idno type="doi">10.1002/mds.20625</idno><idno type="url">https://api.istex.fr/document/9024A63E77257377126A0FC967D49F0520D10BA8/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002942</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Mouse diaphragm assay for detection of antibodies against botulinum toxin type B</title><author><name sortKey="Dressler, Dirk" sort="Dressler, Dirk" uniqKey="Dressler D" first="Dirk" last="Dressler">Dirk Dressler</name><affiliation><mods:affiliation>Department of Neurology, Rostock University, Rostock, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lange, M" sort="Lange, M" uniqKey="Lange M" first="M." last="Lange">M. Lange</name><affiliation><mods:affiliation>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Bigalke, Hans" sort="Bigalke, Hans" uniqKey="Bigalke H" first="Hans" last="Bigalke">Hans Bigalke</name><affiliation><mods:affiliation>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-12">2005-12</date><biblScope unit="vol">20</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1617">1617</biblScope><biblScope unit="page" to="1619">1619</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">9024A63E77257377126A0FC967D49F0520D10BA8</idno><idno type="DOI">10.1002/mds.20625</idno><idno type="ArticleID">MDS20625</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>antibodies</term><term>botulinum toxin type B</term><term>mouse diaphragm assay</term><term>therapy failure</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">With the advent of a commercial preparation of botulinum toxin type B (BT‐B) for treatment of cervical dystonia detection of antibodies against BT‐B (BT‐B‐AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT‐B 3 ng/ml the time to half‐maximal twitch force reduction (paralysis time [PT]) was 69 ± 4 min (n = 25). Addition of sera from patients with antibodies against BT‐A produced a PT of 68 ± 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 ± 6 min (n = 30). When defined amounts of BT‐B‐AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT‐B‐AB added, thus producing a calibration curve. The threshold for BT‐B‐AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 ± 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 ± 2.9) and complete secondary failure of BT‐B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 ± 2,601 MU/injection series, 1.86 ± 0.69 injection series before complete secondary therapy failure; 100.4 ± 15.8 days between injection series with normal therapeutic effect) were tested, BT‐B‐AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT‐B‐AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT‐B‐AB titers in partial BT‐B therapy failure. © 2005 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dirk Dressler MD, PhD</name><affiliations><json:string>Department of Neurology, Rostock University, Rostock, Germany</json:string></affiliations></json:item><json:item><name>M. Lange MD</name><affiliations><json:string>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Hans Bigalke MD, PhD</name><affiliations><json:string>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>mouse diaphragm assay</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>botulinum toxin type B</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>antibodies</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>therapy failure</value></json:item></subject><language><json:string>eng</json:string></language><abstract>With the advent of a commercial preparation of botulinum toxin type B (BT‐B) for treatment of cervical dystonia detection of antibodies against BT‐B (BT‐B‐AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT‐B 3 ng/ml the time to half‐maximal twitch force reduction (paralysis time [PT]) was 69 ± 4 min (n = 25). Addition of sera from patients with antibodies against BT‐A produced a PT of 68 ± 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 ± 6 min (n = 30). When defined amounts of BT‐B‐AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT‐B‐AB added, thus producing a calibration curve. The threshold for BT‐B‐AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 ± 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 ± 2.9) and complete secondary failure of BT‐B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 ± 2,601 MU/injection series, 1.86 ± 0.69 injection series before complete secondary therapy failure; 100.4 ± 15.8 days between injection series with normal therapeutic effect) were tested, BT‐B‐AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT‐B‐AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT‐B‐AB titers in partial BT‐B therapy failure. © 2005 Movement Disorder Society</abstract><qualityIndicators><score>4.92</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1757</abstractCharCount><pdfWordCount>1920</pdfWordCount><pdfCharCount>12065</pdfCharCount><pdfPageCount>3</pdfPageCount><abstractWordCount>281</abstractWordCount></qualityIndicators><title>Mouse diaphragm assay for detection of antibodies against botulinum toxin type B</title><genre><json:string>Serial article</json:string></genre><host><volume>20</volume><pages><total>3</total><last>1619</last><first>1617</first></pages><issn><json:string>0885-3185</json:string></issn><issue>12</issue><subject><json:item><value>Brief Report</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2005</publicationDate><copyrightDate>2005</copyrightDate><doi><json:string>10.1002/mds.20625</json:string></doi><id>9024A63E77257377126A0FC967D49F0520D10BA8</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/9024A63E77257377126A0FC967D49F0520D10BA8/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/9024A63E77257377126A0FC967D49F0520D10BA8/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/9024A63E77257377126A0FC967D49F0520D10BA8/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Mouse diaphragm assay for detection of antibodies against botulinum toxin type B</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2005</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Mouse diaphragm assay for detection of antibodies against botulinum toxin type B</title><author><persName><forename type="first">Dirk</forename><surname>Dressler</surname><roleName type="degree">MD, PhD</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, Rostock University, Gehlsheimer Str. 20, D‐18147 Rostock, Germany</p></note><affiliation>Department of Neurology, Rostock University, Rostock, Germany</affiliation></author><author><persName><forename type="first">M.</forename><surname>Lange</surname><roleName type="degree">MD</roleName></persName><affiliation>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</affiliation></author><author><persName><forename type="first">Hans</forename><surname>Bigalke</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-12"></date><biblScope unit="vol">20</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1617">1617</biblScope><biblScope unit="page" to="1619">1619</biblScope></imprint></monogr><idno type="istex">9024A63E77257377126A0FC967D49F0520D10BA8</idno><idno type="DOI">10.1002/mds.20625</idno><idno type="ArticleID">MDS20625</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>With the advent of a commercial preparation of botulinum toxin type B (BT‐B) for treatment of cervical dystonia detection of antibodies against BT‐B (BT‐B‐AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT‐B 3 ng/ml the time to half‐maximal twitch force reduction (paralysis time [PT]) was 69 ± 4 min (n = 25). Addition of sera from patients with antibodies against BT‐A produced a PT of 68 ± 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 ± 6 min (n = 30). When defined amounts of BT‐B‐AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT‐B‐AB added, thus producing a calibration curve. The threshold for BT‐B‐AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 ± 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 ± 2.9) and complete secondary failure of BT‐B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 ± 2,601 MU/injection series, 1.86 ± 0.69 injection series before complete secondary therapy failure; 100.4 ± 15.8 days between injection series with normal therapeutic effect) were tested, BT‐B‐AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT‐B‐AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT‐B‐AB titers in partial BT‐B therapy failure. © 2005 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>mouse diaphragm assay</term></item><item><term>botulinum toxin type B</term></item><item><term>antibodies</term></item><item><term>therapy failure</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2004-09-01">Received</change><change when="2005-03-01">Registration</change><change when="2005-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9024A63E77257377126A0FC967D49F0520D10BA8/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="120"><doi origin="wiley" registered="yes">10.1002/mds.v20:12</doi><numberingGroup><numbering type="journalVolume" number="20">20</numbering><numbering type="journalIssue">12</numbering></numberingGroup><coverDate startDate="2005-12">December 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="160" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.20625</doi><idGroup><id type="unit" value="MDS20625"></id></idGroup><countGroup><count type="pageTotal" number="3"></count></countGroup><titleGroup><title type="articleCategory">Brief Report</title><title type="tocHeading1">Brief Reports</title></titleGroup><copyright ownership="thirdParty">Copyright © 2005 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2004-09-01"></event><event type="manuscriptRevised" date="2005-02-21"></event><event type="manuscriptAccepted" date="2005-03-01"></event><event type="publishedOnlineEarlyUnpaginated" date="2005-08-02"></event><event type="firstOnline" date="2005-08-02"></event><event type="publishedOnlineFinalForm" date="2005-10-31"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.6 mode:FullText source:FullText result:FullText" date="2010-04-21"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1617</numbering><numbering type="pageLast">1619</numbering></numberingGroup><correspondenceTo>Department of Neurology, Rostock University, Gehlsheimer Str. 20, D‐18147 Rostock, Germany</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS20625.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="14"></count><count type="wordTotal" number="1845"></count></countGroup><titleGroup><title type="main" xml:lang="en">Mouse diaphragm assay for detection of antibodies against botulinum toxin type B</title><title type="short" xml:lang="en">Mouse Diaphragm Assay</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Dirk</givenNames><familyName>Dressler</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email normalForm="dirk.dressler@med.uni-rostock.de">dirk.dressler@med.uni‐rostock.de</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>M.</givenNames><familyName>Lange</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Hans</givenNames><familyName>Bigalke</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, Rostock University, Rostock, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">mouse diaphragm assay</keyword><keyword xml:id="kwd2">botulinum toxin type B</keyword><keyword xml:id="kwd3">antibodies</keyword><keyword xml:id="kwd4">therapy failure</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>With the advent of a commercial preparation of botulinum toxin type B (BT‐B) for treatment of cervical dystonia detection of antibodies against BT‐B (BT‐B‐AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT‐B 3 ng/ml the time to half‐maximal twitch force reduction (paralysis time [PT]) was 69 ± 4 min (n = 25). Addition of sera from patients with antibodies against BT‐A produced a PT of 68 ± 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 ± 6 min (n = 30). When defined amounts of BT‐B‐AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT‐B‐AB added, thus producing a calibration curve. The threshold for BT‐B‐AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 ± 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 ± 2.9) and complete secondary failure of BT‐B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 ± 2,601 MU/injection series, 1.86 ± 0.69 injection series before complete secondary therapy failure; 100.4 ± 15.8 days between injection series with normal therapeutic effect) were tested, BT‐B‐AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT‐B‐AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT‐B‐AB titers in partial BT‐B therapy failure. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Mouse diaphragm assay for detection of antibodies against botulinum toxin type B</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Mouse Diaphragm Assay</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mouse diaphragm assay for detection of antibodies against botulinum toxin type B</title></titleInfo><name type="personal"><namePart type="given">Dirk</namePart><namePart type="family">Dressler</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Rostock University, Rostock, Germany</affiliation><description>Correspondence: Department of Neurology, Rostock University, Gehlsheimer Str. 20, D‐18147 Rostock, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Lange</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hans</namePart><namePart type="family">Bigalke</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Institute of Toxicology, Medizinische Hochschule, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2005-12</dateIssued><dateCaptured encoding="w3cdtf">2004-09-01</dateCaptured><dateValid encoding="w3cdtf">2005-03-01</dateValid><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">1</extent><extent unit="references">14</extent><extent unit="words">1845</extent></physicalDescription><abstract lang="en">With the advent of a commercial preparation of botulinum toxin type B (BT‐B) for treatment of cervical dystonia detection of antibodies against BT‐B (BT‐B‐AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT‐B 3 ng/ml the time to half‐maximal twitch force reduction (paralysis time [PT]) was 69 ± 4 min (n = 25). Addition of sera from patients with antibodies against BT‐A produced a PT of 68 ± 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 ± 6 min (n = 30). When defined amounts of BT‐B‐AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT‐B‐AB added, thus producing a calibration curve. The threshold for BT‐B‐AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 ± 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 ± 2.9) and complete secondary failure of BT‐B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 ± 2,601 MU/injection series, 1.86 ± 0.69 injection series before complete secondary therapy failure; 100.4 ± 15.8 days between injection series with normal therapeutic effect) were tested, BT‐B‐AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT‐B‐AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT‐B‐AB titers in partial BT‐B therapy failure. © 2005 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>mouse diaphragm assay</topic><topic>botulinum toxin type B</topic><topic>antibodies</topic><topic>therapy failure</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Brief Report</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>12</number></detail><extent unit="pages"><start>1617</start><end>1619</end><total>3</total></extent></part></relatedItem><identifier type="istex">9024A63E77257377126A0FC967D49F0520D10BA8</identifier><identifier type="DOI">10.1002/mds.20625</identifier><identifier type="ArticleID">MDS20625</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002942 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 002942 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:9024A63E77257377126A0FC967D49F0520D10BA8
|texte= Mouse diaphragm assay for detection of antibodies against botulinum toxin type B
}}
| This area was generated with Dilib version V0.6.23. |  |