Human cerebrospinal fluid somatostatin in neurologic disease
Identifieur interne : 002E17 ( Main/Corpus ); précédent : 002E16; suivant : 002E18Human cerebrospinal fluid somatostatin in neurologic disease
Auteurs : M. Flint Beal ; Michael F. Mazurek ; Peter Mcl. Black ; Joseph B. MartinSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1985.
Abstract
Concentrations of somatostatin-like immunoreactivity (SLI) were examined in human cerebrospinal fluid (CSF). To validate the assay it was shown that CSF which had been run over a somatostatin immunoaffinity column showed no interference with binding of synthetic standards. Reversed phase HPLC showed that the immunoreactive material coeluted with SS14 and SS28 as well as a higher molecular weight precursor. Concentrations of human CSF SLI were stable at both room temperature and 4 °C for up to 72 h while repeated freezing and thawing resulted in a significant loss of immunoreactive material after the 3rd repetition. In normal control patients less than 55 years of age, CSF SLI was 54.7 ± 1.9 pg/ml, while in those older than 55 CSF SLI was 56.2 ± 2.2 pg/ml. Febrile infants had significantly higher levels (75.4 ± 7.3) pg/ml. CSF SLI was normal in patients with aseptic meningitis (54.4 ± 3.4 pg/ml), suggesting that increased CSF protein and white cell counts do not affect concentrations. Concentrations of CSF SLI were significantly increased in intervertebral disc disease (65.1 ± 5.6 pg/ml), intrinsic spinal cord pathology (101.0 ± 23.9 pg/ml), central nervous system tumors (78.0 ± 7.8 pg/ml) and acute cortical damage of varied etiology (277.8 ± 81.6 pg/ml). Patients with pseudotumor cerebri had concentrations of 43.2 ± 2.5 pg/ml. Concentrations of CSF SLI were significantly reduced (P < 0.01) in multiple sclerosis (38.8 ± 5.5 pg/ml) and old cortical pathology (23.2 ± 3.9 pg/ml). Serial CSF analyses in patients with acute CNS lesions, suggest that CSF SLI may be a neurochemical marker of acute pathology, as the initially elevated levels fell to or below normal with resolution of the pathologic process.
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DOI: 10.1016/0022-510X(85)90039-5
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Black</name><affiliation><mods:affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Martin, Joseph B" sort="Martin, Joseph B" uniqKey="Martin J" first="Joseph B." last="Martin">Joseph B. Martin</name><affiliation><mods:affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:65C373234BD10600B0081005DF500799FC215837</idno><date when="1985" year="1985">1985</date><idno type="doi">10.1016/0022-510X(85)90039-5</idno><idno type="url">https://api.istex.fr/document/65C373234BD10600B0081005DF500799FC215837/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002E17</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Human cerebrospinal fluid somatostatin in neurologic disease</title><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name><affiliation><mods:affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Mazurek, Michael F" sort="Mazurek, Michael F" uniqKey="Mazurek M" first="Michael F." last="Mazurek">Michael F. Mazurek</name><affiliation><mods:affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Black, Peter Mcl" sort="Black, Peter Mcl" uniqKey="Black P" first="Peter Mcl." last="Black">Peter Mcl. Black</name><affiliation><mods:affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Martin, Joseph B" sort="Martin, Joseph B" uniqKey="Martin J" first="Joseph B." last="Martin">Joseph B. Martin</name><affiliation><mods:affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1985">1985</date><biblScope unit="volume">71</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="91">91</biblScope><biblScope unit="page" to="104">104</biblScope></imprint><idno type="ISSN">0022-510X</idno></series><idno type="istex">65C373234BD10600B0081005DF500799FC215837</idno><idno type="DOI">10.1016/0022-510X(85)90039-5</idno><idno type="PII">0022-510X(85)90039-5</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Concentrations of somatostatin-like immunoreactivity (SLI) were examined in human cerebrospinal fluid (CSF). To validate the assay it was shown that CSF which had been run over a somatostatin immunoaffinity column showed no interference with binding of synthetic standards. Reversed phase HPLC showed that the immunoreactive material coeluted with SS14 and SS28 as well as a higher molecular weight precursor. Concentrations of human CSF SLI were stable at both room temperature and 4 °C for up to 72 h while repeated freezing and thawing resulted in a significant loss of immunoreactive material after the 3rd repetition. In normal control patients less than 55 years of age, CSF SLI was 54.7 ± 1.9 pg/ml, while in those older than 55 CSF SLI was 56.2 ± 2.2 pg/ml. Febrile infants had significantly higher levels (75.4 ± 7.3) pg/ml. CSF SLI was normal in patients with aseptic meningitis (54.4 ± 3.4 pg/ml), suggesting that increased CSF protein and white cell counts do not affect concentrations. Concentrations of CSF SLI were significantly increased in intervertebral disc disease (65.1 ± 5.6 pg/ml), intrinsic spinal cord pathology (101.0 ± 23.9 pg/ml), central nervous system tumors (78.0 ± 7.8 pg/ml) and acute cortical damage of varied etiology (277.8 ± 81.6 pg/ml). Patients with pseudotumor cerebri had concentrations of 43.2 ± 2.5 pg/ml. Concentrations of CSF SLI were significantly reduced (P < 0.01) in multiple sclerosis (38.8 ± 5.5 pg/ml) and old cortical pathology (23.2 ± 3.9 pg/ml). Serial CSF analyses in patients with acute CNS lesions, suggest that CSF SLI may be a neurochemical marker of acute pathology, as the initially elevated levels fell to or below normal with resolution of the pathologic process.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>M.Flint Beal</name><affiliations><json:string>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</json:string></affiliations></json:item><json:item><name>Michael F. Mazurek</name><affiliations><json:string>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</json:string></affiliations></json:item><json:item><name>Peter McL. Black</name><affiliations><json:string>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</json:string></affiliations></json:item><json:item><name>Joseph B. Martin</name><affiliations><json:string>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Cerebrospinal fluid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neurological disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Somatostatin</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Concentrations of somatostatin-like immunoreactivity (SLI) were examined in human cerebrospinal fluid (CSF). To validate the assay it was shown that CSF which had been run over a somatostatin immunoaffinity column showed no interference with binding of synthetic standards. Reversed phase HPLC showed that the immunoreactive material coeluted with SS14 and SS28 as well as a higher molecular weight precursor. Concentrations of human CSF SLI were stable at both room temperature and 4 °C for up to 72 h while repeated freezing and thawing resulted in a significant loss of immunoreactive material after the 3rd repetition. In normal control patients less than 55 years of age, CSF SLI was 54.7 ± 1.9 pg/ml, while in those older than 55 CSF SLI was 56.2 ± 2.2 pg/ml. Febrile infants had significantly higher levels (75.4 ± 7.3) pg/ml. CSF SLI was normal in patients with aseptic meningitis (54.4 ± 3.4 pg/ml), suggesting that increased CSF protein and white cell counts do not affect concentrations. Concentrations of CSF SLI were significantly increased in intervertebral disc disease (65.1 ± 5.6 pg/ml), intrinsic spinal cord pathology (101.0 ± 23.9 pg/ml), central nervous system tumors (78.0 ± 7.8 pg/ml) and acute cortical damage of varied etiology (277.8 ± 81.6 pg/ml). Patients with pseudotumor cerebri had concentrations of 43.2 ± 2.5 pg/ml. Concentrations of CSF SLI were significantly reduced (P > 0.01) in multiple sclerosis (38.8 ± 5.5 pg/ml) and old cortical pathology (23.2 ± 3.9 pg/ml). Serial CSF analyses in patients with acute CNS lesions, suggest that CSF SLI may be a neurochemical marker of acute pathology, as the initially elevated levels fell to or below normal with resolution of the pathologic process.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>504 x 735 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>3</keywordCount><abstractCharCount>1727</abstractCharCount><pdfWordCount>5343</pdfWordCount><pdfCharCount>31594</pdfCharCount><pdfPageCount>14</pdfPageCount><abstractWordCount>276</abstractWordCount></qualityIndicators><title>Human cerebrospinal fluid somatostatin in neurologic disease</title><pii><json:string>0022-510X(85)90039-5</json:string></pii><genre><json:string>research-article</json:string></genre><host><volume>71</volume><pii><json:string>S0022-510X(00)X0198-0</json:string></pii><pages><last>104</last><first>91</first></pages><issn><json:string>0022-510X</json:string></issn><issue>1</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Journal of the Neurological Sciences</title><publicationDate>1985</publicationDate></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string><json:string>NEUROIMAGING</json:string><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>1985</publicationDate><copyrightDate>1985</copyrightDate><doi><json:string>10.1016/0022-510X(85)90039-5</json:string></doi><id>65C373234BD10600B0081005DF500799FC215837</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/65C373234BD10600B0081005DF500799FC215837/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/65C373234BD10600B0081005DF500799FC215837/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/65C373234BD10600B0081005DF500799FC215837/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/65C373234BD10600B0081005DF500799FC215837/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Human cerebrospinal fluid somatostatin in neurologic disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1985</date></publicationStmt><notesStmt><note>This work was supported by USPHS grants AM 26252 and NS 16367 (Huntington's Disease Center without Walls) and Alzheimer's Disease Research Center Grant, NIA-IP50AG05134. Dr. Beal is a fellow of the National Huntington Disease Association and holds a Young Investigator Award (IR23NS19867-1). M.F. Mazurek is a Fellow of the Medical Research Council of Canada.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Human cerebrospinal fluid somatostatin in neurologic disease</title><author><persName><forename type="first">M.Flint</forename><surname>Beal</surname></persName><note type="biography">Address reprint requests to: Dr. Beal, Neurology Research, Research 4, Massachusetts General Hospital, Boston, MA 02114 U.S.A.</note><affiliation>Address reprint requests to: Dr. Beal, Neurology Research, Research 4, Massachusetts General Hospital, Boston, MA 02114 U.S.A.</affiliation><affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</affiliation></author><author><persName><forename type="first">Michael F.</forename><surname>Mazurek</surname></persName><affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</affiliation></author><author><persName><forename type="first">Peter McL.</forename><surname>Black</surname></persName><affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</affiliation></author><author><persName><forename type="first">Joseph B.</forename><surname>Martin</surname></persName><affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</affiliation></author></analytic><monogr><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="pISSN">0022-510X</idno><idno type="PII">S0022-510X(00)X0198-0</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1985"></date><biblScope unit="volume">71</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="91">91</biblScope><biblScope unit="page" to="104">104</biblScope></imprint></monogr><idno type="istex">65C373234BD10600B0081005DF500799FC215837</idno><idno type="DOI">10.1016/0022-510X(85)90039-5</idno><idno type="PII">0022-510X(85)90039-5</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1985</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Concentrations of somatostatin-like immunoreactivity (SLI) were examined in human cerebrospinal fluid (CSF). To validate the assay it was shown that CSF which had been run over a somatostatin immunoaffinity column showed no interference with binding of synthetic standards. Reversed phase HPLC showed that the immunoreactive material coeluted with SS14 and SS28 as well as a higher molecular weight precursor. Concentrations of human CSF SLI were stable at both room temperature and 4 °C for up to 72 h while repeated freezing and thawing resulted in a significant loss of immunoreactive material after the 3rd repetition. In normal control patients less than 55 years of age, CSF SLI was 54.7 ± 1.9 pg/ml, while in those older than 55 CSF SLI was 56.2 ± 2.2 pg/ml. Febrile infants had significantly higher levels (75.4 ± 7.3) pg/ml. CSF SLI was normal in patients with aseptic meningitis (54.4 ± 3.4 pg/ml), suggesting that increased CSF protein and white cell counts do not affect concentrations. Concentrations of CSF SLI were significantly increased in intervertebral disc disease (65.1 ± 5.6 pg/ml), intrinsic spinal cord pathology (101.0 ± 23.9 pg/ml), central nervous system tumors (78.0 ± 7.8 pg/ml) and acute cortical damage of varied etiology (277.8 ± 81.6 pg/ml). Patients with pseudotumor cerebri had concentrations of 43.2 ± 2.5 pg/ml. Concentrations of CSF SLI were significantly reduced (P < 0.01) in multiple sclerosis (38.8 ± 5.5 pg/ml) and old cortical pathology (23.2 ± 3.9 pg/ml). Serial CSF analyses in patients with acute CNS lesions, suggest that CSF SLI may be a neurochemical marker of acute pathology, as the initially elevated levels fell to or below normal with resolution of the pathologic process.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Cerebrospinal fluid</term></item><item><term>Neurological disease</term></item><item><term>Somatostatin</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1985-07-01">Registration</change><change when="1985-07-01">Modified</change><change when="1985">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: 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:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>JNS</jid><aid>85900395</aid><ce:pii>0022-510X(85)90039-5</ce:pii><ce:doi>10.1016/0022-510X(85)90039-5</ce:doi><ce:copyright type="unknown" year="1985"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>This work was supported by USPHS grants AM 26252 and NS 16367 (Huntington's Disease Center without Walls) and Alzheimer's Disease Research Center Grant, NIA-IP50AG05134. Dr. Beal is a fellow of the National Huntington Disease Association and holds a Young Investigator Award (IR23NS19867-1). M.F. Mazurek is a Fellow of the Medical Research Council of Canada.</ce:note-para></ce:article-footnote><ce:title>Human cerebrospinal fluid somatostatin in neurologic disease</ce:title><ce:author-group><ce:author><ce:given-name>M.Flint</ce:given-name><ce:surname>Beal</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Michael F.</ce:given-name><ce:surname>Mazurek</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Peter McL.</ce:given-name><ce:surname>Black</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Joseph B.</ce:given-name><ce:surname>Martin</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>Address reprint requests to: Dr. Beal, Neurology Research, Research 4, Massachusetts General Hospital, Boston, MA 02114 U.S.A.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="23" month="1" year="1985"></ce:date-received><ce:date-revised day="1" month="7" year="1985"></ce:date-revised><ce:date-accepted day="1" month="7" year="1985"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Concentrations of somatostatin-like immunoreactivity (SLI) were examined in human cerebrospinal fluid (CSF). To validate the assay it was shown that CSF which had been run over a somatostatin immunoaffinity column showed no interference with binding of synthetic standards. Reversed phase HPLC showed that the immunoreactive material coeluted with SS14 and SS28 as well as a higher molecular weight precursor. Concentrations of human CSF SLI were stable at both room temperature and 4 °C for up to 72 h while repeated freezing and thawing resulted in a significant loss of immunoreactive material after the 3rd repetition. In normal control patients less than 55 years of age, CSF SLI was 54.7 ± 1.9 pg/ml, while in those older than 55 CSF SLI was 56.2 ± 2.2 pg/ml. Febrile infants had significantly higher levels (75.4 ± 7.3) pg/ml. CSF SLI was normal in patients with aseptic meningitis (54.4 ± 3.4 pg/ml), suggesting that increased CSF protein and white cell counts do not affect concentrations. Concentrations of CSF SLI were significantly increased in intervertebral disc disease (65.1 ± 5.6 pg/ml), intrinsic spinal cord pathology (101.0 ± 23.9 pg/ml), central nervous system tumors (78.0 ± 7.8 pg/ml) and acute cortical damage of varied etiology (277.8 ± 81.6 pg/ml). Patients with pseudotumor cerebri had concentrations of 43.2 ± 2.5 pg/ml. Concentrations of CSF SLI were significantly reduced (<ce:italic>P</ce:italic> < 0.01) in multiple sclerosis (38.8 ± 5.5 pg/ml) and old cortical pathology (23.2 ± 3.9 pg/ml). Serial CSF analyses in patients with acute CNS lesions, suggest that CSF SLI may be a neurochemical marker of acute pathology, as the initially elevated levels fell to or below normal with resolution of the pathologic process.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Cerebrospinal fluid</ce:text></ce:keyword><ce:keyword><ce:text>Neurological disease</ce:text></ce:keyword><ce:keyword><ce:text>Somatostatin</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Human cerebrospinal fluid somatostatin in neurologic disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Human cerebrospinal fluid somatostatin in neurologic disease</title></titleInfo><name type="personal"><namePart type="given">M.Flint</namePart><namePart type="family">Beal</namePart><affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</affiliation><description>Address reprint requests to: Dr. Beal, Neurology Research, Research 4, Massachusetts General Hospital, Boston, MA 02114 U.S.A.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael F.</namePart><namePart type="family">Mazurek</namePart><affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter McL.</namePart><namePart type="family">Black</namePart><affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph B.</namePart><namePart type="family">Martin</namePart><affiliation>Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1985</dateIssued><dateValid encoding="w3cdtf">1985-07-01</dateValid><dateModified encoding="w3cdtf">1985-07-01</dateModified><copyrightDate encoding="w3cdtf">1985</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Concentrations of somatostatin-like immunoreactivity (SLI) were examined in human cerebrospinal fluid (CSF). To validate the assay it was shown that CSF which had been run over a somatostatin immunoaffinity column showed no interference with binding of synthetic standards. Reversed phase HPLC showed that the immunoreactive material coeluted with SS14 and SS28 as well as a higher molecular weight precursor. Concentrations of human CSF SLI were stable at both room temperature and 4 °C for up to 72 h while repeated freezing and thawing resulted in a significant loss of immunoreactive material after the 3rd repetition. In normal control patients less than 55 years of age, CSF SLI was 54.7 ± 1.9 pg/ml, while in those older than 55 CSF SLI was 56.2 ± 2.2 pg/ml. Febrile infants had significantly higher levels (75.4 ± 7.3) pg/ml. CSF SLI was normal in patients with aseptic meningitis (54.4 ± 3.4 pg/ml), suggesting that increased CSF protein and white cell counts do not affect concentrations. Concentrations of CSF SLI were significantly increased in intervertebral disc disease (65.1 ± 5.6 pg/ml), intrinsic spinal cord pathology (101.0 ± 23.9 pg/ml), central nervous system tumors (78.0 ± 7.8 pg/ml) and acute cortical damage of varied etiology (277.8 ± 81.6 pg/ml). Patients with pseudotumor cerebri had concentrations of 43.2 ± 2.5 pg/ml. Concentrations of CSF SLI were significantly reduced (P < 0.01) in multiple sclerosis (38.8 ± 5.5 pg/ml) and old cortical pathology (23.2 ± 3.9 pg/ml). Serial CSF analyses in patients with acute CNS lesions, suggest that CSF SLI may be a neurochemical marker of acute pathology, as the initially elevated levels fell to or below normal with resolution of the pathologic process.</abstract><note>This work was supported by USPHS grants AM 26252 and NS 16367 (Huntington's Disease Center without Walls) and Alzheimer's Disease Research Center Grant, NIA-IP50AG05134. Dr. Beal is a fellow of the National Huntington Disease Association and holds a Young Investigator Award (IR23NS19867-1). M.F. Mazurek is a Fellow of the Medical Research Council of Canada.</note><subject><genre>Keywords</genre><topic>Cerebrospinal fluid</topic><topic>Neurological disease</topic><topic>Somatostatin</topic></subject><relatedItem type="host"><titleInfo><title>Journal of the Neurological Sciences</title></titleInfo><titleInfo type="abbreviated"><title>JNS</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">198511</dateIssued></originInfo><identifier type="ISSN">0022-510X</identifier><identifier type="PII">S0022-510X(00)X0198-0</identifier><part><date>198511</date><detail type="volume"><number>71</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>136</end></extent><extent unit="pages"><start>91</start><end>104</end></extent></part></relatedItem><identifier type="istex">65C373234BD10600B0081005DF500799FC215837</identifier><identifier type="DOI">10.1016/0022-510X(85)90039-5</identifier><identifier type="PII">0022-510X(85)90039-5</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/65C373234BD10600B0081005DF500799FC215837/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROIMAGING</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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