Human cerebrospinal fluid somatostatin in neurologic disease
Identifieur interne : 002993 ( Main/Exploration ); précédent : 002992; suivant : 002994Human 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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Martin</name></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><idno type="wicri:Area/Main/Curation">002A34</idno><idno type="wicri:Area/Main/Exploration">002993</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><wicri:noCountry code="subField">MA U.S.A.</wicri:noCountry></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><wicri:noCountry code="subField">MA U.S.A.</wicri:noCountry></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><wicri:noCountry code="subField">MA U.S.A.</wicri:noCountry></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><wicri:noCountry code="subField">MA U.S.A.</wicri:noCountry></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><affiliations><list></list><tree><noCountry><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name><name sortKey="Black, Peter Mcl" sort="Black, Peter Mcl" uniqKey="Black P" first="Peter Mcl." last="Black">Peter Mcl. Black</name><name sortKey="Martin, Joseph B" sort="Martin, Joseph B" uniqKey="Martin J" first="Joseph B." last="Martin">Joseph B. Martin</name><name sortKey="Mazurek, Michael F" sort="Mazurek, Michael F" uniqKey="Mazurek M" first="Michael F." last="Mazurek">Michael F. Mazurek</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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