Oxidative stress in patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS).
Identifieur interne : 000834 ( Ncbi/Merge ); précédent : 000833; suivant : 000835Oxidative stress in patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS).
Auteurs : Rie Miyata [Japon] ; Naoyuki Tanuma ; Masaharu Hayashi ; Takuji Imamura ; Jun-Ichi Takanashi ; Rieko Nagata ; Akihisa Okumura ; Hirohumi Kashii ; Sunao Tomita ; Satoko Kumada ; Masaya KubotaSource :
- Brain & development [ 1872-7131 ] ; 2012.
Descripteurs français
- KwdFr :
- Adolescent, Corps calleux (anatomopathologie), Corps calleux (métabolisme), Cytokines (), Dosage radioimmunologique, Désoxyguanosine (), Désoxyguanosine (analogues et dérivés), Encéphalite (), Encéphalite (sang), Encéphalopathies (), Encéphalopathies (anatomopathologie), Encéphalopathies (sang), Enfant, Enfant d'âge préscolaire, Enolase (métabolisme), Femelle, Humains, Imagerie par résonance magnétique, Mâle, Nourrisson, Protéines tau (), Sodium (sang), Stress oxydatif (physiologie), Test ELISA.
- MESH :
- analogues et dérivés : Désoxyguanosine.
- anatomopathologie : Corps calleux, Encéphalopathies.
- métabolisme : Corps calleux, Enolase.
- physiologie : Stress oxydatif.
- sang : Encéphalite, Encéphalopathies, Sodium.
- Adolescent, Cytokines, Dosage radioimmunologique, Désoxyguanosine, Encéphalite, Encéphalopathies, Enfant, Enfant d'âge préscolaire, Femelle, Humains, Imagerie par résonance magnétique, Mâle, Nourrisson, Protéines tau, Test ELISA.
English descriptors
- KwdEn :
- 8-Hydroxy-2'-Deoxyguanosine, Adolescent, Brain Diseases (blood), Brain Diseases (cerebrospinal fluid), Brain Diseases (complications), Brain Diseases (pathology), Child, Child, Preschool, Corpus Callosum (metabolism), Corpus Callosum (pathology), Cytokines (cerebrospinal fluid), Deoxyguanosine (analogs & derivatives), Deoxyguanosine (cerebrospinal fluid), Encephalitis (blood), Encephalitis (cerebrospinal fluid), Encephalitis (complications), Enzyme-Linked Immunosorbent Assay, Female, Humans, Infant, Magnetic Resonance Imaging, Male, Oxidative Stress (physiology), Phosphopyruvate Hydratase (metabolism), Radioimmunoassay, Sodium (blood), tau Proteins (cerebrospinal fluid).
- MESH :
- chemical , analogs & derivatives : Deoxyguanosine.
- chemical , blood : Sodium.
- chemical , cerebrospinal fluid : Cytokines, Deoxyguanosine, tau Proteins.
- chemical , metabolism : Phosphopyruvate Hydratase.
- chemical : 8-Hydroxy-2'-Deoxyguanosine.
- blood : Brain Diseases, Encephalitis.
- cerebrospinal fluid : Brain Diseases, Encephalitis.
- complications : Brain Diseases, Encephalitis.
- metabolism : Corpus Callosum.
- pathology : Brain Diseases, Corpus Callosum.
- physiology : Oxidative Stress.
- Adolescent, Child, Child, Preschool, Enzyme-Linked Immunosorbent Assay, Female, Humans, Infant, Magnetic Resonance Imaging, Male, Radioimmunoassay.
Abstract
We examined oxidative stress markers, tau protein and cytokines in the cerebrospinal fluid (CSF) in six patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS). In the CSF, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and hexanoyl-lysine adduct levels increased over the cutoff index in four and one out of six MERS patients, respectively. The CSF IL-6 and IL-10 levels were increased in three out of six patients, two of which had extended lesion of the cerebral white matter. The CSF value of tau protein, marker of the axonal damage, was not increased, and neuron specific enolase (NSE) in the CSF was not increased. The increased 8-OHdG levels in the CSF, DNA oxidative stress marker, in four MERS patients, suggesting involvement of oxidative stress in MERS. MERS is occasionally accompanied with hyponatremia, although our patients lacked hyponatremia. It is possible that the disequilibrium of systemic metabolism including electrolytes may lead to facilitation of oxidative stress and reversible white matter lesion in MERS. The increase of cytokine production seems to be involved in the distribution of lesions in MERS.
DOI: 10.1016/j.braindev.2011.04.004
PubMed: 21576007
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pubmed:21576007Le document en format XML
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ELISA</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We examined oxidative stress markers, tau protein and cytokines in the cerebrospinal fluid (CSF) in six patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS). In the CSF, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and hexanoyl-lysine adduct levels increased over the cutoff index in four and one out of six MERS patients, respectively. The CSF IL-6 and IL-10 levels were increased in three out of six patients, two of which had extended lesion of the cerebral white matter. The CSF value of tau protein, marker of the axonal damage, was not increased, and neuron specific enolase (NSE) in the CSF was not increased. The increased 8-OHdG levels in the CSF, DNA oxidative stress marker, in four MERS patients, suggesting involvement of oxidative stress in MERS. MERS is occasionally accompanied with hyponatremia, although our patients lacked hyponatremia. It is possible that the disequilibrium of systemic metabolism including electrolytes may lead to facilitation of oxidative stress and reversible white matter lesion in MERS. The increase of cytokine production seems to be involved in the distribution of lesions in MERS.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21576007</PMID><DateCompleted><Year>2012</Year><Month>05</Month><Day>07</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7131</ISSN><JournalIssue CitedMedium="Internet"><Volume>34</Volume><Issue>2</Issue><PubDate><Year>2012</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Brain & development</Title><ISOAbbreviation>Brain Dev.</ISOAbbreviation></Journal><ArticleTitle>Oxidative stress in patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS).</ArticleTitle><Pagination><MedlinePgn>124-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.braindev.2011.04.004</ELocationID><Abstract><AbstractText>We examined oxidative stress markers, tau protein and cytokines in the cerebrospinal fluid (CSF) in six patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS). In the CSF, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and hexanoyl-lysine adduct levels increased over the cutoff index in four and one out of six MERS patients, respectively. The CSF IL-6 and IL-10 levels were increased in three out of six patients, two of which had extended lesion of the cerebral white matter. The CSF value of tau protein, marker of the axonal damage, was not increased, and neuron specific enolase (NSE) in the CSF was not increased. The increased 8-OHdG levels in the CSF, DNA oxidative stress marker, in four MERS patients, suggesting involvement of oxidative stress in MERS. MERS is occasionally accompanied with hyponatremia, although our patients lacked hyponatremia. It is possible that the disequilibrium of systemic metabolism including electrolytes may lead to facilitation of oxidative stress and reversible white matter lesion in MERS. The increase of cytokine production seems to be involved in the distribution of lesions in MERS.</AbstractText><CopyrightInformation>Copyright © 2011 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Miyata</LastName><ForeName>Rie</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Tokyo-Kita Social Insurance Hospital, Kita-ku, Tokyo, Japan. rie88miyata@ybb.ne.jp</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tanuma</LastName><ForeName>Naoyuki</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Hayashi</LastName><ForeName>Masaharu</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Imamura</LastName><ForeName>Takuji</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Takanashi</LastName><ForeName>Jun-ichi</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Nagata</LastName><ForeName>Rieko</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Okumura</LastName><ForeName>Akihisa</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Kashii</LastName><ForeName>Hirohumi</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Tomita</LastName><ForeName>Sunao</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Kumada</LastName><ForeName>Satoko</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Kubota</LastName><ForeName>Masaya</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>05</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Brain Dev</MedlineTA><NlmUniqueID>7909235</NlmUniqueID><ISSNLinking>0387-7604</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>88847-89-6</RegistryNumber><NameOfSubstance UI="D000080242">8-Hydroxy-2'-Deoxyguanosine</NameOfSubstance></Chemical><Chemical><RegistryNumber>9NEZ333N27</RegistryNumber><NameOfSubstance UI="D012964">Sodium</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 4.2.1.11</RegistryNumber><NameOfSubstance UI="D010751">Phosphopyruvate Hydratase</NameOfSubstance></Chemical><Chemical><RegistryNumber>G9481N71RO</RegistryNumber><NameOfSubstance UI="D003849">Deoxyguanosine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000080242" MajorTopicYN="N">8-Hydroxy-2'-Deoxyguanosine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001927" MajorTopicYN="N">Brain Diseases</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002675" MajorTopicYN="N">Child, Preschool</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003337" MajorTopicYN="N">Corpus Callosum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003849" MajorTopicYN="N">Deoxyguanosine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004660" MajorTopicYN="N">Encephalitis</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004797" MajorTopicYN="N">Enzyme-Linked Immunosorbent Assay</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008279" MajorTopicYN="N">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010751" MajorTopicYN="N">Phosphopyruvate Hydratase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011863" MajorTopicYN="N">Radioimmunoassay</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012964" MajorTopicYN="N">Sodium</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016875" MajorTopicYN="N">tau Proteins</DescriptorName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2011</Year><Month>01</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2011</Year><Month>03</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>04</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>5</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>5</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>5</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">21576007</ArticleId><ArticleId IdType="pii">S0387-7604(11)00093-3</ArticleId><ArticleId IdType="doi">10.1016/j.braindev.2011.04.004</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country><region><li>Région de Kantō</li></region><settlement><li>Tokyo</li></settlement></list><tree><noCountry><name sortKey="Hayashi, Masaharu" sort="Hayashi, Masaharu" uniqKey="Hayashi M" first="Masaharu" last="Hayashi">Masaharu Hayashi</name><name sortKey="Imamura, Takuji" sort="Imamura, Takuji" uniqKey="Imamura T" first="Takuji" last="Imamura">Takuji Imamura</name><name sortKey="Kashii, Hirohumi" sort="Kashii, Hirohumi" uniqKey="Kashii H" first="Hirohumi" last="Kashii">Hirohumi Kashii</name><name sortKey="Kubota, Masaya" sort="Kubota, Masaya" uniqKey="Kubota M" first="Masaya" last="Kubota">Masaya Kubota</name><name sortKey="Kumada, Satoko" sort="Kumada, Satoko" uniqKey="Kumada S" first="Satoko" last="Kumada">Satoko Kumada</name><name sortKey="Nagata, Rieko" sort="Nagata, Rieko" uniqKey="Nagata R" first="Rieko" last="Nagata">Rieko Nagata</name><name sortKey="Okumura, Akihisa" sort="Okumura, Akihisa" uniqKey="Okumura A" first="Akihisa" last="Okumura">Akihisa Okumura</name><name sortKey="Takanashi, Jun Ichi" sort="Takanashi, Jun Ichi" uniqKey="Takanashi J" first="Jun-Ichi" last="Takanashi">Jun-Ichi Takanashi</name><name sortKey="Tanuma, Naoyuki" sort="Tanuma, Naoyuki" uniqKey="Tanuma N" first="Naoyuki" last="Tanuma">Naoyuki Tanuma</name><name sortKey="Tomita, Sunao" sort="Tomita, Sunao" uniqKey="Tomita S" first="Sunao" last="Tomita">Sunao Tomita</name></noCountry><country name="Japon"><region name="Région de Kantō"><name sortKey="Miyata, Rie" sort="Miyata, Rie" uniqKey="Miyata R" first="Rie" last="Miyata">Rie Miyata</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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