Investigation of genes coding for inflammatory components in Parkinson's disease.
Identifieur interne : 003089 ( PubMed/Checkpoint ); précédent : 003088; suivant : 003090Investigation of genes coding for inflammatory components in Parkinson's disease.
Auteurs : Anna H Kansson [Suède] ; Lars Westberg ; Staffan Nilsson ; Silvia Buervenich ; Andrea Carmine ; Björn Holmberg ; Olof Sydow ; Lars Olson ; Bo Johnels ; Elias Eriksson ; Hans NissbrandtSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2005.
English descriptors
- KwdEn :
- 1-Alkyl-2-acetylglycerophosphocholine Esterase (genetics), 1-Alkyl-2-acetylglycerophosphocholine Esterase (metabolism), Age Factors, Alleles, Brain (metabolism), Chemokine CCL2 (genetics), Chemokine CCL2 (metabolism), DNA Primers (genetics), Genotype, Humans, Inflammation (complications), Inflammation (genetics), Inflammation (metabolism), Intercellular Adhesion Molecule-1 (genetics), Intercellular Adhesion Molecule-1 (metabolism), Interferon-gamma (genetics), Interferon-gamma (metabolism), Interleukin-10 (genetics), Interleukin-10 (metabolism), Middle Aged, Parkinson Disease (complications), Parkinson Disease (genetics), Parkinson Disease (metabolism), Polymorphism, Genetic (genetics), Promoter Regions, Genetic (genetics), Receptors, Interferon (genetics), Receptors, Interferon (metabolism), Tumor Necrosis Factor-alpha (genetics), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , genetics : 1-Alkyl-2-acetylglycerophosphocholine Esterase, Chemokine CCL2, DNA Primers, Intercellular Adhesion Molecule-1, Interferon-gamma, Interleukin-10, Receptors, Interferon, Tumor Necrosis Factor-alpha.
- chemical , metabolism : 1-Alkyl-2-acetylglycerophosphocholine Esterase, Chemokine CCL2, Intercellular Adhesion Molecule-1, Interferon-gamma, Interleukin-10, Receptors, Interferon, Tumor Necrosis Factor-alpha.
- complications : Inflammation, Parkinson Disease.
- genetics : Inflammation, Parkinson Disease, Polymorphism, Genetic, Promoter Regions, Genetic.
- metabolism : Brain, Inflammation, Parkinson Disease.
- Age Factors, Alleles, Genotype, Humans, Middle Aged.
Abstract
Several findings obtained recently indicate that inflammation may contribute to the pathogenesis in Parkinson's disease (PD). Genetic variants of genes coding for components involved in immune reactions in the brain might therefore influence the risk of developing PD or the age of disease onset. Five single nucleotide polymorphisms (SNPs) in the genes coding for interferon-gamma (IFN-gamma; T874A in intron 1), interferon-gamma receptor 2 (IFN-gamma R2; Gln64Arg), interleukin-10 (IL-10; G1082A in the promoter region), platelet-activating factor acetylhydrolase (PAF-AH; Val379Ala), and intercellular adhesion molecule 1 (ICAM-1; Lys469Glu) were genotyped, using pyrosequencing, in 265 patients with PD and 308 controls. None of the investigated SNPs was found to be associated with PD; however, the G1082A polymorphism in the IL-10 gene promoter was found to be related to the age of disease onset. Linear regression showed a significantly earlier onset with more A-alleles (P = 0.0095; after Bonferroni correction, P = 0.048), resulting in a 5-year delayed age of onset of the disease for individuals having two G-alleles compared with individuals having two A-alleles. The results indicate that the IL-10 G1082A SNP could possibly be related to the age of onset of PD.
DOI: 10.1002/mds.20378
PubMed: 15648059
Affiliations:
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sort="Nissbrandt, Hans" uniqKey="Nissbrandt H" first="Hans" last="Nissbrandt">Hans Nissbrandt</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="doi">10.1002/mds.20378</idno><idno type="RBID">pubmed:15648059</idno><idno type="pmid">15648059</idno><idno type="wicri:Area/PubMed/Corpus">003161</idno><idno type="wicri:Area/PubMed/Curation">003161</idno><idno type="wicri:Area/PubMed/Checkpoint">003089</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Investigation of genes coding for inflammatory components in Parkinson's disease.</title><author><name sortKey="H Kansson, Anna" sort="H Kansson, Anna" uniqKey="H Kansson A" first="Anna" last="H Kansson">Anna H Kansson</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden. anna.hakansson@pharm.gu.se</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Göteborg</wicri:regionArea><wicri:noRegion>Göteborg</wicri:noRegion></affiliation></author><author><name sortKey="Westberg, Lars" sort="Westberg, Lars" uniqKey="Westberg L" first="Lars" last="Westberg">Lars Westberg</name></author><author><name sortKey="Nilsson, Staffan" sort="Nilsson, Staffan" uniqKey="Nilsson S" first="Staffan" last="Nilsson">Staffan Nilsson</name></author><author><name sortKey="Buervenich, Silvia" sort="Buervenich, Silvia" uniqKey="Buervenich S" first="Silvia" last="Buervenich">Silvia Buervenich</name></author><author><name sortKey="Carmine, Andrea" sort="Carmine, Andrea" uniqKey="Carmine A" first="Andrea" last="Carmine">Andrea Carmine</name></author><author><name sortKey="Holmberg, Bjorn" sort="Holmberg, Bjorn" uniqKey="Holmberg B" first="Björn" last="Holmberg">Björn Holmberg</name></author><author><name sortKey="Sydow, Olof" sort="Sydow, Olof" uniqKey="Sydow O" first="Olof" last="Sydow">Olof Sydow</name></author><author><name sortKey="Olson, Lars" sort="Olson, Lars" uniqKey="Olson L" first="Lars" last="Olson">Lars Olson</name></author><author><name sortKey="Johnels, Bo" sort="Johnels, Bo" uniqKey="Johnels B" first="Bo" last="Johnels">Bo Johnels</name></author><author><name sortKey="Eriksson, Elias" sort="Eriksson, Elias" uniqKey="Eriksson E" first="Elias" last="Eriksson">Elias Eriksson</name></author><author><name sortKey="Nissbrandt, Hans" sort="Nissbrandt, Hans" uniqKey="Nissbrandt H" first="Hans" last="Nissbrandt">Hans Nissbrandt</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Alkyl-2-acetylglycerophosphocholine Esterase (genetics)</term><term>1-Alkyl-2-acetylglycerophosphocholine Esterase (metabolism)</term><term>Age Factors</term><term>Alleles</term><term>Brain (metabolism)</term><term>Chemokine CCL2 (genetics)</term><term>Chemokine CCL2 (metabolism)</term><term>DNA Primers (genetics)</term><term>Genotype</term><term>Humans</term><term>Inflammation (complications)</term><term>Inflammation (genetics)</term><term>Inflammation (metabolism)</term><term>Intercellular Adhesion Molecule-1 (genetics)</term><term>Intercellular Adhesion Molecule-1 (metabolism)</term><term>Interferon-gamma (genetics)</term><term>Interferon-gamma (metabolism)</term><term>Interleukin-10 (genetics)</term><term>Interleukin-10 (metabolism)</term><term>Middle Aged</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Polymorphism, Genetic (genetics)</term><term>Promoter Regions, Genetic (genetics)</term><term>Receptors, Interferon (genetics)</term><term>Receptors, Interferon (metabolism)</term><term>Tumor Necrosis Factor-alpha (genetics)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>1-Alkyl-2-acetylglycerophosphocholine Esterase</term><term>Chemokine CCL2</term><term>DNA Primers</term><term>Intercellular Adhesion Molecule-1</term><term>Interferon-gamma</term><term>Interleukin-10</term><term>Receptors, Interferon</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>1-Alkyl-2-acetylglycerophosphocholine Esterase</term><term>Chemokine CCL2</term><term>Intercellular Adhesion Molecule-1</term><term>Interferon-gamma</term><term>Interleukin-10</term><term>Receptors, Interferon</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Inflammation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Inflammation</term><term>Parkinson Disease</term><term>Polymorphism, Genetic</term><term>Promoter Regions, Genetic</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Inflammation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age Factors</term><term>Alleles</term><term>Genotype</term><term>Humans</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Several findings obtained recently indicate that inflammation may contribute to the pathogenesis in Parkinson's disease (PD). Genetic variants of genes coding for components involved in immune reactions in the brain might therefore influence the risk of developing PD or the age of disease onset. Five single nucleotide polymorphisms (SNPs) in the genes coding for interferon-gamma (IFN-gamma; T874A in intron 1), interferon-gamma receptor 2 (IFN-gamma R2; Gln64Arg), interleukin-10 (IL-10; G1082A in the promoter region), platelet-activating factor acetylhydrolase (PAF-AH; Val379Ala), and intercellular adhesion molecule 1 (ICAM-1; Lys469Glu) were genotyped, using pyrosequencing, in 265 patients with PD and 308 controls. None of the investigated SNPs was found to be associated with PD; however, the G1082A polymorphism in the IL-10 gene promoter was found to be related to the age of disease onset. Linear regression showed a significantly earlier onset with more A-alleles (P = 0.0095; after Bonferroni correction, P = 0.048), resulting in a 5-year delayed age of onset of the disease for individuals having two G-alleles compared with individuals having two A-alleles. The results indicate that the IL-10 G1082A SNP could possibly be related to the age of onset of PD.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">15648059</PMID><DateCreated><Year>2005</Year><Month>05</Month><Day>05</Day></DateCreated><DateCompleted><Year>2005</Year><Month>09</Month><Day>01</Day></DateCompleted><DateRevised><Year>2008</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>20</Volume><Issue>5</Issue><PubDate><Year>2005</Year><Month>May</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Investigation of genes coding for inflammatory components in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>569-73</MedlinePgn></Pagination><Abstract><AbstractText>Several findings obtained recently indicate that inflammation may contribute to the pathogenesis in Parkinson's disease (PD). Genetic variants of genes coding for components involved in immune reactions in the brain might therefore influence the risk of developing PD or the age of disease onset. Five single nucleotide polymorphisms (SNPs) in the genes coding for interferon-gamma (IFN-gamma; T874A in intron 1), interferon-gamma receptor 2 (IFN-gamma R2; Gln64Arg), interleukin-10 (IL-10; G1082A in the promoter region), platelet-activating factor acetylhydrolase (PAF-AH; Val379Ala), and intercellular adhesion molecule 1 (ICAM-1; Lys469Glu) were genotyped, using pyrosequencing, in 265 patients with PD and 308 controls. None of the investigated SNPs was found to be associated with PD; however, the G1082A polymorphism in the IL-10 gene promoter was found to be related to the age of disease onset. Linear regression showed a significantly earlier onset with more A-alleles (P = 0.0095; after Bonferroni correction, P = 0.048), resulting in a 5-year delayed age of onset of the disease for individuals having two G-alleles compared with individuals having two A-alleles. The results indicate that the IL-10 G1082A SNP could possibly be related to the age of onset of PD.</AbstractText><CopyrightInformation>Copyright 2005 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Håkansson</LastName><ForeName>Anna</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden. anna.hakansson@pharm.gu.se</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Westberg</LastName><ForeName>Lars</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Nilsson</LastName><ForeName>Staffan</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Buervenich</LastName><ForeName>Silvia</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Carmine</LastName><ForeName>Andrea</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Holmberg</LastName><ForeName>Björn</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Sydow</LastName><ForeName>Olof</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Olson</LastName><ForeName>Lars</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Johnels</LastName><ForeName>Bo</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Eriksson</LastName><ForeName>Elias</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Nissbrandt</LastName><ForeName>Hans</ForeName><Initials>H</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov 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Molecule-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>130068-27-8</RegistryNumber><NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.47</RegistryNumber><NameOfSubstance UI="D043203">1-Alkyl-2-acetylglycerophosphocholine Esterase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D043203">1-Alkyl-2-acetylglycerophosphocholine Esterase</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000367">Age Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000483">Alleles</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018932">Chemokine CCL2</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017931">DNA Primers</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005838">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007249">Inflammation</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018799">Intercellular Adhesion Molecule-1</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007371">Interferon-gamma</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016753">Interleukin-10</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011110">Polymorphism, Genetic</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011401">Promoter Regions, Genetic</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017471">Receptors, Interferon</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014409">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>1</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>9</Month><Day>2</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>1</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.20378</ArticleId><ArticleId IdType="pubmed">15648059</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Suède</li></country></list><tree><noCountry><name sortKey="Buervenich, Silvia" sort="Buervenich, Silvia" uniqKey="Buervenich S" first="Silvia" last="Buervenich">Silvia Buervenich</name><name sortKey="Carmine, Andrea" sort="Carmine, Andrea" uniqKey="Carmine A" first="Andrea" last="Carmine">Andrea Carmine</name><name sortKey="Eriksson, Elias" sort="Eriksson, Elias" uniqKey="Eriksson E" first="Elias" last="Eriksson">Elias Eriksson</name><name sortKey="Holmberg, Bjorn" sort="Holmberg, Bjorn" uniqKey="Holmberg B" first="Björn" last="Holmberg">Björn Holmberg</name><name sortKey="Johnels, Bo" sort="Johnels, Bo" uniqKey="Johnels B" first="Bo" last="Johnels">Bo Johnels</name><name sortKey="Nilsson, Staffan" sort="Nilsson, Staffan" uniqKey="Nilsson S" first="Staffan" last="Nilsson">Staffan Nilsson</name><name sortKey="Nissbrandt, Hans" sort="Nissbrandt, Hans" uniqKey="Nissbrandt H" first="Hans" last="Nissbrandt">Hans Nissbrandt</name><name sortKey="Olson, Lars" sort="Olson, Lars" uniqKey="Olson L" first="Lars" last="Olson">Lars Olson</name><name sortKey="Sydow, Olof" sort="Sydow, Olof" uniqKey="Sydow O" first="Olof" last="Sydow">Olof Sydow</name><name sortKey="Westberg, Lars" sort="Westberg, Lars" uniqKey="Westberg L" first="Lars" last="Westberg">Lars Westberg</name></noCountry><country name="Suède"><noRegion><name sortKey="H Kansson, Anna" sort="H Kansson, Anna" uniqKey="H Kansson A" first="Anna" last="H Kansson">Anna H Kansson</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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