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Article: Linkage studies on chromosome 22 in familial schizophrenia

TitleLinkage studies on chromosome 22 in familial schizophrenia
Authors
Issue Date1995
Citation
American Journal Of Medical Genetics - Neuropsychiatric Genetics, 1995, v. 60 n. 2, p. 139-146 How to Cite?
AbstractAs part of a systematic search for a major genetic locus for schizophrenia we have examined chromosome 22 using 14 highly polymorphic markers in 23 disease pedigrees. The markers were distributed at an average distance of 6.6 cM, covering 70-80% of the chromosome. We analyzed the data by the lod score method using five plausible genetic models ranging from dominant to recessive, after testing the power of our sample under the same genetic parameters. The most positive lod score found was 1.51 under a recessive model for the marker D22S278, which is insufficient to conclude linkage. However, an excess of shared alleles in affected siblings (P < .01) was found for both D22S278 and D22S283. For D22S278, the A statistic was equal to the lod score (1.51) and therefore did not provide additional evidence for linkage allowing for heterogeneity, but the Liang statistic was more significant (P = .002). Our results suggest the possibility that the region around D22S278 and D22S283 contains a gene which contributes to the aetiology of schizophrenia.
Persistent Identifierhttp://hdl.handle.net/10722/175720
ISSN
2003 Impact Factor: -999.999
2009 SCImago Journal Rankings: 1.100
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVallada, HPen_US
dc.contributor.authorGill, Men_US
dc.contributor.authorSham, Pen_US
dc.contributor.authorLim, LCCen_US
dc.contributor.authorNanko, Sen_US
dc.contributor.authorAsherson, Pen_US
dc.contributor.authorMurray, RMen_US
dc.contributor.authorMcguffin, Pen_US
dc.contributor.authorOwen, Men_US
dc.contributor.authorCollier, Den_US
dc.date.accessioned2012-11-26T09:00:44Z-
dc.date.available2012-11-26T09:00:44Z-
dc.date.issued1995en_US
dc.identifier.citationAmerican Journal Of Medical Genetics - Neuropsychiatric Genetics, 1995, v. 60 n. 2, p. 139-146en_US
dc.identifier.issn0148-7299en_US
dc.identifier.urihttp://hdl.handle.net/10722/175720-
dc.description.abstractAs part of a systematic search for a major genetic locus for schizophrenia we have examined chromosome 22 using 14 highly polymorphic markers in 23 disease pedigrees. The markers were distributed at an average distance of 6.6 cM, covering 70-80% of the chromosome. We analyzed the data by the lod score method using five plausible genetic models ranging from dominant to recessive, after testing the power of our sample under the same genetic parameters. The most positive lod score found was 1.51 under a recessive model for the marker D22S278, which is insufficient to conclude linkage. However, an excess of shared alleles in affected siblings (P < .01) was found for both D22S278 and D22S283. For D22S278, the A statistic was equal to the lod score (1.51) and therefore did not provide additional evidence for linkage allowing for heterogeneity, but the Liang statistic was more significant (P = .002). Our results suggest the possibility that the region around D22S278 and D22S283 contains a gene which contributes to the aetiology of schizophrenia.en_US
dc.languageengen_US
dc.relation.ispartofAmerican Journal of Medical Genetics - Neuropsychiatric Geneticsen_US
dc.subject.meshAllelesen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshChromosome Mappingen_US
dc.subject.meshChromosomes, Human, Pair 22 - Geneticsen_US
dc.subject.meshDna Primers - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenetic Linkageen_US
dc.subject.meshGenetic Markersen_US
dc.subject.meshHumansen_US
dc.subject.meshLod Scoreen_US
dc.subject.meshMaleen_US
dc.subject.meshModels, Geneticen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshPedigreeen_US
dc.subject.meshPolymorphism, Geneticen_US
dc.subject.meshSchizophrenia - Geneticsen_US
dc.titleLinkage studies on chromosome 22 in familial schizophreniaen_US
dc.typeArticleen_US
dc.identifier.emailSham, P: pcsham@hku.hken_US
dc.identifier.authoritySham, P=rp00459en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/ajmg.1320600210-
dc.identifier.pmid7485248-
dc.identifier.scopuseid_2-s2.0-0028937526en_US
dc.identifier.volume60en_US
dc.identifier.issue2en_US
dc.identifier.spage139en_US
dc.identifier.epage146en_US
dc.identifier.isiWOS:A1995QT74500009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVallada, HP=7003742958en_US
dc.identifier.scopusauthoridGill, M=14633481100en_US
dc.identifier.scopusauthoridSham, P=34573429300en_US
dc.identifier.scopusauthoridLim, LCC=36484937000en_US
dc.identifier.scopusauthoridNanko, S=7006294283en_US
dc.identifier.scopusauthoridAsherson, P=35402700900en_US
dc.identifier.scopusauthoridMurray, RM=35406239400en_US
dc.identifier.scopusauthoridMcGuffin, P=22954119700en_US
dc.identifier.scopusauthoridOwen, M=36044041500en_US
dc.identifier.scopusauthoridCollier, D=26642980600en_US

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