Please use this identifier to cite or link to this item: http://repository.kln.ac.lk/handle/123456789/1154
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dc.contributor.authorde Silva, H.J.en_US
dc.contributor.authorHoang, P.en_US
dc.contributor.authorDalton, H.en_US
dc.contributor.authorde Silva, N.R.en_US
dc.contributor.authorJewell, D.P.en_US
dc.contributor.authorPeiris, J.B.en_US
dc.date.accessioned2014-10-29T09:10:23Z-
dc.date.available2014-10-29T09:10:23Z-
dc.date.issued1992en_US
dc.identifier.citationTransactions of the Royal Society of Tropical Medicine and Hygiene. 1992; 86(2): pp.129-131en_US
dc.identifier.issn0035-9203 (Print)en_US
dc.identifier.issn1878-3503 (Electronic)en_US
dc.identifier.urihttp://repository.kln.ac.lk/handle/123456789/1154-
dc.descriptionIndexed in MEDLINE-
dc.description.abstractEvidence for immune activation was investigated in 12 patients with a rare syndrome of self-limiting, delayed onset cerebellar dysfunction following an attack of falciparum malaria which occurred 18-26 d previously. Concentrations of tumour necrosis factor, interleukin 6 and interleukin 2 were all significantly higher in serum samples of patients during cerebellar ataxia than in recovery sera and in the sera of 8 patients who did not develop delayed cerebellar dysfunction following an attack of falciparum malaria. Cytokine concentrations in the cerebrospinal fluid were also significantly higher in ataxic patients than in controls. These findings suggest that immunological mechanisms may play a role in delayed cerebellar dysfunction following falciparum malaria.en_US
dc.publisherOxford University Pressen_US
dc.subjectMalariaen_US
dc.subjectMalaria, Cerebralen_US
dc.subjectMalaria, Cerebral-immunology-
dc.subjectCerebellar Ataxia-
dc.titleImmune activation during cerebellar dysfunction following Plasmodium falciparum malariaen_US
dc.typeArticleen_US
dc.identifier.departmentMedicineen_US
dc.identifier.departmentParasitologyen_US
dc.creator.corporateauthorRoyal Society of Tropical Medicine and Hygieneen_US
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