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dc.contributor.authorGonzález Castañeda, Candelas
dc.contributor.authorPérez Castrillon, José Luis 
dc.contributor.authorRomero Gómez, Mercedes
dc.contributor.authorHerreros Fernández, Vicente
dc.date.accessioned2014-09-05T10:22:12Z
dc.date.available2014-09-05T10:22:12Z
dc.date.issued2002
dc.identifier.citationInternational Journal of Cardiology, 2002, vol. 82, p. 293-295es
dc.identifier.issn0167-5273es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/5836
dc.descriptionProducción Científicaes
dc.description.abstractChlamydia pneumoniae infection has long been suspected as a possible cause of atherosclerosis and has been frequently detected in atheromatous plaques of the coronary arteries. Nevertheless, its distribution is not correlated to the severity or extent of the disease, but it would support the hypothesis that the organism may be an active factor in the pathogenesis of atherosclerosis. A group of patients with stable angina were examined as to whether or not the positivity of antibodies against Chlamydia pneumoniae modified cellular populations as mechanisms responsible for the alterations of inflammatory response. We concluded that the presence of IgG anti-C. pneumoniae antibodies do not participate in the activation of inflammatory mechanisms that may intervene in the genesis of atherosclerosis in patients with stable angina.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherElsevier Science Ireland Ltd.es
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectCardiovascular, Aparato, Efectos de los medicamentos sobre eles
dc.subjectAtherosclerosises
dc.subjectNeumoniaes
dc.titleAntibodies against Chlamydia pneumoniae and their relation to lymphocyte population levelses
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.publicationfirstpage293es
dc.identifier.publicationlastpage295es
dc.identifier.publicationtitleInternational Journal of Cardiologyes
dc.identifier.publicationvolume82es
dc.peerreviewedSIes
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International


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