English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

de li of particular combination are involved in the initial human ortholog protein[3]. Lipoprotein(a) would endothelial damage. The autoimmune theory of the atherosclerotic pro-cess is not new, nor is the idea novel that circulating immunocomplexes may play a role in this and other cardiovascular diseases. The novelty of the study by Glader et al. rather resides in the suggestion that at least some of the C. pneumonia antibodies in circulat-ing immunocomplexes would indeed interact with (recognize?) lipoprotein(a), thus assigning to this risk therefore constitute an additional antigenic target of a C. pneumoniae antigen-primed immune reaction. If this target were an apoprotein epitope, identifying the priming chlamydia antigen could be more easily achieved now that the C. pneumonia genome has been sequenced and shown to code for at least 1000 proteins[4]. Less conventional, and more intriguing, would be another theoretical possibility, i.e. the anti-genic determination of the lipid moiety of the lipo-European Heart Journal (2000) 21, 599–600 doi:10.1053/euhj.1999.2034, available online a

Chlamydia pneumoniae and lipoprotein(a): the right combination for atherosclerosis?