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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R.

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Rank 5 out of 30 in category Medical Laboratory Technology in the 2014 Thomson Reuters Journal Citation Report/Science Edition

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Source Normalized Impact per Paper (SNIP) 2015: 0.982
Impact per Publication (IPP) 2015: 2.238

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Polymorphisms in the Lipopolysaccharide-Binding Protein and Bactericidal/Permeability-Increasing Protein in Patients with Myocardial Infarction

Jaroslav A. Hubacek / Jan Pitha / Zdena Skodová / Vera AdámkovÁ / Ivana Podrapska / Gerd Schmitz / Rudolf Poledne

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 40, Issue 11, Pages 1097–1100, ISSN (Print) 1434-6621, DOI: 10.1515/cclm.2002.191, June 2005

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Gram-negative bacterial infection, namely Chlamydia pneumoniae has been recently discussed as a risk factor for myocardial infarction. The lipopolysaccharide-binding protein (LBP) and the bactericidal/permeability-increasing protein (BPI) play a role in the processes leading to recognition and neutralisation of the Chlamydia pneumoniae and their endotoxins – lipopolysaccharides (LPS). LPS interact with plasma LBP, and LBP-LPS complex activates monocytes/ macrophages, which can influence the atherosclerotic process. BPI is cytotoxic for Gram-negative bacteria and BPI-LPS complexes do not activate monocytes. We have analysed the polymorphisms in the LBP gene (Gly98→Cys; Pro436→Leu) and BPI gene (Lys216→Glu; PstI polymorphism in intron-5; G545→C) in 313 patients after myocardial infarction (MI) and in 302 control individuals. Genotype frequencies in the LBP gene and BPI gene did not differ between MI patients and control individuals. Our findings suggest that LBP and BPI polymorphisms do not influence the risk of MI.

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