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      Association of Mannan-Binding Lectin Deficiency with Venous Bypass Graft Occlusions in Patients with Coronary Heart Disease


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          We investigated the effect of mannan-binding lectin (MBL) deficiency on the susceptibility to bypass graft occlusion in 62 patients with coronary heart disease. MBL deficiency appeared to be associated with occlusion (p = 0.0099). A high level of anti-cardiolipin IgG as well as the number of venous bypass grafts were also involved (p = 0.0018 and p = 0.0104, respectively). Since early occlusion (<5 years after surgery) of a venous bypass graft is considered to be caused by thrombosis or fibro-intimal hyperplasia superimposed by thrombosis, our finding also implies an association of MBL deficiency with thrombotic events. It remains unclear whether the previously confirmed effect of MBL deficiency in coronary disease is mediated through this possible thrombotic mechanism, or whether plaque formation is also involved in the process. Further studies are clearly warranted.

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          Glycosylation changes of IgG associated with rheumatooid arthritis can activate complement via the mannose-binding protein

          The glycosylation of the circulating immunoglobulin-gamma (IgG) antibody molecules changes in rheumatoid arthritis. The extent of the changes correlates with the disease severity and reverses in remission. We demonstrate here that the alteration in glycosylation associated with rheumatoid arthritis can create a new mode for the interaction of IgG with complement through binding to the collagenous lectin mannose-binding protein (MBP). Rheumatoid arthritis is associated with a marked increases in IgG glycoforms that lack galactose (referred to as G0 glycoforms) in the Fc region of the molecule and that terminate in N-acetyl glucosamine (GlcNAc). We show, using nuclear magnetic resonance (NMR) and X-ray data, that these terminal GlcNAc residues become accessible for MBP binding. We further demonstrate that multiple presentation of IgG-G0 glycoforms to MBP results in activation of the complement. This suggests that a contribution to the chronic inflammation of the synovial membrane could arise from the localization of the IgG-G0 glycoforms in the affected joint and from resulting activation of complement.
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            Markers of endothelial dysfunction.

            The endothelium is a functional barrier between vessel wall and blood stream. Assuming the total human vascular and capillary system occupies a surface area of more than 1,000 m2 which is covered by 1,013 endothelial cells, the complex role of the endothelium for hemostasis and immunological and metabolic processes becomes obvious. Dysfunction of the endothelium is a critical factor in the pathogenesis of vascular diseases and thrombus formation. This paper provides a brief review of physiological endothelial functions and summarizes measurable changes in products released from endothelial cells under pathological conditions which were associated with endothelial dysfunction.
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              Phospholipid-binding activity of human mannan-binding lectin.

              Some C-type lectins possess phospholipid-binding ability, which may be of physiological importance. Human mannan-binding lectin (MBL) was found to bind specifically to solid-phase phosphatidylserine (PS), phosphatidylinositol (PI) and phosphatidylcholine (PC), but not cardiolipin (CL), in a concentration-dependent manner. This property was inhibited by EDTA and by monosaccharides, and exhibited a similar pH dependence to the carbohydrate (mannan)-binding activity of MBL. These findings may be of immunological relevance.

                Author and article information

                S. Karger AG
                November 2002
                07 November 2002
                : 98
                : 3
                : 123-126
                aDepartment of Medicine and bDepartment of Clinical Microbiology, Centre for Laboratory Medicine, Tampere University Hospital, Tampere, cDepartment of Biochemistry, National Public Health Institute, Helsinki, dLaboratory of Atherosclerosis Genetics, Department of Clinical Chemistry, Centre for Laboratory Medicine, Tampere University Hospital and University of Tampere Medical School, Tampere, and eLaboratory of Immunobiology, National Public Health Institute, Helsinki, Finland
                66313 Cardiology 2002;98:123–126
                © 2002 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                : 17 April 2002
                : 27 August 2002
                Page count
                Tables: 2, References: 21, Pages: 4
                Cardiac Surgery

                General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Thrombosis,Venous bypass graft occlusion,Coronary heart disease,Anti-β2-glycoprotein I antibodies,Mannan-binding lectin,Anti-cardiolipin antibodies


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