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Your search keyword '"Christine Alessi M"' showing total 2 results
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2 results on '"Christine Alessi M"'

1. Fibrinolytic function and coronary risk

Author

Juhan-Vague I, Christine Alessi M, and Morange P

Subjects
medicine.medical_specialty, Adipose tissue, Coronary Disease, Inflammation, Insulin resistance, Antigen, Risk Factors, Polymorphism (computer science), Internal medicine, Plasminogen Activator Inhibitor 1, medicine, Humans, Obesity, Myocardial infarction, Polymorphism, Genetic, business.industry, Fibrinolysis, Prognosis, medicine.disease, Endocrinology, Gene Expression Regulation, Tissue Plasminogen Activator, Insulin Resistance, medicine.symptom, Cardiology and Cardiovascular Medicine, business, Plasminogen activator
Abstract

Plasminogen activation potential in the blood is controlled by an equilibrium between plasminogen activators, mainly tissue-type plasminogen activator (t-PA), and inhibitors, mainly plasminogen activator inhibitor (PAI)-1. In cardiovascular practice, imbalance of this fibrinolytic potential is encountered primarily in the insulin-resistance syndrome. This syndrome leads to increased plasma PAI-1 and t-PA antigen levels (reflecting inactive t-PA/PAI-1 complexes) with a consequent decrease in fibrinolytic activity. Increased plasma PAI-1 and t-PA antigen both are predictive of myocardial infarction. The prognostic value of PAI-1 disappears after adjustments for insulin resistance markers, whereas the prognostic value of t-PA antigen disappears after simultaneous adjustments for insulin resistance and inflammation markers, suggesting an additive role of inflammation in inducing plasma fibrinolytic markers. Recently the production of PAI-1 by adipose tissue, in particular by tissue from the omentum, has been shown. PAI-1 produced in this way could be an important contributor to the elevated plasma PAI-1 levels observed in insulin-resistant patients. These results support the notion that PAI-1 may be a link between obesity, insulin resistance, and cardiovascular disease. Genetic control of PAI-1 expression has also been shown, involving a -675 4G/5G polymorphism, the 4G/4G genotype being associated with higher plasma PAI-1 levels; its proper influence on the development of myocardial infarction is still debated.

Published
1999

2. Heterogeneity of anti-beta2-glycoprotein I antibodies. A factor of variability in test results.

Author

Sanmarco M, Bardin N, Blank M, Pascal V, Christine Alessi M, Dignat-George F, Shoenfeld Y, and Harlé JR

Subjects
Antibody Affinity, Antiphospholipid Syndrome immunology, Cross Reactions, Enzyme-Linked Immunosorbent Assay standards, Glycosylation, Humans, Reproducibility of Results, beta 2-Glycoprotein I, Antibody Diversity, Autoantibodies immunology, Glycoproteins immunology
Abstract

The aim of this study was to evaluate the heterogeneity of IgGanti-beta2-glycoprotein I antibodies (IgG-abeta2GPI) as regarding their reactivity pattern against different sources of human beta2 GPI, their avidity and their association with clinical events of antiphospholipid syndrome (APS). Three thousand six hundred and eighty-four consecutive patient sera were routinely tested for IgGabeta2 GPI over 1 year using an in-house ELISA with 2 different commercial preparations of human purified beta2GPI. Of the 340 sera found positive, all those clinically documented were included in this study; 61 were positive with only one preparation (S1) and 59 with both (S2). The results of ELISA were confirmed by Western blot. Heterogeneity was stressed by testing sera with a human recombinant protein and 3 beta2GPI-related peptides. No contribution of glycosylation in the binding to beta2GPI was found. The avidity indices for each protein were significantly higher in S1 than in S2 (p=0.0021). S2 were more associated with antiphospholipid antibodies than S1 (75% versus 21% ; p<0.0001). A similar frequency of the main clinical features of APS was found in S1 and S2 sera (69% and 71%, respectively). In conclusion, our data show a heterogeneity in the antigenic reactivity pattern of IgG- abeta2 GPI and a relationship between a binding profile and antibody avidity. This heterogeneity could represent a crucial factor of variability in test results and underlines the difficulty of getting standardisation.

Published
2005
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