Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02749 (beta2-glycoprotein I)
 836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was made of the level of alpha- and beta-lipoproteins, apolipoprotein H and tissue protein alpha 2-glycoprotein of the arteriosclerotically changed aortic wall in the blood serum of 129 patients with coronary arteriosclerosis, 50 patients with various diseases of the internal organs without clinical signs of arteriosclerosis and in 26 healthy patients by the immunodiffusion method using standard assays. A significant increase in beta- and alpha-lipoprotein indices was revealed in the groups of patients with coronary heart disease as compared to the healthy persons. alpha 2-glycoprotein of the arteriosclerotically changed aortic wall was undetectable in the blood serum of the healthy persons; in the group of patients without clinical signs of coronary heart disease this protein was detected in 5 patients only in the concentration of 4-8 micrograms/ml. alpha 2-glycoprotein concentration in the blood serum of the patients with the ischemic, thrombonecrotic and fibrous stages of arteriosclerosis was much higher (23.5 +/- 1.0; 27.5 +/- 2.9 and 35.3 +/- 2.2 micrograms/ml respectively). The proposed immunochemical determination of some indices of the blood serum can be of use to assess the activity of arteriosclerotic processes in patients with coronary heart disease. The determination of the level of alpha 2-glycoprotein of the arteriosclerotically changed aortic wall serves this purpose most adequately.
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PMID:[Immunochemical study of the alpha 2-glycoprotein from the atherosclerotically altered aortic wall in the blood serum of ischemic heart disease patients]. 241 47

Low-density lipoprotein (LDL) size, a coronary heart disease risk factor, is influenced by both genetic and environmental factors. Results from the Quebec Family Study (QFS) revealed that the LDL peak particle diameter (LDL-PPD) aggregates in families with a heritability coefficient above 50% and is affected by a major quantitative trait locus on chromosome 17q (LOD=6.8). Complex segregation analyses have consistently demonstrated a major gene effect influencing LDL size. In the present study, we report a similar analysis in the QFS cohort, which suggests that a major gene explains 23% of the variance in age-body mass index and triglyceride-adjusted LDL-PPD. The most intuitive positional candidate gene on chromosome 17q is the apolipoprotein H gene. Direct sequencing of the promoter, coding regions, and exon-intron splicing boundaries of this gene revealed the presence of three missense mutations and two polymorphisms in the untranslated regions. Using family-based association tests, none of these variants was individually associated with LDL-PPD. However, analysis of the haplotypes constructed from the three missense mutations, suggested that one particular haplotype (frequency=20.9%) was associated with a significant increase in LDL-PPD trait values (p=0.046). Taken together, these results suggest the presence of a major gene effect influencing LDL-PPD and a positive association with a positional candidate gene located on chromosome 17q. Replication of the association between apolipoprotein H gene haplotype and LDL-PPD is required before reaching firm conclusion.
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PMID:Detection of a major gene effect for LDL peak particle diameter and association with apolipoprotein H gene haplotype. 1615 95

Systemic autoimmune diseases, which comprise a family of conditions which share common pathogenetic mechanisms, are frequently associated to cardiac involvement and to a high prevalence of ischemic coronary events often occurring at a younger age than in normal population. A large increase in mortality is related to premature atherosclerosis with coronary artery disease and stroke in patients with connective tissue diseases. Coronary heart disease is responsible for 40-50% of the death of patients with rheumatoid arthritis. Moreover, a growing body of evidence supports the view that autoimmune mechanisms are involved in the pathogenesis of cardiovascular disease. Inflammatory heart disease is a rising concern worldwide. Similar mechanisms link autoimmune diseases, including the association of increased disease with proinflammatory cytokines and the importance of regulatory mechanisms in the control of chronic inflammation. The role of the immune system in modulating atherosclerosis has recently been well documented. Studies have revealed that cellular and humoral immunity plays crucial roles in atherogenic plaque formation. This includes macrophages, CD4+ T cells and dendritic cells as well as autoantigens such as oxidized low-density lipoprotein (oxLDL), heat shock proteins and beta2-glycoprotein I. The inflammatory component is not localized to the "culprit" plaque, but it is diffused to the entire coronary vascular bed, and involves also the myocardium. The aim of the conference (2nd conference on heart, rheumatism and autoimmunity) was to focus the attention of the participants on some pathogenetic, clinical and therapeutic aspects at the boundary between cardiology and rheumatology and to encourage the debate among clinicians and basic researchers with different backgrounds and experiences.
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PMID:2nd conference on heart, rheumatism and autoimmunity, Pescara, Italy, May 19-20, 2005. 1633 12