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Interaction of the lipoprotein lipase asparagine 291-->serine mutation with body mass index determines elevated plasma triacylglycerol concentrations: a study in hyperlipidemic subjects, myocardial infarction survivors, and healthy adults.

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A mutation in the lipoprotein lipase (LPL) gene, resulting in the substitution of asparagine by serine at residue 291 (LPL-S291), was found to occur in young survivors of a myocardial infarction from Sweden, combined hyperlipidemic subjects from the United Kingdom, and type III hyperlipidemic

[Sensitivity of creatine phosphokinase in early diagnosis of myocardial infarction and improvement of the test's specificity by determination of the rate of increase of enzyme activity].

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The activity of serum enzymes: creatine phosphokinase (CPK), CPK isoenzyme MB and asparagine aminotransferase--was examined every 1-3 hours after the onset of a painful attack in 68 patients with "determined" (according to the 1979 WHO classification) myocardial infarction (DMI) and 32 patients with

Molecular and functional differences induced in thrombospondin-1 by the single nucleotide polymorphism associated with the risk of premature, familial myocardial infarction.

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A serine (Ser-700) amino acid rather than an asparagine (Asn-700) at residue 700 of thrombospondin-1 has been linked to an increased risk for development of premature, familial heart attacks. We now have identified both functional and structural differences between the Ser-700 and Asn-700

[Myocardial infarction--symptoms and procedures. Longitudinal observation of a population of 280,000 women and men--Project POL-MONICA in Krakow. VI: Enzymatic diagnosis and myocardial infarction].

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Different combinations of serum enzymes activity determinations are used in the diagnostics of myocardial infarction. The goal of the present paper was: 1) to assess the frequency of determinations of asparagine aminotransferase (AspAT) and to compare it with the frequency of determinations of

Association between the LPL-D9N mutation in the lipoprotein lipase gene and plasma lipid traits in myocardial infarction survivors from the ECTIM Study.

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Using polymerase chain reaction (PCR) based techniques, we have identified individuals in the ECTIM study of myocardial infarction survivors (cases) and healthy matched controls who are carriers for a mutation of the gene for lipoprotein lipase (LPL) which alters amino acid 9 from aspartic acid to

Molecular imaging of angiogenesis after myocardial infarction by (111)In-DTPA-cNGR and (99m)Tc-sestamibi dual-isotope myocardial SPECT.

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BACKGROUND CD13 is selectively upregulated in angiogenic active endothelium and can serve as a target for molecular imaging tracers to non-invasively visualise angiogenesis in vivo. Non-invasive determination of CD13 expression can potentially be used to monitor treatment response to pro-angiogenic

Specific haplotypes of the P-selectin gene are associated with myocardial infarction.

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P-selectin is a cellular adhesion molecule that may be involved in the development of atherosclerosis and its complications. We have previously identified thirteen polymorphisms of the P-selectin gene among which five were located in the coding region of the gene (S290N, N562D, V599L, T715P, T741T

PET imaging of cardiac wound healing using a novel [68Ga]-labeled NGR probe in rat myocardial infarction.

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OBJECTIVE Peptides containing the asparagine-glycine-arginine (NGR) motif bind to aminopeptidase N (CD13), which is expressed on inflammatory cells, endothelial cells, and fibroblasts. It is unclear whether radiolabeled NGR-containing tracers could be used for in vivo imaging of the early

Apolipoprotein B gene polymorphisms, lipoproteins and coronary atherosclerosis: a study of young myocardial infarction survivors and healthy population-based individuals.

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Association studies were carried out in a sample of 87 patients from Sweden who had survived a myocardial infarction (MI) before the age of 45, and 91 age-matched healthy individuals, to compare the impact of polymorphisms at the apolipoprotein (apo) E and B gene loci on among-individual differences

Functional SNPs in the lymphotoxin-alpha gene that are associated with susceptibility to myocardial infarction.

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By means of a large-scale, case-control association study using 92,788 gene-based single-nucleotide polymorphism (SNP) markers, we identified a candidate locus on chromosome 6p21 associated with susceptibility to myocardial infarction. Subsequent linkage-disequilibrium (LD) mapping and analyses of

A novel polymorphism of apolipoprotein A-IV is the result of an asparagine to serine substitution at residue 127.

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We have identified a hitherto unknown genetic polymorphism of apolipoprotein A-IV (apoA-IV). The molecular basis for this polymorphism is an A to G substitution at nucleotide 1687 resulting in an Asn to Ser change of amino acid 127. The frequencies of the two apoA-IV alleles (designated

Heterogeneity of Escherichia coli-expressed human muscle creatine kinase.

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Creatine kinase (CK) plays an important role in maintaining a constant ATP:ADP ratio during periods of high energy usage. Elevated levels of CK give an early indication of myocardial infarction. The enzyme has four major isozymes with heterogeneity being observed for each of them. In many cases the

Boy with pseudohypoparathyroidism type 1a caused by GNAS gene mutation (deltaN377), Crouzon-like craniosynostosis, and severe trauma-induced bleeding.

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We report on a 6-month-old boy with craniosynostosis, pseudohypoparathyroidism type 1a (PHP1A), and a GNAS gene mutation. He had synostoses of the coronal, frontal, and sagittal sutures, brachyturricephaly, and hydrocephaly. He also had congenital hypothyroidism, round face, full cheeks, shortness

Coronary artery disease and the thrombospondin single nucleotide polymorphisms.

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GeneQuest was a high throughput, large-scale analysis of single nucleotide polymorphisms (SNPs) to identify gene associated with familial, premature coronary artery disease and myocardial infarction. The three SNPs showing the highest and most significant associations with disease were all members

Hypoxic regulation of NF-kappaB signaling.

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Hypoxia and inflammation are coincidental events in an array of diseased tissues, including chronically inflamed sites (e.g., inflammatory bowel disease, rheumatoid arthritis), growing tumors, myocardial infarcts, atherosclerotic plaques, healing wounds, and sites of bacterial infection (Murdoch et

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