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Remodeling after myocardial infarction in humans is not associated with interstitial fibrosis of noninfarcted myocardium.
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OBJECTIVE
This study was specifically designed to evaluate whether noninfarcted hypertrophic myocardium in patients with end-stage heart failure after myocardial infarction (MI) is associated with an increase in interstitial fibrous tissue.
BACKGROUND
Postinfarction remodeling consists of complex
Mass spectrometric mapping of protein epitope structures of myocardial infarct markers myoglobin and troponin T.
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Monoclonal antibodies are widely used analytical tools in biochemical research. The knowledge of their corresponding epitopes is of major interest. One possible approach for epitope characterization is the application of protein antigen proteolysis in combination with mass spectrometric peptide
Radioimmunoassay for serum myoglobin.
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A column flow-through radioimmune assay for serum myoglobin has been developed. The assay uses antibodies to human or rhesus monkey myoglobin coupled to Sepharose by cyanogen bromide activation and myoglobin labeled by the Chloramine-T method. The labeled myoglobin is stable over two to three
[Development and optimization of the methods for determining activity of plasminogen activator inhibitor-1 in plasma].
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The activity and content of plasminogen activator inhibitor-1 (PAI-1) are important indicators of pathological processes, because its content in plasma increases at acute myocardium infarction, tumor, diabetes mellitus, etc. The present work is dedicated to the development and optimization of the
The nature of post-translational formation of MM creatine kinase isoforms.
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Isoforms (derived from the same isoenzyme but distinguished by differences in isoelectric point) of MM creatine kinase appear in plasma after myocardial infarction. They are formed by conversion of the tissue form of creatine kinase (MM-A, pI 7.80) to progressively more acidic species (MM-B, pI
Characterization of MB creatine kinase isoform conversion in vitro and in vivo in dogs.
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Time-dependent removal of the COOH-terminal lysine residue from each subunit of tissue MM creatine kinase by plasma carboxypeptidase N produces two additional isoforms that are readily separated, thereby permitting sensitive, early detection of acute myocardial infarction. Only two isoforms of MB
Variants of human tissue-type plasminogen activator. Fibrin binding, fibrinolytic, and fibrinogenolytic characterization of genetic variants lacking the fibronectin finger-like and/or the epidermal growth factor domains.
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Tissue-type plasminogen activator (t-pa) is a serine protease comprising four different putative structural domains with homologies to fibronectin finger-like structures (finger), epidermal growth factor, kringle structures, and the active site of serine proteases. Only the finger and epidermal
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