Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioimmunoassay for quantitation of serum myoglobin in healthy individuals and patients with different diseases is described. Purified myoglobin was labelled by an 125I-labelled ester (N-succinimidyl 3-(-4 hydroxy, 5-[125I]iodophenyl) propionate), a commercially available antiserum was used, and the antigen-antibody complex was precipitated with polyethylene glycol 6000. The rapid assay can be performed within 1 h at 37 degrees C with a detection limit of 45 micrograms/l. Prolonged incubation at 4 degrees C for 18 or 72 h gives a detection limit of 6 and 2 micrograms/l, respectively. The mean coefficient of variation of the routine assay was 11%. In healthy human subjects a significant difference in mean serum myoglobin concentration was found between 43 women (34 +/- 17 micrograms/l) and 51 mean 47 +/- 15 micrograms/l). In twenty patients admitted to hospital with the clinical diagnosis acute myocardial infarction, the serum myoglobin concentration profiles were in close agreement with the final diagnosis. In three patients with myocardial infarction serum samples were taken every 2 h after the acute episode, and serum myoglobin levels were compared with the levels of creatine kinase, lactate dehydrogenase, aspartate aminotransferase and creatine kinase isoenzyme-MB.
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PMID:Rapid and sensitive radioimmunoassays for human myoglobin. 53 83

Myoglobin and the enzymatic activity of creatine phosphokinase CK), MB-isoenzyme of CK (CK-MB), aspartate aminotransferase (GOT), alanine aminotransferase (GPT) and lactic acid dehydrogenase (LDH) were serially determined in 10 patients with acute myocardial infarction. Additionally the same parameters were assessed in 5 patients with angina pectoris for 24 hours after bicycle ergometry. 10 in-patients served as controls. Myoglobin was determined by radioimmunoassay and the other enzyme activities according to the current kinetic methods. Comparison of myoglobin with the enzymatic parameters showed that the myoglobin peak occurs 5.6 hours after the beginning of the sampling period, i.e. 7.3 hours earlier than CK and CK-MB and 11.6 hours earlier than GOT. In analogy to this finding the descending limb of the myoglobin curve was significantly earlier at a level of one third of the peak value, i.e. 8.2 hours earlier than CK-MB, 18.8 hours earlier than CK and 27.3 hours earlier than GOT. No signs of myocardial necrosis in terms of myoglobin or enzymatic activity could be detected after bicycle ergometry. It is concluded that myoglobin is a more sensitive parameter for assessment of the acute phase in patients with myocardial infarction than the usualy enzymatic parameters.
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PMID:[Plasma myoglobin level as a course criterium in patients with acute myocardial infarct]. 53 58

Rhabdomyolysis, secondary to exertion is known to result in myoglobinuria and is occasionally associated with acute renal failure. In this study myoglobinaemia occurred in 25 of 44 runners completing a 99 km marathon. A marked rise in the values of myoglobin, lactate and the enzymes creatine kinase (CPK), aspartate transaminase (AST) and lactic dehydrogenase (LDH) was noted. A linear correlation was demonstrated between the level of serum myoglobin and the serum concentrations of urate, CPK, AST and LDH. Both the myoglobin itself and the increased concentration of urate may contribute to the acute renal failure. The pathophysiology of rhabdomyolysis during exertion is discussed in the context of other causes of myoglobinuria. A classification of rhabdomyolysis and myoglobinuria is suggested.
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PMID:Myoglobinuria, rhabdomyolysis and marathon running. 75 Oct 88

It was demonstrated in experiments on 60 dogs that in hyporeactive myocardial infarction (MI) myoglobin (MG) concentration and the activity of creatine kinase (CK) and aspartate aminotransferase (ASAT) increase at a slower rate and reach maximum values later. In hyperreactive MI the rate of their increase and the time of attainment of maximum values are, respectively, greater and earlier than in normoreactive MI. The connection of MG, CK, and ASAT changes with reactivity allows them to be used in prognosticating MI healing.
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PMID:[Kinetics of myoglobin, creatine kinase and aspartate aminotransferase in uncomplicated and complicated forms of healing of experimental myocardial infarction]. 162 20

The time course of changes in serum proteins and other blood constituents after eccentric exercise of the forearm flexors by six nonweight-trained female subjects (age, 19.7 +/- 1.9 years) was investigated. Eccentric muscle actions are those in which the muscle lengthens as it exerts force, as when a person lowers a weight. Serum levels of creatine kinase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, myoglobin, as well as urea nitrogen, uric acid, creatinine, calcium, and phosphorus were examined before and for 6 days after exercise. Creatine kinase increased dramatically (peak value ranged from 6740 to 24,200 U/L) and aspartate aminotransferase, lactate dehydrogenase, alanine aminotransferase, and myoglobin followed the same time course as creatine kinase, but their peak values were lower. These proteins did not increase significantly until 48 hours after exercise and reached peak values 3 to 5 days after exercise. Alkaline phosphatase, gamma-glutamyl transpeptidase, uric acid, urea nitrogen, creatinine, calcium, and phosphorus showed no change. There is either a delay in muscle protein release by damaged muscle fibers, or the proteins are unable to leave the interstitial area for the 24 to 48 hour period after exercise. Because of the long delay, care should be taken when blood protein levels are interpreted in persons who have exercised strenuously (even if only for a short period of intense effort) several days before any diagnostic tests are performed.
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PMID:Time course of serum protein changes after strenuous exercise of the forearm flexors. 174 Jun 32

The clinical significance of the serum enzymes creatine kinase (CK, EC 2.7.3.2), lactate dehydrogenase (LD, EC 1.1.1.27) and aspartate aminotransferase (EC 2.6.1.1), and the isoenzymes CK 1-3 and LD 1-5, in acute myocardial infarction (AMI) is reviewed. Particular attention is given to electrophoretic analysis of the isoenzymes (and the CK isoforms/subforms) following AMI and thrombolytic therapy. Other protein markers for the monitoring of AMI, including myoglobin and muscle contractile proteins, are also discussed and the potential for the detection of new marker proteins using high-resolution two-dimensional electrophoretic methods is demonstrated. Whilst emphasis is placed upon electrophoretic methods the value of complementary immunoassays is acknowledged in order to maintain a balanced perspective.
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PMID:Electrophoresis of serum isoenzymes and proteins following acute myocardial infarction. 193 92

The serum myoglobin (MG) was assayed by the radio-immunological method in 30 patients, all victims of a recent myocardial infarction (MI) and in 30 tests subjects suffering (21 cases) or not (9 cases) from heart diseases, but none from myocardial infarction (MI). The blood samples have been collected on hospital admission of the patient, then every four hours during the first 48 hours and finally, every 12 hours from the 48th to 72nd hour. The normal value is less than 85 micrograms/l. The creatine-kinase (CK), the aspartate aminotransferase (ASAT), the alanine aminotransferase (ALAT) and the lactate dehydrogenase (LDH) were also assayed each time. In MI, there is a significant increase in the serum MG level (731 +/- 323 micrograms/l against 174 +/- 198 micrograms/l in the test subjects; p less than 0.001). The sensitivity of this assay reaches 97%, its specificity 80%, its positive predictive value 83% and its negative predictive value 96%. Starting from the beginning of the characteristic pain of infarction, the MG level exceeds the normal values after 3.3 +/- 1.6 hours, reaches its maximum after 9.3 +/- 3.7 hours and comes back to normal after 38 +/- 8.1 hours. On the other hand, the MG level does not enable any conclusion regarding either the transmural/not transmural nature, or the site, or the acuteness of the MI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Value of the assay of serum myoglobin in recent myocardial infarction]. 218 59

The detection rate was examined for ECG (EchoECG) equivalents of clinical coronary heart disease (CHD) forms, such as angina pectoris, focal myocardial dystrophy, small and large myocardial infarction, at various levels of the peak activity of blood creatine phosphokinase in the acute period of the disease. A series of investigations revealed in the acute period the time when myoglobin, CPK, CPK MB, AST, and LDH attained their maximal blood content, which were directly related to the molecular weight of proteins. The findings allowed the author to consider a relationship between the values obtained by diagnostic techniques and the time course of an infarct process, the mass of ischemic necrosis and its topography in the myocardium.
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PMID:[Correlations of laboratory and instrumental method parameters in the diagnosis of acute ischemic lesion of the myocardium]. 229 Feb 68

Administration of testosterone after exercises led to suppression of the hormone production during the anabolic phase within 72-120 hrs of muscles adaptation to physical loading. Content of the androgen receptors was also altered. The supercompensatory phase in content of proteins (myoglobin and aspartate aminotransferase as index) was absent due to an impairing effect of testosterone on muscle adaptation. These data suggest that administration of testosterone could not serve as an adequate model of a body androgenization which was observed in anabolic phase of muscle adaptation to physical exercises.
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PMID:[Androgen regulation of the level of tissue-specific proteins in skeletal muscles during physical exercise]. 238 30

For the diagnosis of myocardial injury, particularly AMI, CK-MB has become the gold standard. Changing CK-MB activities in serially collected blood from patients with suggestive signs and symptoms of AMI is almost pathognomonic for infarction. Nevertheless, an increased CK-MB cannot be equated with AMI owing to the many other types of inflammatory, traumatic, and miscellaneous forms of injury to the heart and the trace activities of CK-MB in skeletal muscle. Other enzyme tests for AMI are less efficient. In order of decreasing efficiency, the tests are CK-MB, CK, LD1 greater than LD2 or LD1/LD2 greater than 0.76, AST and LD; the latter two tests are not cost effective and add little or nothing when results for CK-MB, CK, and LD isoenzymes are available. The value of the isoforms of CK-MM and CK-MB remains to be established. Early evidence suggests that they could be helpful in the diagnosis of AMI; however, owing to the greater technical difficulties in performing these tests, their use is necessarily more restricted. Enzyme testing on admission and then every 12 hours for 2 days is sufficient and effective in making the initial diagnosis. In patients presenting early after an attack, CK and CK-MB are often normal. Decisions on AMI cannot be made on blood tests collected in the emergency department. Clot-lysing agents like streptokinase, urokinase, and tPA have changed the therapy of AMI dramatically. Enzyme tests clearly separate patients with and without successful therapeutic or spontaneous reperfusion. With successful reperfusion, the uniform finding has been a "washout" phenomenon with significantly earlier peaking times for CK and CK-MB. The isoforms of CK and myoglobin give the earliest peaks after successful reperfusion. With faster turnaround times for these tests, they may become important tools in patient management.
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PMID:Differential diagnosis of patients with abnormal serum creatine kinase isoenzymes. 268 5


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