Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The diagnostic value of serum myoglobin as compared to MB iso-enzyme of creatine phosphokinase and aspartate aminotransferase was investigated in 25 patients admitted on suspicion of acute myocardial infarction with a duration of symptoms less than 6 hours. In group 1 (acute myocardial infarction group), the first blood sample, obtained at a mean time of 3.27 hours after onset of infarction, invariably showed increased myoglobin (mean 2.6-fold normal) whereas MB iso-enzyme of creatine phosphokinase and aspartate aminotransferase were often normal. Peak myoglobin values occurred earlier than peak serum MB iso-enzyme of creatine phosphokinase values. The highest peak values of serum myoglobin were found in patients with extensive myocardial infarction. In group 2 (non-acute myocardial infarction or control group) serial determinations of serum myoglobin, serum MB iso-enzyme of creatine phosphokinase and aspartate aminotransferase were within normal limits. Hence the importance lies with the early detection of serum myoglobin in acute myocardial infarction.
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PMID:The roles of myoglobin, MB iso-enzyme of creatine phosphokinase and aspartate aminotransferase in serum in the acute phase of myocardial infarction. 793 Jun 58

The diagnostic significance of ischemia-sensitive laboratory parameters in respect to possible interference with shed blood autotransfusion was assessed in a prospective study with 100 patients undergoing elective coronary artery bypass grafting. Serum levels of creatine kinase, creatine kinase MB activity, creatine kinase MB mass concentration, 2-hydroxybutyrate dehydrogenase, lactate dehydrogenase-1, troponin-T, myoglobin, and glutamicoxaloacetic transaminase were repeatedly assessed up to the sixth postoperative day. Thirty-seven patients were excluded from the study due to postoperative development of myocardial infarction (n = 4), transient ischemic events (n = 25), and left bundle-branch blocks (n = 8). In the remaining group of 63, 37 patients were retransfused with 580 +/- 370 mL shed blood up to the twelfth postoperative hour, and 26 patients did not receive autotransfusion due to minimal mediastinal blood loss. The results of our study show that the ischemia-sensitive laboratory parameters were significantly influenced by shed blood autotransfusion: 8 hours postoperatively, creatine kinase (272%), creatine kinase MB fraction (151%), 2-hydroxybutyrate dehydrogenase (130%), lactate dehydrogenase-1 (133%), troponin-T (200%), myoglobin (159%) and glutamic-oxaloacetic transaminase levels (153%) were significantly elevated (p < 0.05) in patients with postoperative autotransfusion, although there were no electrocardiographic signs of myocardial ischemia in this group of patients. Our study shows that postoperative autotransfusion of mediastinal shed blood may interfere with the diagnosis of perioperative myocardial ischemia by laboratory parameters in coronary bypass patients.
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PMID:Shed blood autotransfusion influences ischemia-sensitive laboratory parameters after coronary operations. 817 1

Six horses with a history of recurrent exertional rhabdomyolysis (RER) (Horses A-F) and 7 control horses performed a submaximal and later a near-maximal treadmill exercise test. Blood samples were obtained before, during and after exercise and muscle biopsies were taken before and after exercise. At rest, plasma aspartate aminotransferase (AST) activities in horses with RER were above 95% confidence intervals for control horses. During submaximal exercise, 3 horses with RER (A, B and C) had much greater increases in plasma AST, creatine kinase (CK) and myoglobin concentrations than did Horses D, E and F and control horses. Clinical signs of muscle stiffness and pain were only obvious in Horse A. During near-maximal exercise, only Horse C showed a substantial increase in CK activity and myoglobin concentrations without any associated clinical signs of rhabdomyolysis. Muscle biopsies from Horses A, B and C contained necrotic type II fibres which, on electron microscopic examination, contained disrupted myofibrils and swollen mitochondria. These results suggest that, in RER, subclinical episodes of muscle fibre necrosis and associated increases in plasma AST, CK and myoglobin occur with exercise more frequently than could be detected clinically. Furthermore, the pattern of increase in muscle enzymes and myoglobin concentrations in the 6 horses with RER suggested that the high plasma AST and CK activities commonly observed at rest in symptom-free Standardbred horses are probably a result of repeated subclinical episodes of rhabdomyolysis after exercise, rather than leakage due to abnormal sarcolemmal permeability.
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PMID:Muscle histopathology and plasma aspartate aminotransferase, creatine kinase and myoglobin changes with exercise in horses with recurrent exertional rhabdomyolysis. 842 77

There is a large inter-subject variability in serum creatine kinase (CK) response after eccentric exercise. This study examined and compared the variability of CK activity, other serum protein increases (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, aldolase, myoglobin),changes in muscle damage indicators (maximal isometric force: MIF, relaxed and flexed elbow joint angle: RANG and FANG, circumference: CIR, and muscle soreness level: SOR), and changes in magnetic resonance (MR) images. Ten male subjects (21.7 +/- 1.6 yrs) performed 24 maximal eccentric actions of the elbow flexors, and measurements except MR images were taken immediately before and after, and for 10 days after exercise. MR images were taken 7 days after exercise. A large variability in peak CK response (236 - 25,244 IU.I(-1) was found among subjects. Spearman rank-order correlation coefficients (r) revealed significant correlations of peak CK with peak serum protein levels (r = 0.79-0.95), peak changes in MIF (r = 0.73-0.79), RANG (r = 0.69), and CIR (r = 0.91). The higher the peak CK levels, the more profound the abnormality in the MR images and the larger the changes in MR signal intensity (r = 0.90-0.94). It is concluded that the large variability in CK response after exercise seems to be related to the variability in exercise-induced muscle damage.
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PMID:Variability in serum creatine kinase response after eccentric exercise of the elbow flexors. 883 14

Acceptable biochemical markers of ischaemic heart disease are now considered to include myoglobin, CK-MB isoforms, CK-MB, and cardiac troponins T and I. AST (SGOT), total LD and LD isoenzymes, and total CK activity measurements are regarded as obsolete for this purpose. All acceptable biochemical markers must be available, if required, with a turnaround time of < 20 min. Such a service can either be provided by quantitative assays in a well-equipped laboratory or by qualitative point-of-care (bedside) devices (except for the CK-MB isoform assay) which can also be used in patients' homes and ambulances. There is, however, a pressing need for the careful side-by-side assessment of the relative merits of each of these biochemical markers to permit definitive conclusions about their future usage. A particular problem is the lack of primary standards for CK-MB and troponin I assays. The sensitivity of the initial ECG is about 50% for detecting myocardial damage; thus the use of biochemical markers may contribute to the early diagnosis and monitoring of thrombolytic therapy and these possible applications are examined. In addition, biochemical markers are presently the gold standard for the diagnosis of minor myocardial damage. There is now good evidence that biochemical markers, particularly the cardiac troponins, have a prognostic function in ischaemic heart disease although such findings pose unanswered clinical management questions. At the same time, it is recognized that there is often no need at all for the use of any biochemical marker when the clinical diagnosis is unequivocal, other than for prognosis, monitoring thrombolytic therapy, or diagnosing reinfarction.
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PMID:The use of biochemical markers in ischaemic heart disease: summary of the roundtable and extrapolations. 958 61

Diagnosis of acute myocardial infarction is made with the aid of biomarkers such as structural myocardial proteins, myoglobin (MG) or specific enzymes, creatine phosphokinase isoenzyme MB (CK-MB) or non specific enzymes, lactic dehydrogenase (DHL) and aspartate aminotransferase (AST). We found good sensitivity (71%-50%), specificity (85%-100%) and predictive values (Pos. 77%-100%, Neg. 82%-72%) for Mg and CK-MB, supporting their clinical usefulness. In contrast DHL and AST were not clinically useful for early diagnosis.
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PMID:[The usefulness of determining myoglobin, creatine phosphokinase MB isoenzyme, lactate dehydrogenase and aspartate aminotransferase in the diagnosis of acute myocardial infarct]. 981 Mar 42

This is the first confirmed report of exertional rhabdomyolysis in a non-human primate. The monkey was singly housed and presented with anorexia and reluctance to move. There was no external evidence of trauma. Clinicopathologic findings included mild azotemia, marked elevation in serum creatine phosphokinase (CPK), alanine aminotransferase, aspartate aminotransferase, and myoglobinuria. Two days post-incident, the peripheral skeletal muscle had marked multifocal myonecrosis and fibrillar disruption without an inflammatory reaction. Treatment included diuresis and pain relief, and urinary output was monitored. The monkey recovered over the next two weeks. The major significance of skeletal muscle damage is the potential of released myoglobin to cause acute renal failure in the presence of other co-factors such as hypovolemia, acidosis, or ischemia. CPK levels can be highly variable and are inconsistent with the degree of muscle damage; however, CPK is thought to be the most sensitive enzyme marker for muscle necrosis. Because of the potential life-threatening sequelae, exertional rhabdomyolysis should be included as a differential diagnosis when similar clinical and pathological signs are observed.
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PMID:Review of exertional rhabdomyolysis and a case in a rhesus monkey (Macaca mulatta). 1020 11

A 66-year-old female was admitted to our hospital in January, 1998, complaining of low grade fever and muscle weakness of her legs. Physical examination revealed muscle weakness of her neck (4/5) and proximal skeletal muscles of her bilateral legs (3/5-4/5). She showed proteinuria and microhematuria. Her serum levels of ureanitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, creatinekinase, aldolase and myoglobin were all within the normal ranges. Antinuclear antibodies were negative, but her serum levels of pANCA (743 EU) and C reactive protein (18.0 mg/dl) were elevated. Neuroconduction velocity of her left common peroneal nerve was decreased to 40.8 m/sec and electric myograph showed neurogenic changes. Magnetic resonance images (MRI) of her bilateral thigh depicted high signal intensity in quadriceps by T 2 weighed images, but the signals were not enhanced by gadolinium injection. Muscle and renal biopsies revealed necrotizing vasculitis of the small arteries. Crescentic glomerulonephritis was also observed by renal biopsy. These findings supported the diagnosis of microscopic PN. On 16 th admission day, she developed acute cardiac and respiratory failures due to cardiac and respiratory muscle involvements with PN, and was assisted by mechanical ventilation. She was treated with methylprednisolone pulse therapy (500 mg/day, three consecutive days) on 18 th admission day, followed by 40 mg of oral prednisolone daily. However, her symptoms deteriorated, and herserum creatinine levels increased to 2.4 mg/dl. On 24 th admission day, intravenous cyclophosphamide pulse therapy (500 mg/day) was instituted. Her cardiac wall motion on echocardiography and serum creatinine levels gradually improved, but her skeletal and respiratory muscle weakness did not improve. On 38 th admission day, she was complicated with respiratory infection by methicillin resistant Staphylococcus aures. On 62 th admission day, she died of endotoxic shock. This is the first report describing respiratory muscle involvement with PN, and the second report describing MRI findings of muscle involvement by PN. Therefore, our case provides important clinical information for the diagnosis and treatment of the disease.
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PMID:[A case of microscopic polyangiitis with severe cardiac and respiratory muscle involvement]. 1061 70

Assays of serum enzymes, such as aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and isoenzyme MB, are widely performed in the early phase of suspected ischemic myocardial injury. However, these enzymes are not restricted to cardiac muscle tissue and increases in their serum concentrations have been observed in non-cardiac conditions. The levels of CK, and especially those of the myocardial specific isoform (CK-MB), have served as essential components for clinical decision in emergency rooms for over 25 years. This standard diagnostic test is far from perfect in specificity and the time delay necessary for the detection of a rise in levels. The clinician needs specific and sensitive biological parameters that can be rapidly measured in serum immediately after ischemic damage. In the last years, several new serum markers of myocardial damage have been developed. Currently, an important place is reserved for some non-enzyme muscle constituents, such as myoglobin and troponin sub-units, which have better specificity and allow an earlier detection of myocardial damage. The immunoassay of human cardiac troponin is a specific and sensitive diagnostic method for acute and sub-acute myocardial damage. It is ideal for the detection of myocardial necrosis in complex clinical situations when the usual enzymatic markers may be ineffective. An important prognostic value of troponin levels, especially troponin T, is currently under investigation. Myoglobin is a protein with low molecular weight that is abnormally high in serum two hours after myocardial infarction. Despite their high sensitivity, the use of serum measurements in the emergency room is controversial because of their low specificity, requiring the exclusion of skeletal muscle damage. Sensitivity could be lost in patients with renal function damage. The measurement of CK-MB protein weight (CK-MBmass) is another marker that has been confirmed as more accurate than CK-MB activity assays, especially in patients presented within four hours after the onset of chest pain, but could be inaccurate in several circumstances. In this research article, the authors describe the most important parameters of enzymatic and non-enzymatic markers, the kinetics of serum release, the clinical applications and the problems.
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PMID:[Serum markers for ischemic myocardial damage]. 1066 Oct 20

A 29-year-old male who had a past history of mild ECG abnormality of arrhythmia at the age of 14 years, was referred to our hospital because of elevated serum creatine kinase (CK) level. He had never been aware of muscular weakness nor cardiac symptoms. Neurological examination revealed normal muscle strength of all extremities except marked back muscle weakness. He had normal intelligence. On laboratory examination, serum AST, ALT, LDH, aldolase, CK and myoglobin levels were elevated. Both lactate and pyruvate levels were normally responded after an ischemic exercises test. Acid maltase activity was normal in white blood cells. A muscle biopsy obtained from rectus femoris muscle revealed vacuolar myopathy with mildly increased PAS positive material. On electron microscopy, there were autophagic vacuoles scavenging glycogen particles and cytoplasmic debris, and sarcolemmal indentation, compatible with the findings of lysosomal glycogen storage disease with normal acid maltase. This patient had unusual clinical features of absent mental retardation and no apparent cardiomyopathy. Accordingly, mental retardation is probably not necessary to see later onset of cardiac muscle involvement.
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PMID:[Lysosomal glycogen storage disease with normal acid maltase (Danon) without apparent cardiomyopathy and mental retardation]. 1088 38


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