Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Differential diagnosis of patients who present with chest pain remains problematical. It has been shown that 11.8-7% of patients with acute myocardial infarction (AMI) are sent home from the emergency department (ED). Audit of our own ED has shown the incidence of missed prognostically significant myocardial damage to be 6.7%. Diagnostic criteria for AMI have classically been based on the triad of history, ECG and measurement of cardiac enzymes. The choice of 'cardiac enzymes' has been dictated by the evolution of laboratory techniques, commencing with measurement of aspartate transaminase and progressing to measurement of creatine kinase (CK) and its MB isoenzyme (CK-MB). Measurement of CK-MB has been shown by both clinical studies and rigorous statistical analysis to represent the best test for the diagnosis of AMI. The advent of real time immunoassay together with advances in therapeutic options for management of acute coronary syndromes (ACS) has resulted in a paradigm shift in the approach to laboratory testing. Immunoassay for CK-MB (CK-MB mass measurement) is diagnostically superior to CK-MB activity measurement and is the test of choice for 'classical' AMI. Development of immunoassays for the cardiac troponins, i.e. cardiac troponin T (cTnT) and cardiac troponin I (cTnI), has enhanced diagnostic specificity. These measurements are completely specific for cardiac damage, allow quantitation of the extent of infarction and are diagnostically superior to CK-MB measurement. Applications of this specificity have included the differential diagnosis of CK elevation in arduous physical training, detection of myocardial damage after DC cardioversion and prediction of ejection fraction. Of more interest is the utility of these markers in management of patients presenting without clear electrocardiographic changes. Diagnosis and management of patients presenting with ST segment elevation has been clarified by large clinical trials of thrombolytic agents. In such patients, thrombolysis is the treatment of choice. Patients presenting with ST segment elevation represents the minority of patients with probable ACS 9.6% of all patients presenting to our hospital. The majority require risk stratification into high- and low-risk groups. It is here that cardiac troponins have a major role. The measurement of cTnT has been shown in a large number of studies to enable risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification of patients with unstable angina. The combination of cTnT, admission ECG and stress ECG can be used for a comprehensive risk stratification which can be completed by 24 h from admission, as well as allowing a safe discharge policy from the ED. Measurements of cardiac troponins can also be used to predict prognosis in patients with other diagnostic categories. Patients with cardiac failure can be risk stratified according to cTnT status. cTnT status on admission allows subdivision into high- and low-risk groups in patients presenting with ST segment elevation. Certainly, cTnT measurement can be incorporated into a clinical decision-making strategy to assign patients to investigation and management pathways. There is evidence that cTnT may be useful to guide therapeutic options. The major issue is one of cost. In the U.K. model of managed care with undemanding diagnostic standards, the role of cTnT will be to enhance clinical decision-making strategies, to provide accurate diagnosis and to reduce lengths of stay. This can be shown to have potential for major improvements in cost efficiency. Improvements in diagnostic accuracy can reduce inappropriate long-term drug therapy. In systems with a more aggressive laboratory investigation strategy, rationalization of test numbers will provide an immediate cost reduction while improving quality. Finally, use of point-of-care testing (POCT) means that biochemical testing can be pe
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PMID:Troponin T or troponin I or CK-MB (or none?). 985 34

The pericardial fluid was examined in 26 patients without morphological signs of severe damage to cardiac histiocytes, who died unexpectedly from ischemic heart disease (IHD)--main group. The control group comprised 26 persons, who died from other (not heart diseases-asphyxia, acute blood loss, crania-cerebral trauma). The mean age of the died was 57.4 +/- 1.5 years in the main group and 51.8 +/- 2.7 years in the control group. Cardiac markers were examined in the pericardial fluid of the died in both groups, i.e. the activity of aspartate aminotransferase (AsAT), of creatine kinase (CK), of isoenzyme KK-MB, of lactate dehydrogenase (LDG), and its isoenzyme spectrum, and, finally, the content of the cardiac troponin I (cTnI). The statistically reliable differences were found between the two groups according to the activity of AsAT, LDG, its isoenzyme spectrum and the cTnI content. Isoenzymes LDG1 and LDG2 constituted up to 60% of the LDG activity in the pericardial fluid of those who unexpectedly died from IHD. As for the control group, the LDG activity was virtually evenly distributed between all isoenzymes. No differences were found in the activity of CK and isoenzyme KK-MB between the main and control groups. Thus, the obtained data are indicative of the "cardiac" origin of enzymes in the pericardial fluid. Finally, a number of assumptions were put forward on mechanisms of hyper-fermentation in the ischemic damage of the cardiac muscle.
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PMID:[Cardiac markers in the pericardial fluid in sudden coronary death]. 1282 98

Cardiac troponins are invaluable tools for the detection of minimal myocardial injury. No study to date has analyzed the effect of permanent cardiac pacing on minimal myocardial injury detection by cardiac troponin I (cTnI) measurement. We investigated 76 clinically stable patients (mean age 75 years, range 31-93 years, 59% men) listed for elective endocardial permanent pacemaker insertion. Patients were required to have normal levels of cardiac cTnI, aspartate transaminase (AST) and creatinine kinase (CK) on a venous blood sample taken immediately prior to elective pacemaker implantation. Repeat measurements of AST, CK, and cTnI were performed at a mean of 19.2 post implantation. There was a detectable small rise in cTnI levels above normal in 21% of patients in a second blood sample taken 18-21 hours later (mean cTnI 0.39 +/- 0.37 microg/L, normal < 0.15 microg/L). The only factor that correlated with this rise was prolonged x ray screening time for lead implantation.
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PMID:Effects of transvenous pacing on cardiac troponin release. 1546 17

The postmortem diagnostics of acute forms of coronary heart disease showed that third-degree cardiomyocytic damages, primary lumpish destruction, and intracellular myocytolysis are attended by elevated cardiac troponin I levels in pericardial fluid and by enhanced activity aspartate aminotransferase and lactate dehydrogenase.
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PMID:[Relationship of microscopic myocardial changes to the biochemical parameters of pericardial fluid in acute forms of coronary heart disease]. 1683 Jun 18

The current study was designed to determine the changes of the cardiac troponin I (cTnI) expression in blood and tissue during the myocardial degeneration in calves with foot-and-mouth disease (FMD). Seventeen crossbred calves presenting pathological signs for FMD confirmed by viral analysis were studied. A biochemistry panel and immunohistochemistry were performed on 17 diseased calves and 7 calves used as controls. Creatine kinase (CK), CK-myocardial band (CK-MB), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities were analyzed for both groups. Cardiac troponin I levels were measured by a commercially available enzyme-linked immunosorbent assay kit. Mean cTnI (14.8 +/- 1.9 ng/ml) concentration and CK (573 +/- 407 U/l), CK-MB (238 +/- 37 U/l), AST (84 +/- 7), and LDH (298 +/- 29 U/l) activities were higher in FMD cases compared with controls. Immunohistochemistry revealed loss or depletion of cTnI expression in myocardium of all cases. None of the 7 controls showed loss of cTnI expression. Increased serum cTnI concentration correlated with myocardial injury and loss of cTnI immunolabeling in cardiomyocytes of calves with FMD.
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PMID:Determination of cardiac troponin I in the blood and heart of calves with foot-and-mouth disease. 1877 92

Since cardiac and skeletal myotoxicity affect the development of drug candidates, it is important to detect their toxicity at an early stage of drug development. For that purpose, in this study, the usefulness of several cardiac and skeletal myotoxic biomarkers in blood were evaluated using two rat models treated intraperitoneally with an acetylcholinesterase inhibitor carbofuran (CAF) or a synthetic catecholamine isoproterenol (ISO). The biomarkers assayed were fatty acid binding protein 3 (Fabp3), myosin light chain 1 (MLC1), cardiac troponin I (cTnI), cardiac troponin T (cTnT), aspartate transaminase (AST), lactate dehydrogenase (LDH) and creatine kinase (CK). CAF and ISO treatment of rats induced greater increases in the levels of Fabp3, MLC1, cTnI and cTnT than in the levels of AST, LDH and CK. A kinetic analysis indicated that the levels of all of the biomarkers had returned to the basal level by 24h after drug administration. Pathological examination revealed lesions in the heart, mainly at the left ventricle and septum, in both CAF- and ISO-treated rats. CAF-treated rats showed widespread lesions of skeletal muscle that were independent of muscle fiber type, while in ISO-treated rats locoregional lesions were observed only in slow twitch muscle. Receiver operating characteristic curve analysis of the sensitivity of the tested biomarkers indicated that MLC1 and cTnT were the most effective biomarkers of cardiotoxicity. For skeletal myotoxicity, Fabp3 and MLC1 were the most effective biomarkers based on the specific tissue distribution of these proteins. Conversely, the rapid blood clearance of these markers should be taken into account when considering the use of these biomarkers.
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PMID:Evaluation of the usefulness of biomarkers for cardiac and skeletal myotoxicity in rats. 1985 36

The aim of this study was to evaluate the canine blood and urinary profiles after envenomation by Tityus serrulatus venom. Twelve dogs were randomly distributed into two equal groups. Control group animals received 0.5 mL phosphate buffered saline (PBS) injected subcutaneously into the internal portion of the left thigh, whilst dogs in the envenomed group were injected with scorpion venom (250 microg/kg in 0.5 mL PBS). No significant alterations were detected in the urine of envenomed dogs. Levels of plasma glucose and serum urea, creatinine, total protein, potassium, alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK), lactate dehydrogenase (LDH), and amylase were determined. Semi-quantitative analysis of serum cardiac troponin I (cTnI) was performed using an immunochromatographic test. The concentrations of cortisol and insulin were determined using commercial radioimmunoassay kits. Increases in serum cortisol levels in experimental group animals coincided with hyperglycaemia and was probably a response to pain. Increased insulin levels were observed during the hyperglycaemic peaks. Envenomed dogs presented discreet increases in ALT, AST and CK, but no alterations in LDH, amylase, cTnI, urea, creatinine and potassium levels were observed. It was concluded that the venom of T. serrulatus induces blood and urinary biochemical changes in dogs.
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PMID:Biochemical profile of dogs experimentally envenomed with Tityus serrulatus scorpion venom. 2006 Apr 4

Tei index (myocardial performance) and cardiac biomarkers were evaluated in dogs with parvoviral enteritis (PVE). Tei index was calculated as isovolumic contraction time plus isovolumic relaxation time divided by ejection time. Myocardial and skeletal muscle damages were assessed by serum levels of cardiac troponin I (cTnI), creatine (phospho) kinase, lactate dehydrogenase and aspartate aminotransferase. Serum magnesium level was also determined. According to treatment response, dogs were divided into the survivor (n=20) and non-survivor groups (n=23). Seven healthy dogs served as controls. The mean value of the Tei index was higher in non-survivors, compared with survivors (p<0.02) and healthy controls (p<0.01). Serum level of cTnI in non-survivors was higher than that of survivors and controls (p<0.05). Tei index showed the highest sensitivity and specificity to predict mortality. The findings of an elevated Tei index and an increase in serum cTnI are factors associated with a poor prognosis in cases of canine parvovirosis.
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PMID:Tei index (myocardial performance index) and cardiac biomarkers in dogs with parvoviral enteritis. 2107 28

N,N-dimethylformamide (DMF) is a colorless liquid with a faint amine odor, which is widely used in the world. DMF exposure may induce adverse effects on liver, but few studies showed damage to heart after exposure to DMF. In the present study, DMF was administered to ICR mice with the doses of 0.32, 0.63 and 1.26 g/kg of body weight by gavage for 90 days. The increase in the relative liver weight is accompanied with the presence of the centrilobular hepatocellular hypertrophy as well as increased serum levels of aspartate transaminase (AST) and alanine transaminase (ALT). An increase of malondialdehyde (MDA) level was shown in liver homogenate, while superoxide dismutase (SOD) and glutathione (GSH) activities decreased. Heart damage was also shown in mice exposed to DMF for 90 days, although pathological examination showed only slight inflammatory cell infiltration. Increased levels of serum lactate dehydrogenase (LDH), isoenzymes of creatine kinase (CK-MB) and cardiac troponin I (cTnI) were shown. Increased level of MDA was also shown in heart homogenate, in contrast with the decreased activity of SOD. These data suggested that the administration of DMF could induce liver and heart injuries and oxidative stress was involved in the toxic effects.
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PMID:Liver and heart toxicity due to 90-day oral exposure of ICR mice to N,N-dimethylformamide. 2178 5

The aim of this study is to investigate the effects of enalapril, an angiotensin-converting enzyme inhibitor, on multiple organ damage after scald injury. Healthy adult rats (half male and half female; 8-12 weeks old) were randomly assigned to the following treatments: sham operation, scald injury, and intraperitoneal enalapril (1, 2, and 4 mg/kg body weight) treatment after scalding. At 1, 12, and 24 H postscald, left ventricular and aortic hemodynamics were measured using a multichannel physiological recorder. Functional and pathological changes of the heart, liver, and kidney were examined by biochemical and histological methods. Compared with sham controls, untreated scalded animals showed decreased hemodynamic parameters and increased myocardial angiotensin II, serum creatine kinase heart isoenzyme, and serum cardiac troponin I and histopathological inflammation in the myocardium 12 H postscald. These hemodynamic, functional, and pathological changes were attenuated by 1 mg/kg enalapril. Enalapril reversed scald-induced elevations in aspartate aminotransferase, alanine aminotransferase, blood urea nitrogen, and blood creatinine 12 H postscald, and ameliorated focal necrosis in the liver and erythrocyte cast formation in renal tubules. However, higher doses of enalapril yielded less or no improvement in organ dysfunction. Enalapril at 1 mg/kg attenuates scald-induced multiple organ damage in rats.
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PMID:Protective effects of enalapril, an angiotensin-converting enzyme inhibitor, on multiple organ damage following scald injury in rats. 2358 64


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