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)

Serum gamma-glutamyl transferase (GGT, EC. 2.3.2.2. was measured in 173 patients with diseases of the hepatobiliary system (including metastatic cancer) and in 90 patients who were subsequently shown to have primary diseases of other etiology. All patients had been selected because they had abnormal alkaline phosphatase, aspartate aminotransferase or bilirubin on SMA 12/60 screening. Serum GGT was elevated in 97% of patients with primary hepatobiliary disease. The magnitude of the increase in GGT was variable in all groups and was unhelpful in differential diagnosis, even between medical and surgical cases. Moreover, GGT was abnormal in 69 patients who did not have primary hepatobiliary disease (77%), an incidence higher than that for other enzyme tests performed. We conclude that because GGT was more susceptible than other tests to spurious elevation in the absence of hepatobiliary disease and was unhelpful in differential diagnosis, it has little value apart from monitoring alcohol abuse and enzyme induction.
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PMID:Lack of value of serum gamma-glutamyl transferase in the diagnosis of hepatobiliary disease. 3 86

We used the previously described [Clin. Chem. 19, 1114 (1973)] and evaluated [Clin. Chem. 19, 1122 (1973)] computer-controlled instrument system for sequential chemical testing to select and perform tests of hepatic status, to aid the clinician in the diagnosis of liver disease. Results for total bilirubin, aspartate aminotransferase, and alkaline phosphatase obtained from the continuous-flow analysis (SMA 12/60) admission screen were used by the instrument system to determine selectively the values for gamma-glutamyltransferase, alanine aminotransferase, creatine kinase, and total and direct bilirubin. Kit methods for the latter four tests were evaluated on the system; results were similar to manual procedures. A software, enzymatic ratemeter was found to be better than the previously described hardware ratemeter. The follow-up tests of serum prescribed by the system are compared to clinician-prescribed follow-up tests and discharge diagnoses. In 10 of 19 cases, the system and clinician ordered similar follow-up tests; in three cases follow-up differed, and in six cases, the system ordered follow-up tests and the clinician ordered none.
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PMID:Computer-controlled instrument system for sequential chemical testing III. Application to liver assessment. 34 61

A study of cardiovascular risk factors in middle-aged twin men provided an opportunity to test for genetic variability in the SMA 12/60 (Technicon) battery of clinical chemistry tests. Classical twin methodology was used to analyze the variation of monozygotic and dizygotic twins. In addition, frequency of co-twin contact was used to control for effects of differences in shared environment. Genetic variability played a definite role in controlling four of the 11 reported tests: one-hour serum glucose, serum urea nitrogen, uric acid, and bilirubin. No genetic variation was found for lactate dehydrogenase, phosphorus, and alkaline phosphatase. Significantly higher means for calcium, total protein, albumin, and aspartate aminotransferase in monozygotic twins precluded any statement about heredity and environment for these tests.
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PMID:Genetic variability of clinical chemical values. 55 78

Malate dehydrogenase (EC 1.1.1.37) was immobilized on the lower groove of the dialyzer plate used for serum aspartate aminotransferase determination in the AutoAnalyzer II system. Immobilization was effected by covalently attaching malate dehydrogenase to the inner surface of the groove which was previously activated by treatment with glutaraldehyde at room temperature. The immobilized malate dehydrogenase catalyzed the reaction between oxaloacetate and NADH to form NAD in the coupled reaction originally proposed by Karmen. Results of the present method correlated well with those obtained by the Technicon SMA II system in which malate dehydrogenase is in solution (n = 99; r = 0.99; t = 0.30). The activity of immobilized malate dehydrogenase on the dialyzer groove was sufficient to measure serum aspartate aminotransferase for at least one month with continuous use. The stability of immobilized malate dehydrogenase was also dependent on the number of samples determined. The dialyzer plate is a reusable solid matrix for malate dehydrogenase immobilization. The expense of the present method is only half the cost of the method in which malate dehydrogenase is in solution.
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PMID:Use of malate dehydrogenase immobilized on the dialyzer groove of the Autoanalyzer II for serum aspartate aminotransferase determination. 311 24

I compared results for aspartate aminotransferase (EC 2.6.1.1) obtained with a reaction-rate analyzer (LKB 2086 Mark Two), based on IFCC methodology, and a continuous-flow analyzer (the Technicon SMA 2) for 115 patients' sera and seven commercial quality-control sera. The data from the SMA 2 showed a clear positive bias in those sera with activities exceeding 40 U/L (the upper limit of the reference range). Independent data to support the bias of the SMA 2 and other continuous-flow analyzer systems are presented. Application of a correction factor to the SMA 2 data above the upper limit of the range significantly decreased this bias. Failure to apply such a factor to data obtained from continuous-flow analyzers could lead to serious clinical misinterpretation.
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PMID:Discrepancies in measurement of aspartate aminotransferase by continuous-flow analysis. 664 Sep 5

The effects of diltiazem on an experimental study of Superior Mesenteric Artery ligation were studied on three rat groups comprising controls (N = 5), SMA ligation (N = 8), and SMA ligation and diltizem (0.25 mg/kg injection), (N = 8). Creatine phosphokinase, lactic dehydrogenase, aspartate transaminase and alanine transaminase venous blood levels were significantly decreased after diltiazem injection compared with the SMA ligation group. Histopathologic examinations revealed that diltiazem partly protected the small intestine from ischemic changes.
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PMID:The effects of diltiazem on superior mesenteric artery ligation. An experimental study. 912 98

Fibrosis-related changes in livers of cirrhotic rats induced by dimethylnitrosamine (DMN) have not yet been fully clarified. The aim of this study was to investigate changes in molecular and biochemical markers in DMN-intoxicated rats. DMN was administered to Sprague-Dawley rats for 2 and 5 weeks to induce different degrees of hepatic fibrosis. Liver tissues were assessed for the degree of fibrosis and gene expression. Histological examination of the liver showed a progressive increase in fibrosis scores (1.33 +/- 0.21 and 3.03 +/- 0.29, respectively) and expansion of fibrous septa with collagen-staining fibers in rats after 2 and 5 weeks of DMN administration. Hepatic protein contents of alpha-smooth muscle actin (alpha-SMA) and total collagen were significantly higher in rats administered DMN for both 2 and 5 weeks compared with those in control rats. Hepatic mRNA expressions of alpha-SMA, transforming growth factor-beta1 (TGF-beta1), connective tissue growth factor, tissue inhibitor of metalloproteinase-1, and procollagen I and III were increased in DMN rats after 2 and 5 weeks. Abnormal increases in plasma alanine transaminase (ALT) and aspartate transaminase (AST) levels, plasma and mitochondrial MDA levels, and portal venous pressure were also noted in DMN rats. DMN administration to rats for 2 and 5 weeks induced progressive increases in hepatic fibrosis scores, hepatic mRNA expressions of TGF-beta1 and procollagen I and III genes, plasma levels of ALT and AST, and portal venous pressure, as well as progressive decreases in both liver and body weights. Our results suggest that DMN administration in rats induces biochemical and molecular changes related to fibrogenesis in the liver.
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PMID:Increases in fibrosis-related gene transcripts in livers of dimethylnitrosamine-intoxicated rats. 1506 25

The suppressive effects of Platycodi Radix (Changkil: CK), the root of Platycodon grandiflorum A. DC (Campanulaceae), on the progress of acute carbon tetrachloride (CCl4)-induced hepatic fibrosis were investigated in the rat. CK significantly suppressed CCl4-induced hepatic necrosis and inflammation, as determined by the serum enzymatic activities of alanine and aspartate aminotransferase and serum tumor necrosis factor-alpha levels, in dose-dependent manners. In addition, the increased hepatic fibrosis after acute CCl4 treatment was suppressed by the administration of CK. CK also significantly prevented the elevation of hepatic alpha1 (I) procollagen (type I collagen) mRNA and alpha-smooth muscle actin (alpha-SMA) expressions in the liver of CCl4-intoxicated rats and also suppressed the induction of alpha-SMA and type I collagen in cultured hepatic stellate cells, in dose-dependent manners. These results suggest that the suppressive effects of CK against the progress of acute CCl4-induced hepatic fibrosis possibly involve mechanisms related to its ability to block both hepatic inflammation and the activation of hepatic stellate cells.
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PMID:Suppressive effects of Platycodon grandiflorum on the progress of carbon tetrachloride-induced hepatic fibrosis. 1564 98

Excessive oxidative stress is implicated in hepatic fibrogenesis. Extracts of Salvia miltiorrhiza (Sm) have been shown to protect cells against oxidative stress. In this study we investigated the in vitro and in vivo effects of Sm on hepatic fibrosis. A cell line of rat hepatic stellate cells (HSC-T6) was stimulated with transforming growth factor-beta1 (TGF-beta1). The inhibitory effects of Sm (50-400 microg/ml) on TGF-beta1-induced alpha-smooth muscle actin (alpha-SMA) secretion and the mRNA expressions of fibrosis-related genes, including alpha-SMA, connective tissue growth factor (CTGF), and tissue inhibitor of metalloproteinase-1 (TIMP-1), were assessed. Fibrosis was induced by dimethylnitrosamine (DMN) administration in rats. DMN-treated rats were randomly assigned to 1 of 4 groups: saline, Sm (20 mg/kg), Sm (100 mg/kg), or silymarin (100 mg/kg), each given by gavage twice daily for 5 weeks starting from the onset of DMN administration. Sm (200 and 400 microg/ml) significantly inhibited TGF-beta1-stimulated alpha-SMA secretion and the mRNA expressions of alpha-SMA, CTGF, and TIMP-1 in HSC-T6 cells. Fibrosis scores of livers from DMN-treated rats with either a low (1.8 +/- 0.2) or high (1.8 +/- 0.1) dose of Sm, or silymarin (1.4 +/- 0.2) were significantly reduced in comparison with DMN-treated rats receiving saline (3.1 +/- 0.1). Hepatic collagen contents were also significantly reduced by either Sm or silymarin treatment. The mRNA expression levels of alpha-SMA, TGF-beta1, and procollagen I were all attenuated in Sm- and silymarin-treated rats. Moreover, levels of plasma aspartate transaminase activities were reduced by Sm and silymarin treatment. In conclusion, our results show that Sm exerted antifibrotic effects in both HSC-T6 cells and in rats with DMN-induced fibrosis.
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PMID:Antifibrotic effects of Salvia miltiorrhiza on dimethylnitrosamine-intoxicated rats. 1586 49

Morin, a plant-derived flavonoid, has been reported to exhibit a wide range of pharmacological properties. In this study, we investigated the protective effect of morin on hepatic fibrosis induced by dimethylnitrosamine (DMN) in rats. Oral administration of morin remarkably prevented weight loss in the body and liver from DMN and inhibited the elevation of serum alanine transaminase (ALT), aspartate transaminase (AST), and total bilirubin levels. For the evaluation of hepatic fibrosis-related factors, we investigated expressions of collagen type I, transforming growth factor beta(1) (TGF-beta(1)), and alpha-smooth muscle actin (alpha-SMA) in mRNA and protein levels. We observed that morin significantly reduced the expression of collagen type I, TGF-beta(1), and alpha-SMA on hepatic fibrosis induced by DMN. Taken together, this study demonstrated that morin showed hepatoprotective and antifibrogenic effects against DMN-induced hepatic injury. This suggests that morin may be useful in preventing the development of hepatic fibrosis and cirrhosis.
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PMID:Protective effect of morin on dimethylnitrosamine-induced hepatic fibrosis in rats. 1862 40


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