Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The expression of soluble GPT (E.C. 2. 6. 1. 2) was analysed in seventeen independent rat hepatoma/human somatic cell hybrids and in forty-one subclones derived from two of these hybrids. 2. As judged by electrophoretic mobility, twelve hybrid clones expressed rat GPT activity only and three expressed strong rat and weak human GPT activity but no heteromeric isozymes. In the remaining two hybrids, only human GPT was demonstrable. 3. The segregation of GPT and marker enzymes in the primary hybrid cells and the subclones suggests that the human structural GPT locus is on chromosome 8. 4. The re-expression of rat GPT in segregating subclones derived from two primary hybrids which had extinguished this function, could not be correlated with presence or absence of any particular human chromosome(s).
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PMID:Regulation of expression of liver-specific enzymes. II. Activation and chromosomal localization of soluble glutamate-pyruvate transaminase. 711 91

A group of 48 patients (42 suffering from hepato-biliary diseases and 6 without hepatic diseases) was followed by the authors for a period lasting from 5 to 8 years, 13 out of them for longer. The hepatic disease was assessed on the basis of physical examination, current liver chemistry and proper and specific instrumental procedures. Initial and final diagnosis and the aminotransferases (AST, ALT) trend in years were carefully considered. First of all it was concluded that no advantage is obtained in monitoring the two aminotransferases instead of one alone. Moreover it is stressed the opportunity of referring aminotransferases activities in a simple way such as per cent of variation as referred to considered upper normal value differing from one to the other laboratory. The aminotransferase increase maintains an important and diagnostic significance in acute liver damage such as in acute hepatitis. An inappreciable prognostic value may be drawn from the follow up of these enzymatic parameters: for example the development of posthepatic fibrosis, or cirrhosis or hepatoma cannot be foreseen on the basis of the aminotransferases trend. A greater variability and sharp increases in AST-ALT values are recorded in patients with biliary gallstones.
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PMID:[Diagnostic-prognostic significance of long-term (5-11 years) variations in serum GOT-GPT levels in the blood]. 717 59

Dedifferentiated rat hepatoma variant cells of clone Faof1 fail to express most of the liver-specific functions characteristic of its line or origin, H4IIEC3. When Faof1 cells are cultivated for 48 hr in the form of aggregates two cell types can be recovered from monolayer cultures established from the aggregates: the majority of cells are similar to the Faof1 parental line, but a new cell type (designated dag) that adheres only weakly to the substrate is present at a frequency of 2--12 X 10(-2). Eight dag populations and eight clones are characterized as being different from Faof1 cells by the production of serum albumin, aldolase B and in some cases activity of alcohol dehydrogenase and alanine aminotransferase. No dag cells are recovered after 18 or 24 hours of aggregation, but after 48 or 96 hrs 1--5% of the cells give rise to clones of dag cells. During aggregation cells are committed to become dag cells but their new phenotype is expressed only after 5--12 days. The fraction of dag cells in colonies that grow out from aggregates suggests that dag transformation is not a clonal event. These experiments demonstrate that a transitory change in the culture conditions of Faof1 cells can lead to a heritable modification in phenotypic expression. Since dag cells fail to express the liver-specific gluconeogenic enzymes that permit cells to grow in glucose-free medium, it is possible to select from dag populations revertants in which expression of these activities is restored. The frequency of appearance of such dag revertants is not increased by the action of EMS.
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PMID:Dedifferentiated variants of a rat hepatoma: partial reversion induced by cell aggregation. 744 71

The indication and the evaluation of IFN treatment for chronic hepatitis type C has been discussed. Good response to IFN depend on the level of HCV RNA just before the treatment. The patients who has low level of HCV RNA (less than 1 Meq/ml by DNA probe assay) could be able to estimate the response more than 80%. On the contrary, it is less than 10% for the patients with high level of HCV RNA. The evaluation of IFN treatment for chronic hepatitis were divided into 3 groups. Cure was defined as the continuous normalization of serum ALT and disappearance of HCV RNA during 12 month or more after the treatment. Partial response was defined as continuous normalization of ALT level but positive for HCV RNA. The others were defined as non responder. First and second group should be evaluated for the IFN treatment. Final purpose for IFN treatment should be prevent to develop liver cirrhosis or hepatocellular carcinoma.
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PMID:[The indication and the evaluation of IFN treatment of chronic hepatitis C]. 752 17

ELISA was used to detect anti-HCV antibody in 179 serum samples of patients with various types of liver diseases and 41 serum samples of blood recipients in Baise district of Guang Xi. The results showed that 17.9% of patients with various types of liver diseases and 31.7% of blood recipients were anti-HCV positive. Among patients with liver diseases, the anti-HCV positive rate was 4.3% (1/23) in acute hepatitis (AH), 12.8% (10/78) in chronic hepatitis (CH), 28.6% (12/42) in liver cirrhosis (LC) and 25.0% (9/36) in hepatocellular carcinoma (HCC). As liver diseases became chronic, the anti-HCV positive rate tended to rise. The anti-HCV positive rate in LC was significantly higher than that in AH or CH (P < 0.05). The anti-HCV positive rate in HCC was not significantly different from that in AH or CH (P > 0.05 or 0.1). It was found that the anti-HCV positive rate in HBsAg-negative patients was significantly higher than that in HBsAg-positive patients (P < 0.05). The anti-HCV positive rate in liver diseases was not related to ALT (P > 0.05). In blood recipients, the anti-HCV positive rate was closely related to the number of transfusion and the activity of ALT.
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PMID:[An investigation on the present situation of HCV infection patients with liver diseases and in blood recipients in Baise District of Guang Xi]. 753 8

Two hundred cases of various kinds of viral hepatitis and hepatocellular carcinoma were tested for serum anti-HCV. The positive rates of anti-HVC in patients with severe hepatitis and patients with cirrhosis were 42.86% and 46.15%, respectively. They were significantly higher than those in patients with other kinds of hepatitis (P < 0.05). The positive rate of anti-HCV was 67.5% in patients with posttransfusion hepatitis, 20.47% in healthy blood donors. In posttransfusion hepatitis B it was only 2.5%. Our results demonstrated that blood transfusion played an important role in transmitting HCV. Our findings also indicated that dual infection of HBV and HCV was important in the course of chronic hepatitis, cirrhosis and severe hepatitis. 50% of the anti-HCV positive patients with chronic hepatitis had slightly elevated serum alanine aminotransferase level. This showed that liver damage caused by HCV may be a chronic course.
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PMID:[The anti-HCV assay in viral hepatitis and hepatoma and the relationship between HCV infection and blood transfusion]. 753 55

Our aim was to verify whether the presence of antibodies to HCV envelope protein might mark the occurrence of liver damage, as recently suggested in the literature. Sera from 104 patients (62 male, 42 female) were tested: 84 were positive and 20 were negative to a second generation enzyme immunoassay for anti-HCV antibodies; 51 patients had mild chronic liver disease (44 chronic hepatitis, seven steatosis), 43 had liver cirrhosis (superimposed by hepatocellular carcinoma in 18) and ten were asymptomatic anti-HCV positive subjects with normal liver function tests. Besides, all sera were tested by means of an enzyme immunoassay for the presence of serum antibodies to the synthetic peptide S24A (SIYPGHVSGH RMAWDMMMNW SPTA) derived from amino acids 307-330 of HCV polyprotein. Anti-S24A antibodies were detected in 40/84 sera positive and 1/20 negative at anti-HCV testing (Pearson chi 2 12.29; p = 0.005). Among anti-HCV positive sera, no significant difference existed in anti-S24A status with regard to clinical evidence of liver disease, ALT concentration or HCV RNA positivity. Thus, anti-S24A antibodies are detectable in approximately half of HCV-positive sera, but they do not seem to add significant clinical information to existing tests or to be useful as putative markers of viraemia.
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PMID:Anti-envelope antibodies in anti-hepatitis C virus (HCV) positive patients with and without liver disease. 753 99

We have developed a new multienzyme control serum, Seraclear-HE, which was designed to function not only as an accuracy and precision control serum but also as an intermethod calibrator for unifying interlaboratory clinical enzyme data in terms of reference method values. Seraclear-HE contains as analytes the following enzymes of human origin only: aspartate aminotransferase (AST, EC 2.6.1.1) and lactate dehydrogenase (LD, EC 1.1.1.27) from erythrocytes; alanine aminotransferase (ALT, EC 2.6.1.2) from a hepatoma cell line; alkaline phosphatase (ALP, EC 3.1.3.1) from an amnion cell line; creatine kinase (CK, EC 2.7.3.2) from an embryo kidney cell line; gamma-glutamyltransferase (GGT, EC 2.3.2.2) from a macrophage cell line; and amylase (AMY, EC 3.2.1.1) from urine and saliva. The seven partly purified enzymes were lyophilized in partially delipidated human serum containing sucrose (50 g/L), pyridoxal 5'-phosphate (30 mmol/L), and other stabilizers. The material is stable for at least 2 years at temperatures < or = 10 degrees C. For two concentrations of this preparation, reference method values (mainly International Federation of Clinical Chemistry and Japan Society of Clinical Chemistry) obtained at both 30 degrees C and 37 degrees C are assigned.
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PMID:Multienzyme control serum (Seraclear-HE) containing human enzymes from established cell lines and other sources. 1: Preparation and properties. 753 43

Chronic hepatitis B virus (HBV) infection is a serious problem because of its world wide distribution and possible adverse chronic sequalae such as cirrhosis and hepatocellular carcinoma. Over the past 20 years, many antiviral or immunomodulatory agents, or both, have been used in patients with chronic HBV infection. Among immunomodulatory agents, levamisole, BCG, picibanil and interleukin-2 have been shown to be ineffective. Corticosteroid therapy is also ineffective and can cause deleterious effects in chronic HBV infection. Thymosin-alpha 1 therapy is currently in phase III clinical trial. Among antiviral agents, acyclovir, dideoxynucleosides, suramin, zidovudine and ganciclovir have been shown to be ineffective and have intolerable side effects. While adenine arabinoside (Ara-A) and its monophosphate derivative (Ara-AMP) are effective agents if the treatment course is long enough, they have been withdrawn from investigative use because of their substantial neuromuscular toxicity. Interferon-alpha may directly inhibit HBV replication and enhance hepatocyte HLA class I antigen expression with subsequent increase of T-cell mediated cytotoxicity. Randomized, controlled clinical trials have shown that 25% to 50% of adult patients with elevated alanine transaminase (ALT) levels lost HBeAg and HBV-DNA when treated with IFN-alpha at a dose of 5MU daily or 10 MU three times a week for 3 to 6 months. In view of the fact that the response rate is far from satisfactory, particularly in Asian patients, combination therapies including interferon alpha with Ara-AMP, acyclovir, didoxynucleoside or interferon-gamma have been studied. Most forms of combination therapy have been shown to be of limited effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Drug therapy in patients with chronic type B hepatitis]. 754 84

Patients with chronic active hepatitis C and cirrhosis often develop hepatocellular carcinoma. Interferon (IFN) seems to be effective in some patients but whether it prevents carcinogenesis is unknown. In a prospective randomised controlled trial, we evaluated the effects of IFN-alpha in cirrhotic patients with HCV infection because of their high risk of hepatocellular carcinoma. 90 patients with compensated chronic active hepatitis C with cirrhosis were randomly allocated to receive IFN-alpha (6 MU three times weekly for 12-24 weeks) (45 patients) or symptomatic treatment (45 controls), and were followed up for 2-7 years. In nine controls, alanine aminotransferase (ALT) decreased to less than 80 IU/L but did not stay in the normal range. In 19 patients given IFN-alpha, ALT decreased to less than 80 IU/L (in seven patients, it became and stayed normal; p = 0.011, Wilcoxon rank-sum test). However, the mean change in ALT was not significantly different between the two groups. The mean change in peak alpha-fetoprotein values was smaller in patients given IFN-alpha than in controls (p = 0.021). The mean change in the serum albumin level was higher in the IFN-alpha group (p < 0.001). The histological activity index in the 12 IFN-alpha patients undergoing a second biopsy after therapy was improved (p = 0.031). Hepatitis C viral RNA disappeared in seven (16%) of the 45 IFN-alpha patients (95% CI, 7-29%) and in none of the 45 controls (0-8%; p = 0.018). Hepatocellular carcinoma was detected in two (4%, 1-15%) IFN-alpha patients and 17 (38%, 24-54%) controls (p = 0.002, Wilcoxon signed-rank test). The risk ratio of IFN-alpha treatment versus symptomatic treatment was 0.067 (0.009-0.530; p = 0.010 Cox's proportional hazards). IFN-alpha improved liver function in chronic active hepatitis C with cirrhosis, and its use was associated with a decreased incidence of hepatocellular carcinoma.
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PMID:Randomised trial of effects of interferon-alpha on incidence of hepatocellular carcinoma in chronic active hepatitis C with cirrhosis. 854 66


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