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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the clinical usefulness of serum tripeptide aminopeptidase (EC 3.4.11.4) activity in diagnosing liver diseases. We found that increased tripeptide aminopeptidase activity accompanied an elevation in alanine aminotransferase activity (ALT) in the sera of patients with non-cancerous liver diseases and that these enzyme activities were correlated (r = 0.826-0.972). In contrast, an increase in tripeptide aminopeptidase activity did not coincide with an elevation in ALT activity in the sera of patients with cancerous liver diseases. We also observed a correlation in acute hepatitis and in patients following transcatheter arterial embolization of hepatoma throughout their subsequent clinical courses. The difference in serum enzyme activities for cancerous and non-cancerous liver diseases seems to result from changes in enzyme activities in cancerous liver tissues. We found that the ratio of tripeptide aminopeptidase to ALT activity in hepatoma tissues (1.9) was 4 times higher than that in normal liver tissues (0.5).
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PMID:Clinical usefulness of serum tripeptide aminopeptidase activity in diagnosing liver diseases. 243 31

At the Center for Experimental Plants and Animals, Hokkaido University, two inbred strains, Long Evans Cinnamon (LEC) and Long Evans Agouti (LEA), which were selected for coat colour, were isolated from a closed colony of Long Evans rats. While the two inbred strains were maintained by sibmating, only LEC rats, over 24-generation, spontaneously developed acute hepatitis with sudden appearance of systemic jaundice at around four months after birth. The frequency of acute hepatitis was 80 to 90% and the disease in nearly 80% of these rats were progressive and they died within two weeks after onset, with their clinical course and histopathological findings similar to those of human fulminant hepatitis. LEC rats with spontaneous hepatitis had strong-conversion of urine-bilirubin, ultimate increase of blood-bilirubin and abnormal increase of serum-transaminases (GOT, GPT; GOT greater than GPT). Histopathological findings of the livers in the rats with acute hepatitis showed spotty necrosis and abnormal hepatocytes containing giant bizarre nuclei and in the rats with fulminant-type hepatitis showed central or coagulated necrosis and marked infiltration of inflammatory cells. Serum levels of albumin in LEC rats before being affected by hepatitis were low compared with those of LEA rats and especially characteristic fact was that cellulose-acetate electrophoresis could not reveal gamma-globulin fraction in LEC rats of 6-week and 12-week old, which will be a clue to analyze the etiology of hepatitis in LEC rats.
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PMID:[Establishment of an inbred strain of LEC (Long Evans Cinnamon) rats with spontaneous hepatitis]. 247 50

To evaluate the level of serum thyroxine-binding globulin (TBG) in various liver diseases, TBG and T4, T3, FT4 were measured by radioimmunoassay in 29 HBsAg carriers (C), 27 patients with acute hepatitis (AH), 18 patients with inactive chronic hepatitis, 70 patients with chronic active hepatitis (CAH), 31 patients with active cirrhosis (AC), 20 patients with inactive cirrhosis (IC), 38 patients with hepatocellular carcinoma (HCC), 12 patients with metastatic Ca to the liver (Met.) and in 81 normal controls. All the patients were clinically euthyroid. The TBG as well as T4 in patients with AH, CAH, AC HCC and, Met. were significantly higher than those in controls. The T3 level was significantly elevated in CAH and AC patients. The TBG level did not correlate with serum albumin or bilirubin levels, but did correlate significantly with alanine transaminase (ALT) (r = 0.54, p less than 0.01). However, the correlation was positive in chronic active hepatitis (r = 0.40, p less than 0.01) but negative in hepatocellular carcinoma (r = -0.32, p less than 0.05). The data suggested: (1) Significant TBG and T4 elevation was found in all active liver diseases and HCC. (2) In the presence of high T4 in patients with liver disease, normal FT4 excluded the diagnosis of hyperthyroidism. (3) The elevation of TBG levels in chronic hepatitis appeared to parallel the severity of hepatocytolysis, and therefore might be the result of hepatocytolysis; while the elevation of TBG in HCC might be due to increased synthesis by the malignant cells.
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PMID:[Changes in thyroid hormone concentration in liver disease]. 250 36

In order to clone hepatitis C (blood-borne non-A, non-B hepatitis) virus, lambda gt11-cDNA library was constructed from RNA extracted from 100 liters serum collected from 1,047 donors with elevated ALT levels and negative for hepatitis B virus-DNA. The library was immunoscreened on Y1090 cells with pooled serum obtained from patients with acute hepatitis C or chronic hepatitis C. By screening 29 clones specific for Japanese hepatitis C infection were isolated. The specificity of these clones for hepatitis C infection was determined by panels constructed in 3 laboratories. Of these, 12 clones were specific for American hepatitis C infection as well. The nucleotide sequence (201 bp) of one of them was determined to be unique compared to known human viruses including hepatitis A virus, hepatitis B virus and hepatitis D virus. Southern blot analysis showed the absence of the sequence of the human genome in the clone. The predicted amino acid sequence is rich in residues of lysine, arginine, glutamic acid and asparagine, while lacking leucine, cysteine and methionine.
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PMID:Cloning of a cDNA associated with acute and chronic hepatitis C infection generated from patients serum RNA. 250 78

We have retrospectively studied the clinical and histological features of 55 cases of acute post-transfusion non-A, non-B hepatitis. Histological findings in the liver biopsies taken in the acute stage covered the whole spectrum of acute and chronic hepatitis, the incidence of acute hepatitis or non-specific reactive hepatitis was 12.7% and 16/4%, respectively, while that of chronic active hepatitis was 56.4%. There was no correlation between histological features in acute stage and the mean peak levels in serum alanine aminotransferase (ALT). Post-transfusion hepatitis, non-A, non-B with histological signs of chronic hepatitis in acute stage frequently results in biochemical evidence of chronic liver disease during long-term follow-up periods. Therefore, our results suggest that the histological features of chronic hepatitis in the acute stage are indicative of long-term elevation in serum ALT level.
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PMID:[Clinical and histological features of acute post-transfusion non-A, non-B hepatitis: histological diagnosis in acute stage and clinical outcome]. 251 63

Serum pregnancy-associated alpha 2-glycoprotein (alpha 2-PAG) levels were evaluated in a follow-up study of patients with hepatitis B virus (HBV) infection and compared with biochemical and virological parameters. In a study of 25 patients with acute hepatitis, an association was found between high alpha 2-PAG values, ALT levels, and HBsAg in 20 patients (80%) (P less than 0.05), 18 recovered completely, and 2 had a protracted course. In five patients serum alpha 2-PAG levels were similar to those in the control group. On the other hand, eight (100%) chronic persistent HBV patients showed high levels of alpha 2-PAG (P less than 0.05) during the study period, and these levels correlated well with inflammatory activity and failure of HBsAg elimination. There were no significant differences in alpha 2-PAG values between asymptomatic HBsAg carriers and controls. Serial analysis of alpha 2-PAG, in correlation with viral markers, biochemical parameters, and histological data, would contribute to the ability to predict the final outcome of HBV infection.
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PMID:Serum pregnancy-associated alpha 2-glycoprotein levels in the evolution of hepatitis B virus infection. 252 83

The peptide which is encoded by the pre-S(2) region of hepatitis B virus DNA, the pre-S(2) antigen, was determined quantitatively by an enzyme immunoassay system employing monoclonal antibodies. The prevalence and titer of pre-S(2)Ag were 91.9% (91/99) and 10,356 +/- 19,053 units (mean +/- S.D., arbitrary units) for hepatitis B e antigen (HBeAg)-positive patients with acute and chronic HBV infection and 86.0% (74/86) and 952 +/- 1,565 units for HBeAg-negative subjects. In four patients with acute hepatitis B, pre-S(2)Ag titers changed in parallel with HBV DNA levels, and the disappearance of pre-S(2)Ag from serum was associated with a rapid fall of ALT levels into the normal range, whereas the fluctuation of pre-S(2)Ag titer correlated with persistence of ALT elevations. In all of the 19 episodes of acute exacerbation of hepatitis which occurred in nine patients with chronic active hepatitis B, a significant elevation of pre-S(2)Ag titer was observed, closely overlapping an increase or appearance of HBV DNA, and its peak preceded peaks of ALT by 1 to 11 weeks (mean +/- S.D. = 4.26 +/- 2.57 weeks). These observations suggest that quantitative measurement of pre-S(2)Ag would be useful for estimation of the magnitude of HBV replication and would help predict the prognosis of acute hepatitis B and of acute exacerbation in chronic hepatitis B.
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PMID:Serum titers of pre-S(2) antigen in patients with acute and chronic type B hepatitis: relation to serum aminotransferase activity and other hepatitis B virus markers. 264 43

We investigated the expression of Pre-S2 antigen (Ag) and antibody (Ab) in sera quantitatively using ELISA. Four patients with acute hepatitis B and 87 chronic HBV carriers were included in this study. We also investigated the expression of Pre-S2Ag in the liver tissues obtained from 26 chronic HBV carriers by direct fluorescent antibody method. There was a significant correlation between Pre-S2Ag titers and HBsAg titers in sera. Pre-S2Ag titers were higher in sera positive for HBeAg, HBV-related DNA polymerase or HBV-DNA than in sera negative for those markers. The ratio of Pre-S2Ag titers to HBsAg titers, however, was constant irrespective of virus replicative markers. Pre-S2Ag in the liver had almost same intracellular localization with HBsAg in the liver. It was suggested that Pre-S2Ag was expressed with an intimate relation to the expression of HBsAg and was not useful as a virus replicative marker. Pre-S2Ag titers/HBsAg titers tended to be high in patients with chronic active hepatitis and high serum GPT levels compared to patients with chronic inactive hepatitis. This may be explained by the release of Pre-S2Ag in the liver. In addition, all patients positive for Pre-S2Ag on the membrane of hepatocytes had chronic active hepatitis. The overproduction of Pre-S2-containing surface proteins in the liver may have some implication related to cell injury via the immune response to Pre-S2Ag etc. Pre-S2Ab was detected only in few cases of chronic HBV infected patients. The lack of immune response to Pre-S2 region may play a role in the persistence of HBV infection.
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PMID:[Expression of Pre-S2 antigen and antibody in patients with hepatitis B virus infection]. 268 90

Serum-soluble Tac peptide was measured by an enzyme-linked immunosorbent assay in 12 patients with acute type B hepatitis, 33 patients with chronic type B hepatitis, and 15 age- and sex-matched controls. All 12 patients with acute type B hepatitis had elevated levels of soluble Tac peptide with a mean (+/- SD) of 1527 +/- 432 U/ml, significantly higher than that of normal controls (264 +/- 74 U/ml) or patients with chronic type B hepatitis (646 +/- 399 U/ml). Serial follow-up showed that serum levels of soluble Tac peptide tended to return to normal 2-4 months after onset of acute hepatitis along with the normalization of alanine aminotransferase and seroconversion of hepatitis B surface antigen (HBsAg) to anti-HBs. Patients with chronic type B hepatitis also had significantly higher levels of soluble Tac peptide than normal controls, although only 63.6% (21/33) of them had a level greater than the upper limit of normal. Serum levels of soluble Tac peptide in patients with chronic type B hepatitis varied considerably with the inflammatity in liver. The hepatitis B e antigen (HBeAg)-positive patients with chronic active liver disease had significantly higher levels of soluble Tac peptide (928 +/- 424 U/ml) than HBeAg-positive (412 +/- 146 U/ml) or anti-HBe-positive (424 +/- 175 U/ml) patients with chronic persistent hepatitis or minimal histological change. In addition, there was a significant positive correlation between serum levels of soluble Tac peptide and alanine aminotransferase. These findings suggested that activation of T cells might play an important role in the pathogenesis of acute and chronic type B hepatitis. Assay of serum-soluble Tac peptide might provide a simple and useful means to better understand the immune mechanisms of acute and chronic hepatitis B virus infection.
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PMID:Serum levels of soluble Tac peptide in acute and chronic hepatitis B virus infection. 278 45

Four chronic hepatitis B virus (HBV) carrier chimpanzees, which had apparently cleared hepatitis D virus (HDV) after a first experimental challenge with HDV, were reinoculated with a homologous strain of HDV. All animals had reappearance of low levels of serum HDV RNA and transient, mild alanine aminotransferase (ALT) elevations, which in two cases correlated with HDV RNA positivity. Plasmas obtained from two chimpanzees after rechallenge were inoculated into two other chronic HBV carrier animals that had recovered from a previous HDV infection. A similar reappearance of HDV RNA in serum (without ALT elevation) was noticed. These same plasmas, however, when inoculated into a chronic HBV carrier chimpanzee never exposed to HDV caused a severe acute hepatitis D. Rechallenge with HDV in chimpanzees apparently recovered from a first HDV infection resulted in the reappearance of HDV replication, sometimes associated with hepatitis. This can be interpreted as reinfection with HDV, but other explanations are possible. Although the serum level of HDV RNA observed after rechallenge with HDV is low, its transmission to individuals susceptible to HDV infection can result in severe acute hepatitis D.
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PMID:Reappearance of hepatitis D virus (HDV) replication in chronic hepatitis B virus carrier chimpanzees rechallenged with HDV. 279 55


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