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)

Two IgG1 type monoclonal antibodies ALT-01 and ALT-04 were prepared by two different immunization schedules. ALT-01 was generated by fusing murine myeloma NS-1 cells with splenocytes from a BALB/c mouse immunized by human lung squamous carcinoma cells, which were coated by antisera to mixed human lymphocytes. For preparation of ALT-04, human lung squamous carcinoma xenograft-bearing nude mice were injected I. P. with the spleen cells of normal BALB/c mice in order to acquire immunofunction. The spleen cells from these tumor-bearing nude mice were fused with NS-1 cells. Then, these hybridomas were screened and cloned for 3 times. Two antibodies were shown to recognize the surface antigen on human lung carcinoma cells and several kinds of tumor cell lines but not those on normal cell lines. ALT-01 reacted to neither human lung carcinoma tissue nor its xenograft. ALT-04 reacted to human lung carcinoma tissue, of which, reaction to adenocarcinoma was the strongest but not to various normal tissues. Immunoprecipitation followed by SDS-polyacrylamide gel electrophoresis and autoradiography was used to detect the associated antigen in 35S-labeled human lung carcinoma cells. Antigens, reacting to ALT-01, show one band of Mr 38,000 but those to ALT-04 reveal two bands of Mr 48,000 and 36,000.
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PMID:[Reactivity of monoclonal antibodies ALT-01 and ALT-04 and identification of lung cancer-associated antigens]. 344 54

A hepatitis B surface antigen (HBsAg) chronic carrier chimpanzee experimentally superinfected with delta virus (DV) developed chronic DV infection. Over a period of 12 months, serologic and biochemical changes were correlated with morphologic abnormalities of the liver. Severe hepatic necrosis and inflammation accompanied the initial acute episode of hepatitis on Day 35 after inoculation, followed by complete resolution of these lesions over the next 3 months. A second episode of hepatitis occurred on Day 145, and severe necrosis and inflammation recurred along with the reappearance of delta antigen in the hepatocytes. Delta antigen persisted in the liver following the second episode of hepatitis and has remained positive throughout the observation period of 1 year. During the initial acute episode, the hepatocytes exhibited foamy cytoplasmic changes resembling microvesicular fat. However, ultrastructural studies of the same cells revealed only vacuolization of the cytoplasm without evidence of fat droplets. The inflammatory infiltrate during both episodes of hepatitis demonstrated a striking predominance of macrophages over lymphocytes. Hepatocyte abnormalities observed by electron microscopy included vacuoles, proliferated endoplasmic reticulum, and tubules similar to those seen in posttransfusion non-A, non-B hepatitis. However, the tubular and reticular abnormalities coincided with delta antigen expression in liver biopsies detected by direct immunoperoxidase staining and abnormal alanine aminotransferase levels in the serum, which suggests a possible causal relationship. Nuclear abnormalities were not seen.
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PMID:Pathologic and ultrastructural changes of acute and chronic delta hepatitis in an experimentally infected chimpanzee. 351 26

In 86 Chinese patients with histologically proven hepatitis B surface antigen (HBsAg) positive chronic hepatitis and serum alanine aminotransferase levels exceeding 200 U/l, antibody to hepatitis D antigen (HDAg) was detected more frequently in sera from hepatitis B e antigen (HBeAg) negative patients (11/35, 31.4%) than in HBeAg positive (4/51, 7.8%) patients (p less than 0.02). 10 liver biopsy specimens (76.9%) from 13 chronic hepatitis B patients with superimposed hepatitis D virus (HDV) infection, showed positive staining for HDAg in their hepatocytes. Neither HBsAg nor hepatitis B core antigen (HBcAg) was found in the liver in 12/13 patients with superimposed HDV infection. However, in liver biopsy specimens from 42 patients without HDV superinfection, HBsAg was stained positively in 41 patients (97.6%), and HBcAg in 24 patients (47.1%). Using dot blot hybridization technique, serum hepatitis B virus (HBV) DNA was detected in 62.1% (41/66) of patients without HDV superinfection, while it was detected only in 10.0% (1/10) of patients who had HDV superinfection. It is concluded that HDV superinfection plays a significant role in Taiwan in HBeAg negative chronic hepatitis B patients with clinical "exacerbation". The data show clear evidence of HDV interfering with the replication of HBV.
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PMID:Hepatitis D virus (delta agent) superinfection in an endemic area of hepatitis B infection: immunopathologic and serologic findings. 361 86

Separation of 7-8S and 19S forms of serum immunoglobulin M (IgM) hepatitis B core antibody (anti-HBc) by rate-zonal centrifugation was carried out on serum from 80 American chronic carriers of hepatitis B surface antigen (HBsAg), all of whom were positive for IgM anti-HBc and had elevated levels of serum alanine aminotransferase (mean 164 IU/L). Seventy-three of the 80 sera showed a predominance of one or the other form of IgM anti-HBc. Fifty-four (68%) had predominantly 7-8S IgM anti-HBc, and 19 (24%) had predominantly 19S IgM anti-HBc. Sex, age, length of HBsAg-carrier state, mean alanine aminotransferase, mean total IgM anti-HBc level, presence of hepatitis B e antigen, and liver histology were similar in both groups. 19S IgM anti-HBc was detected in 11 (41%) of 27 male homosexuals compared with only 8 (17%) of 46 heterosexual patients (p = 0.03). Despite this apparent association, an explanation for the variable presence of 19S and 7-8S IgM anti-HBc predominance in chronic hepatitis B remains lacking.
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PMID:Clinical significance of low molecular weight (7-8S) immunoglobulin M antibody to hepatitis B core antigen in chronic hepatitis B virus infections. 371 66

We conducted a clinical trial to study the effects of a 10-week course of prednisone therapy and its withdrawal on serum aminotransferase levels and on hepatitis B virus (HBV) markers in patients with hepatitis B surface antigen (HBsAg) positive chronic active hepatitis (CAH-B). Eighteen patients with CAH-B were treated with prednisone, while another 18 patients matched for age, sex, race and sexual preference were followed simultaneously without treatment for the same duration. Nine of 18 prednisone-treated patients became transiently DNA polymerase positive. All nine patients developed a transient rise in serum alanine aminotransferase (ALT) levels of greater than 300 U/L above baseline values, which was associated with a drop in HBsAg levels from a mean of 186 micrograms/ml prior to therapy to 92 micrograms/ml at 6 months following treatment. Six of these patients developed fatigue, anorexia and dark urine, and four also developed either ascites or hemorrhage from esophageal varices, which was accompanied by hepatic encephalopathy. All six of these patients had histologic evidence of CAH with cirrhosis. In comparison, none of the control, untreated patients with CAH-B had any change in either HBV markers or serum ALT levels. Therefore, even a short course of prednisone in patients with CAH-B with cirrhosis is detrimental and its use should be discouraged.
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PMID:Effects of short-term, high-dose prednisone treatment of patients with HBsAg-positive chronic active hepatitis. 388 51

We compared the clinical and serologic features of 118 hepatitis B surface antigen carriers with hepatitis B e antibody (anti-HBe) followed up for 3-10 yr (mean 6.1 yr), separated according to the presence or absence of hepatitis B virus-deoxyribonucleic acid (HBV-DNA) in serum. The test was performed by molecular hybridization. There were 28 carriers with and 90 without viral DNA. Carriers with serum anti-HBe/HBV-DNA had major liver disease; cirrhosis developed during the follow-up period in 9 of the patients. All had the hepatitis B "core" antigen in the liver, localized prevalently in the cytoplasm of the hepatocytes. Among carriers of anti-HBe alone, 73 had persistently normal tests of liver function and 17 had abnormal levels of alanine transaminase and usually minor forms of liver damage at histology. In a group of 24 carriers of hepatitis B e antigen who spontaneously seroconverted to anti-HBe, hepatitis and a prevalent nuclear distribution of intrahepatic hepatitis B core antigen were found in temporal correlation with the presence of hepatitis B e antigen in serum. The replication of the hepatitis B virion terminated and liver disease remitted after seroconversion to anti-HBe. A positive HBV-DNA test in anti-HBe carriers is associated with a severe and evolutive liver disease and may provide an indication for treatment with drugs inhibiting the synthesis of HBV-DNA.
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PMID:Chronic hepatitis in HBsAg carriers with serum HBV-DNA and anti-HBe. 395 45

Little is known about the replicative forms of hepatitis B virus (HBV) in the liver in chronic liver disease. We therefore analyzed HBV DNA and the changes in DNA signals after endonuclease digestion in liver tissues taken from 64 patients with hepatitis B surface antigen-positive chronic liver disease. The "active" replication pattern, which included various replicative intermediates, was seen in 36 of 38 (95%) hepatitis B e antigen-seropositive patients. This pattern was also found in 5 of 26 (19%) hepatitis B e antigen-seronegative patients who showed the highest mean serum alanine aminotransferase level (403 +/- 184 mU/ml). Most of them had advanced liver disease. Episomal viral DNA of an "inactive" type having only the supercoiled form was found in 3 patients; they showed the lowest mean serum alanine aminotransferase level (27 +/- 7 mU/ml) and only mild liver disease. As with duck HBV infection, episomal replicative forms of human HBV could be resolved by Southern blot analysis and seem to have clinical implications in human HBV infection.
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PMID:Active and inactive replication of hepatitis B virus deoxyribonucleic acid in chronic liver disease. 401 3

Peripheral T-cell subsets in 77 patients with hepatitis B surface antigen (HBsAg)-positive chronic liver diseases were studied by indirect immunofluorescence using murine monoclonal antibodies against all peripheral T cells (OKT3), T-helper/inducer cells (OKT4), and T-cytoxic/suppressor cells (OKT8). OKT4/OKT8 ratios were significantly reduced in patients with hepatitis B e antigen (HBeAg)-positive chronic liver diseases, including 28 patients with chronic active hepatitis (CAH) (P less than 0.001) and 15 with chronic persistent hepatitis (CPH) (P less than 0.001). OKT4/OKT8 ratios were significantly lower in 21 HBeAg-negative patients with CAH (P less than 0.05), as compared to those of 17 normal controls, while T-cell subsets in 13 patients with HBeAg-negative CPH were essentially normal. Low OKT4/OKT8 ratios significantly correlated with HBeAg positivity (P less than 0.001) and CAH (P less than 0.05), as assessed with multiple regression. There was a significant negative correlation between OKT4/OKT8 ratios and serum glutamic-pyruvic transaminase (SGPT) levels (r = -0.37; P less than 0.01). It was concluded that in chronic hepatitis B virus infection, low OKT4/OKT8 ratios are closely related to active viral replication and more severe histological and biochemical activity.
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PMID:Peripheral T-cell subsets in chronic type B hepatitis: correlation with biochemical and histological activities and hepatitis B e antigen/antibody status. 623 72

The relationship between glutaraldehyde-treated polymeryzed human serum albumin (pHSA) and HBe antigen (HBeAg)-positive serum was examined by the use of a new enzyme-linked immunosorbent assay (ELISA). The author succeeded in measuring the pHSA binding activity (pHSA-BA) of HB surface antigen (HBsAg) particles in the present ELISA method using horseradish peroxidase-labelled pHSA after fixation of HBsAg on an anti-HBs-coated well of polystyrene microplates. In HBeAg-positive group, the pHSA-BA of sera of 40 asymptomatic carriers and 2 chronic persistent hepatitis (CPH) patients were higher than those of 8 chronic active hepatitis (CAH) (p less than 0.01) and 8 liver cirrhosis sera (p less than 0.05). On the contrary, in the anti-HBe-positive group the pHSA-BA of 17 asymptomatic carriers and 3 CPH sera were lower than those of 8 CAH (p less than 0.005) and 10 liver cirrhosis patient sera (p less than 0.005). In the both-negative group the pHSA-BA of 8 asymptomatic carrier and 3 CPH sera were also lower than that of 8 CAH (p less than 0.05). In acute exacerbation of HBsAg-positive CAH the pHSA-BA elevated one to two months before the peak of S-GPT level, being correlated with the DNA-polymerase activity. Because of its apparent reproducibility, it is concluded that low cost and some advantages may have clinical utility in the same setting as the HBeAg is now used.
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PMID:Detection of serum albumin receptor in hepatitis B virus carriers by enzyme-linked immunosorbent assay. 629 49

Delta antigen was detected by means of direct immunofluorescence in the liver of 20 out of 118 chronic carriers of hepatitis B surface antigen (HBsAg). Delta antigen was frequently found in young chronic HBsAg carriers with chronic active hepatitis. Positivity for anti-HBe occurred in almost all cases. A peculiar aspect of delta infection was a predominance in patients from Southern, rather than from Northern or Central Italy. Another interesting finding is the higher mean values of GOT and GPT in delta-positive patients compared with those in delta-negative patients. The follow-up of some patients confirmed that chronic delta hepatitis is a particularly progressive disease.
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PMID:Chronic delta hepatitis: a difficult problem for the hepatologist. 638 95


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