Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the agglutination of sheep red cells by human antibodies as an indicator of microbial antibody activity, a highly significant association was found between the response to the e antigen of the hepatitis B virus and the formation of strong antibody levels to microbial substances (chi 2(1) = 33). This kind of association was not found among chronic carriers of the hepatitis B virus who do not produce antibodies to the e antigen (chi 2(1) = 3,7). In the presence of e antigen activity, patients with acute virus B hepatitis almost always show significantly reduced levels of antibodies to microbial substances (chi 2(1) = 20). The findings indirectly reveal that e activity is associated with the inability of the liver to trap bacterial antigens. Circumstantial evidence further suggests that the e factor may bear antigens on its immunoglobulin-like structure very similar to microbial cell wall components. Accepting that human antibodies to the T (Thomsen-Friedenreich) antigen represent reactions to cryptantigenic membrane structure of autologous tissues, it was significant to record that increased anti-t activity is always demonstrated when virus B infections progress from the acute to the chronic carrier stage (chi 2(1) = 73). The most intense anti-T activity is commonly found in subjects who produce antibodies to the hepatitis B surface antigen (chi 2(1) = 138). In the presence of e antigen the amount of anti-T in circulation is always significantly depressed. Since this type of depression is not seen in patients with acute virus B hepatitis who lack the e antigen, we suspect that the reduced anti-T levels in e antigen-positive patients are linked with the in vivo exposure of T receptors by microbial neuraminidase.
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PMID:Hepatic infections. Part II. The effect of acute and chronic hepatitis B antigenaemia on the reaction to antibodies to sheep red cells (microbial antigens) and human T-activated cells (exposed autologous tissue antigens). 31 18

Significant percentages of patients suffering from non-A non-B hepatitis (43%) and B hepatitis (35%) were found to release an Ig-binding factor in their stools. This factor, which we called "protein F" was less frequently observed (20%) in patients suffering from other liver disorders, and was found in only 6.7% of healthy subjects (p less than 10(-7), less than 10(-4), and less than 0.03, respectively). The specificity of the detection test (a nonimmune ELISA-like assay) was confirmed by inhibition experiments. Binding was located on the F(ab) fragment of Ig, irrespectively of their isotype. Protein F was inactivated by pepsin, neuraminidase, and high concentrations of subtilisin, whereas it was resistant to trypsin and chymotrypsin. Molecular sieving by HPLC indicated an apparent molecular mass of 175 kDa. In preparative SDS-PAGE, the molecular mass was 85 kDa in favor of a dimer disrupted under dissociating conditions. Preparative IEF showed the isoelectric charge to lie between 3.9 and 4.1. Analysis of liver extracts from two patients suffering fron non-A non-B hepatitis, and from a transplant donor, revealed the presence of the factor in the three cases.
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PMID:Protein F. A novel F(ab)-binding factor, present in normal liver, and largely released in the digestive tract during hepatitis. 224 21

Four murine MoAbs, KM191(IgM), KM206(IgM), KM230(IgG1) and KM231(IgG1), against human gastric cancer were generated using mice which underwent tolerance treatment to stomach tissues. They exhibited very similar high reactivities to stomach adenocarcinoma cells and low reactivities to normal cells in both membrane binding assay and immunohistochemical analysis. Their antigens were neuraminidase and protease sensitive and existed as macromolecules (1,000Kd) in body fluids. Binding of each antibody was inhibited by the others and KM231 showed the highest binding avidity. When they were used to detect the antigens shed in ascitic fluids and pleural effusions of cancer patients, KM231 allowed the most efficient detection of the antigen. The above results indicated that the four MoAbs bound to closely related epitopes on the same antigen and that the nature of its high binding avidity enabled KM231 to show the greatest efficiency in the detection of the antigen in body fluids. KM231 was applied to serum diagnosis and gave high positive percentages in pancreatic cancer(86%), hepatocarcinoma(87%), gall bladder cancer(50%), and gastric cancer(34%), whereas in healthy persons (0%) and benign diseases except for hepatitis(29%) the percentages were low. KM231 was similar to NS19-9, but quite different from NS19-9 in the high positive percentages of hepatocarcinoma in serum diagnosis.
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PMID:Comparative studies on monoclonal antibodies raised against human gastric cancer for application to serum diagnosis of cancer. 245 69

1. The LEC rats, a novel animal model of hepatitis and liver tumor, were found to have charge variants of serum alpha 1-antitrypsin (alpha 1AT) at the stage of liver tumor as judged by isoelectric focusing. 2. Treatment of the sera with neuraminidase showed that acidic variants of alpha 1AT in LEC rats seemed to be highly sialylated forms. 3. The concentration and enzymatic activity of serum alpha 1AT in LEC rats were not affected before the onset of hepatitis and even during the development of fulminant hepatitis and hepatocarcinogenesis. This indicates that hereditary hepatitis and subsequent liver tumor in LEC rats do not appear to be associated with alpha 1AT deficiency.
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PMID:Hepatoma-associated alterations of serum alpha 1-antitrypsin in hereditary hepatitis LEC rats as a new animal model of liver disease. 285 94

Australia antigen [Au(1)], a particle associated with viral hepatitis, was isolated from the plasma of a patient with chronic anicteric hepatitis and leukemia who had received radioactive phosphorus. We have found that the immunoreactivity and appearance of Au(1) in the electron microscope were not altered by treatment with enzymes including trypsin, pronase, lipase, phospholipase C, ribonuclease, deoxyribonuclease, amylase, and neuraminidase. In contrast, other serum constituents were degraded by these enzymes. Therefore, treatment of the patient's plasma with many enzymes was exploited as an initial step for the isolation of Au(1). Subsequently, Au(1) was purified from the enzyme-treated (32)P-labeled plasma by gel filtration through Sephadex G-200 and centrifugation through sucrose and in cesium chloride gradients. There were no detectable human serum components in the purest fractions, as tested by immunoelectrophoresis and immunodiffusion. The density of the purified Au(1) was 1.21 in CsCl. The particle measured about 200 A in diameter, was predominantly spherical in shape and appeared to be composed of subunits. Nucleic acids were not detected by spectrophotometric, radiochemical, and chemical analyses. Immunoreactivity of purified Au(1) was destroyed by heating for 1 hr at 85 degrees C but was stable at 56 degrees C. Treatment with Carnoy's solution (3 parts ethanol:1 part glacial acetic acid) followed by pronase disrupted the particles as seen with the electron microscope. These findings, combined with other published information on Australia antigen and viral hepatitis, suggest that the bulk of Australia antigen in the blood of this patient is an incomplete virus or virus capsid.
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PMID:Australia antigen (a hepatitis-associated antigen): purification and physical properties. 424 40

The addition of excess sodium citrate to plasma was found to inhibit fibrin polymerisation (clot opacity) from patients with cirrhosis, hepatitis and hepatoma but not from normal controls. Abnormal clot opacity in plasma from patients with liver disease could be partly or completely abolished by removal of citrate ions by dialysis against citrate-free buffer, but not by dialysis against buffer containing citrate. Similar results were observed in plasma freed of calcium ions by treatment with EGTA. Treatment of plasma with neuraminidase largely abolished the inhibitory effect of excess citrate, and the thrombin times and clot opacity of asialofibrinogen were less affected by citrate than native fibrinogen. In addition, the effects of citrate on the clotting of purified, calcium-free fibrinogen from cirrhotic patients correlated with the sialic acid content. It is concluded that binding of citrate ions to fibrinogen renders the molecule acutely more sensitive to elevations in the sialic acid content, and that a simple plasma clot opacity test in the presence of excess citrate may be a useful aid in the differential diagnosis of liver disease. These findings may also explain why defects in fibrin polymerisation observed in plasma are not always reproduced in purified fibrinogen or fibrin monomer preparations.
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PMID:The role of sodium citrate in the dysfibrinogenaemia of liver disease. 672 77

The presence of liver IgG Fc receptor sites was demonstrated in the liver tissue from 23 patients with liver diseases and 2 patients without liver lesions by the localization of soluble immune complexes of peroxidase-antiperoxidase (PAP). Cryostat sections of liver tissues were incubated with the complexes and the peroxidase activity was revealed histochemically. In the normal liver tissue, PAP were localized on the liver cell membrane, the Kupffer cells, and some of the sinusoidal walls. In acute hepatitis, a strongly positive reaction on swollen Kupffer cells was remarkable but positive reaction on the liver cell membrane was very weak. In chronic aggressive hepatitis, PAP were strongly positive on multiplied Kupffer cells and many PAP-positive infiltrated cells were observed at the area of piecemeal necrosis. However, the positive reaction on the liver cell membrane in patients with chronic aggressive hepatitis was generally fainter than in the normal cases without liver diseases. These results correlated well with the severity of liver cell necrosis. In chronic persistent hepatitis, the number of PAP-positive infiltrated cells in the portal area and positive Kupffer cells were fewer than in chronic aggressive hepatitis. Similar results were obtained with liver cirrhosis, and in particular, the liver cell membrane with regenerative nodules gave a positive reaction. A negative result was obtained by incubation with PAP-F(ab')2 alone. PAP reaction was significantly inhibited by pretreatment with aggregated human IgG, trypsin, and pronase but not with neuraminidase.
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PMID:Detection of liver IgG Fc receptors using soluble immune complexes of peroxidase-antiperoxidase. I. Detection in liver tissue from patients with liver diseases. 701 47

Serum alpha-fetoprotein (AFP) from cord blood and from patients with hepatitis, cirrhosis, hepatocellular carcinoma, gastrointestinal tumors and yolk sac tumor was analyzed by extended agarose gel electrophoresis coupled with our sensitive detection method of antibody-affinity blotting. AFP was separated into AFP-A, AFP-B and AFP-C from the anode to the cathode, corresponding to disialo-, monosialo- and asialo-AFP, respectively, as revealed by the results of neuraminidase digestion of serum AFP. AFP-Af, which migrated ahead of AFP-A as band or leading smear and varied widely in intensity, was eliminated in calculating the proportions of other band intensities. Disialo-AFP was the major component and monosialo-AFP the minor one in benign conditions, the latter being 4.2 +/- 6.0% in chronic hepatitis and 9.0 +/- 8.9% in cirrhosis. Monosialo-AFP in hepatocellular carcinoma was increased significantly, the proportion being 29.9 +/- 11.2%. AFP in other malignancies was further characterized by the appearance of asialo-AFP.
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PMID:Increased serum levels of monosialo-alpha-fetoprotein in hepatocellular carcinoma and other malignancies. 769 51

Sera from 14 normal control subjects, 30 patients with alcoholic liver diseases (fatty liver, n = 8; hepatitis, n = 13; liver cirrhosis, n = 9), 7 controls with chronic hepatitis B, and 8 controls with chronic hepatitis C were masured for their concentrations of antibodies against HepG2 membrane protein by a binding assay utilizing 125I-labeled protein A. When the cut-off level was set as the mean value plus 2 SD of normal control subjects, the incidence of positivity was 75%, 69.2%, and 77.8% in patients with alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis, respectively. Both the mean serum antibody values and the positive incidence were significantly higher in patients with alcoholic liver diseases than in either the normal controls or in the control patients with chronic hepatitis. Sodium dodecylsulfate polyacrylamide gel electrophoresis of 125I-labeled HepG2 membrane protein precipitated with IgG from patients with alcoholic liver diseases revealed an immunoreactive band at a molecular weight of 78,000 daltons (gp78). The antibody activity remained after immunoabsorption by human liver-specific lipoprotein (LSP) but decreased when HepG2 cells were pre-treated with trypsin or neuraminidase. Consequently, gp78 appears to be a glycoprotein distinct from LSP, and is specifically recognized by IgG from patients with alcoholic liver diseases. This assay may provide a new system to measure autoantibody to hepatocytes in alcoholic liver diseases.
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PMID:Autoantibody against a 78 kDa membrane protein of HepG2 cell in the sera of patients with alcoholic liver diseases. 896 93

Haptoglobin phenotypes have been shown in human medicine to be related to the prevalence of various diseases. Furthermore, abnormal glycosylation of haptoglobin has been reported as a consequence of liver disease, cancer and immunological disorders in man. To our knowledge, similar findings have not, so far, been reported in canine disease. The present paper describes a method for investigation of canine haptoglobin phenotypes and of microheterogeneity caused by altered glycosylation. The method consisted of isoelectric focusing (IEF) of dog serum, followed by immunoblotting. The results indicated the existence of only one canine haptoglobin phenotype with a characteristic microheterogeneity pattern in healthy dogs. Changes in this pattern were found in serum from dogs with liver disease, predominantly chronic progressive hepatitis, and with different kinds of anaemia. Pretreatment of serum with neuraminidase or glycopeptidase F (PNGase F) resulted in identical IEF patterns of haptoglobin from healthy and diseased dogs. Moreover, a fucose-specific lectin was capable of binding to some of the abnormal haptoglobin fractions, mainly those found in association with anaemia. The changes described were interpreted as alterations of the carbohydrate content, with or without fucosylation, of some haptoglobin fractions.
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PMID:Disease-related variations of the glycosylation of haptoglobin in the dog. 980 25


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