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)

In confirmation of earlier descriptions by Huang et al. (Huang S-N, Millman I, O'Connell A, Aronoff A, Gault H, Blumberg BS: Am J Pathol 67: 453, 1972) nuclear eosinophilic inclusions due to excess HBcAg particles have been identified in cases of chronic hepatitis B virus infection. As the euchromatin space of affected nuclei is "sanded" by numerous core particles with concomitant dissolution of the chromatin network, spiky, finely granular, and eosinophilic inclusions without a limiting membrane become visible in hematoxylin and eosin-stained paraffin sections. These HBcAg inclusions stain greyish pink with chromotrope aniline blue and are negative for orcein, the periodic acid-Schiff reaction, and the Feulgen reaction for DNA. Sanded nuclei were detected, although not always and only few in number, exclusively in HBAg-positive patients when a focal (as in chronic aggressive hepatitis) or a generalized core formation (as in immunosuppressed kidney transplant recipients) could be demonstrated by electron microscopy or immunofluorescence. Therefore, the positive finding of sanded nuclei in a persistent hepatitis B virus infection indicates an excessive core formation the extent of which should be verified by specific methods.
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PMID:Sanded nuclei in hepatitis B: eosinophilic inclusions in liver cell nuclei due to excess in hepatitis B core antigen formation. 78 2

This study reproduces in experimental animals the sequential development of all the liver lesions seen in the human alcoholic: in 15 baboons fed ethanol, all developed fatty liver, five progressed to hepatitis, and five had cirrhosis. Maintenance of a nutritionally adequate regimen despite the intake of inebriating amounts of ethanol (50% of total calories) was achieved by incorporation of the ethanol in a totally liquid diet. Upon ethanol withdrawal, signs of physical dependence, such as seizures and tremors, developed. Ultrastructural changes of the mitochondria and the endoplasmic reticulum were already present at the fatty liver stage and persisted throughout the hepatitis and cirrhosis. The lesions were similar to those observed in alcoholics (including the inflammation and the central sclerosis) and differed from the alterations produced by choline and protein defiencies. At the fatty liver stage, some "adaptive" increases in activity of microsomal enzymes [aniline hydroxylase (EC 1.14.14.1) and the microsomal ethanol oxidizing system] were observed, but these tended to disappear with the development of hepatitis and cirrhosis. Fat accumulation was also much more pronounced in the animals with the hepatitis as compared with those with simple fatty liver (an 18-fold compared with 3- to 4-fold increase in liver triglycerides). The demonstration that these lesions can develop despite an adequate diet indicates that in addition to correction of the nutritional status, control of alcohol intake is mandatory for the management of patients with alcoholic liver injury.
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PMID:Sequential production of fatty liver, hepatitis, and cirrhosis in sub-human primates fed ethanol with adequate diets. 105 27

Clinical studies are performed on 15 workers from the chemical and pharmaceutic plant "Stanke Dimitrov". Seven of the workers are with acute poisoning from aniline and phenylhydrazine, and eight are exposed to a chronic combined effect of a large group of organic solvents. The clinic and laboratory examinations aim at clarifying the liver and kidney functions, the state of the blood and nervous systems. The tests embrace also blood test morphology and osmotic resistance of erythrocytes, iron, correlation of haemoglobin types, electrolytes, transaminase, GGTP, lipid metabolism, iron-binding capacity. Moderately increased transaminase activity is found in 2/3 of the examined. In four of the workers is registered expressed anaemic and lung syndrome. The following diagnoses are accepted: chronic combined effect of organic solvents--in 3 workers; chronic poisoning with aniline and other solvents--in 1; toxic hepatitis--in 4, with no data for poisoning--in 7. The leading clinical syndromes in acute and chronic combined effect of organic solvents are discussed.
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PMID:[Toxic lesions in workers in the pharmaceutical industry]. 136 44

The hepatoprotective agents silybinin, essentiale and eplir (the complex of phospholipids and caratinoids from the mud) prevent in D-galactosamine-induced intoxication of rats the development of hepatitis, hepatocyte necrosis, a decrease in hepatocytes of the activity of the enzymes of mitochondria and endoplasmic reticulum, labilization of lysosomes. These drugs stimulate D-galactosamine-suppressed antitoxic function of the liver: they increase the contents of RNA, cytochromes P-450, b5, the activity of amidopyrine-D-demethylase, hydroxylases of hexobarbital and aniline, improve the activity of the respiratory chain of microsomes, counteract inactivation of cytochrome P-450 into cytochrome P-420. Essentiale and eplir activate conjugation of xenobiotics with reduced glutathione.
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PMID:[The correction with hepatic protectors of structural metabolic disorders in the liver in D-galactosamine poisoning]. 236 52

Adult female B6C3F1 mice were gavaged with 4,4'-thiobis-(6-t-butyl-m-cresol) (TBBC) in corn oil at doses of 10, 100, or 200 mg/kg daily for 14 consecutive days. There was no overt toxicity, as manifested by grossly observable behavioral changes, decreased growth rate over the exposure period, or mortality. There were also no marked effects on serum chemistries or hematology, with the exception of a significant increase (41%) in the number of leukocytes at the highest dose. Absolute differential counts indicated that significant increases occurred in the number of lymphocytes (31%) and neutrophils (177%). Studies with bone marrow indicated a significant 30% increase in the number of cells/femur from animals treated with the highest dose of TBBC. The number of macrophage progenitors (CFU-M)/femur was significantly increased by 28%, while the number of granulocyte-monocyte progenitors (CFU-GM)/femur was nonsignificantly increased by 20% in the high dose animals. The weight of both the spleen and liver was increased in a dose-related fashion, although the histopathology of the spleen of TBBC-treated mice was not different from control. The livers of mice receiving the high dose showed mild focal hydropic degeneration, mild hepatitis, and a slight increase in the number of Kupffer cells. No other organs were affected. Liver microsomal protein and cytochrome P-450 levels were increased in a dose-related fashion. Enzyme activities of aminopyrine demethylase and aniline hydroxylase, but not arylhydrocarbon hydroxylase, were also increased in a dose-related fashion.
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PMID:An immunotoxicological evaluation of 4,4'-thiobis-(6-t-butyl-m-cresol) in female B6C3F1 mice. 1. Body and organ weights, hematology, serum chemistries, bone marrow cellularity, and hepatic microsomal parameters. 339 95

We have investigated in detail the higher order structure of the genomic hepatitis delta virus (HDV) ribozyme using various base-specific chemical probes under native, semi-denaturing, and denaturing conditions. The bases of the HDV ribozyme were probed by treatment with dimethyl sulfate [which reacts with A (at N1) and C (at N3)] and a carbodiimide [which reacts with U (at N3) and G (at N1)]. In addition, for probing G residues (at N7), RNA samples were treated with NaBH4 and aniline after modification by treatment with dimethyl sulfate. The sites of modified positions were identified by primer extension analysis with reverse transcriptase. In general, our results are consistent with the proposed pseudoknot model of secondary structure, a model that is based on data from ribonucleolytic cleavage experiments. Our results provide clues to the identification of interacting bases in the HDV ribozyme. Furthermore, using this method we identified local conformational changes in several stem variants.
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PMID:Chemical probing studies of variants of the genomic hepatitis delta virus ribozyme by primer extension analysis. 828 89

We attempted to produce a model mouse with a liver injury resulting from an immunological mechanism in C57BL/6J mice, and the effect of hepatitis on the hepatic microsomal mixed-function oxidase system was studied. An experimental immunological liver injury model was caused by the intravenous injection of an anti-basic liver protein (BLP) antibody in mice which had been previously immunized with normal rabbit IgG (RGG) and complete Freund's adjuvant. C57BL/6J strain mice showed the highest susceptibility to the immunological liver injury. Typical histopathological changes in the liver included submassive hepatocellular necrosis and infiltration of lymphocytes into the portal tract and sinusoid area in a necrotic lesion. The liver injury in this model was markedly inhibited by the administration of prednisolone (20 mg/kg, p.o.), cyclophosphamide (15 mg/kg, i.p.), levamisole (10 mg/kg, p.o.), glycyrrhizin (50 mg/kg, i.p.) and cepharanthine (10 mg/kg, i.p.), which act on the immune system. Twenty-four hours after the injection of anti-BLP antibody, the activities of aminopyrine N-demethylase, aniline hydroxylase and NADPH-cytochrome c reductase and the content of cytochrome P-450 were mostly reduced, whereas cytochrome b5 and NADH-ferricyanide reductase were not. These results suggest that the experimental liver injury model in C57BL/6J mice is useful as a model of liver injury model, and its hepatitis was shown to inhibit the cytochrome P-450-dependent biotransformation of drugs in the mouse.
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PMID:Effect of anti-basic liver protein antibody-induced liver injury on hepatic drug-metabolizing enzymes in C57 BL/6J mice. 828 50

The professionals and patients involved in dental examinations are at risk for infection by various disease-causing bacteria, viruses, and fungi, such as those responsible for hepatitis, tuberculosis, herpes, and AIDS. It is known that aerosols and spatter containing pathogenic microorganisms can spread during an examination. Nevertheless, some dental clinics are designed to have multiple examination areas in the same room, with no physical barriers between them. The objective of this study was to verify the reach of spatter resulting from the use of a triple syringe and high-rotation turbine during five simulated exams in a collective clinic, bearing in mind that spatter can contain the patient's saliva and blood. To facilitate tracking of the spatter, aniline dye (pink, blue, yellow, green, and brown) was added to the water in the appropriate receptacle in each of the five units. The room, the equipment, and the patient's and operator's clothing were covered with white paper. A high concentration of spatter was observed on the chair, the operator, and the floor of each unit, and it also appeared on the chairs and trays of the surrounding units. The maximum distance reached by spatter was 1.82 m from a point on the chair corresponding to the position of the patient's mouth. During real simultaneous examinations, the surrounding chairs and their patients and operators, as well as the trays containing sterilized instruments, are within spatter range. Therefore, there is a real possibility of cross-infection, and physical barriers should be placed between the units. This study also confirmed the need for protection of the operator's face, body, hair, and arms, since these regions were heavily affected by spatter.
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PMID:[Determination of the dispersion of microorganisms in the course of dental surgical activity]. 954 44

Aim of this study was to determine and further characterize the serum aminopeptidase-M in children with liver diseases. Based on our new assay, we have shown two fractions of the enzyme. Activity of the first fraction is expressed in undiluted serum at pH adjusted from 8.5 (pH of storaged serum) to 7.4. Activity of the second fraction (cryptic activity) appears in the serum (pH 7.4) as a result of dilution and/or addition of aniline naphthalene sulfonic acid. In children with Alagille syndrome, extrahepatic biliary duct atresia, Byler's disease, and acute hepatitis due to hepatitis B virus infection, activities of both fractions are highly elevated as compared to healthy children or those with chronic viral hepatitis. Moreover, serum aminopeptidase-M seems to reflect other aspects of the pathological process than those reflected by the alanine aminotransferase and gamma-glutamyltranspeptidase. Due to increased activity and broad substrate specificity, the enzyme seems to be also a cofactor of cholestasis and hepatitis.
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PMID:Further studies on aminopeptidase-M in blood in children with cholestatic liver diseases and viral hepatitis. 995 39

To investigate the role of nitric oxide (NO) in hepatitis-induced endotoxemia, we injected mice intraperitoneally with 250 mg/kg galactosamine (GalN) and 1 mg/kg lipopolysaccharide (LPS) separately and in combination. NO synthesis increased in a dose-dependent manner with LPS. NO generation at 5 hr after administration of LPS was greater than that at 24 hr. Enhancement of NO generation was demonstrated in mice administered GalN and LPS in combination. A nitrosyl-heme signal in 10,000 g supernatant of liver homogenate, due to cytochrome P450 (P450) combining with NO, NO-P450, was detected at more than ten hr and even more after administration of LPS by electron spin resonance (ESR) measurements at 77 degrees K. The strongest NO-P450 signal and most extreme elevation of aspartate oxoglutarate aminotransferase (AST), alanine oxoglutarate aminotransferase (ALT), and lactate dehydrogenase (LDH) in serum and of lysosomal enzyme activity in plasma were observed in the GalN + LPS group. Their potency was greater than in the 10 mg/kg LPS group, which was even greater than in the LPS 1 mg/kg group. The aniline hydroxylase activity was inversely proportional to NO-P450 signal intensity. It appears that NO might contribute to LPS-induced hepatic damage in GalN-sensitized mice through degeneration and inactivation of liver microsomal enzymes by binding P450 active sites.
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PMID:NO contribution to lipopolysaccharide-induced hepatic damage in galactosamine-sensitized mice. 1007 39


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