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)

Long-Evans Cinnamon (LEC) rats, characterized by a gross accumulation of hepatic Cu and the spontaneous onset of hepatitis, have been established to be an animal model for Wilson disease. They were used to estimate the relationships among copper (Cu), metallothionein (MT), and reduced glutathione (GSH) in biliary excretion in this study. Even though a huge amount of MT existed in the LEC rat liver (5016 micrograms/g liver) compared to that (63 micrograms/g liver) of controls (Fischer rats), the biliary excretion of MT (65 ng/ml bile) did not reflect the accumulated MT level in LEC rats. It seems likely that MT does not excrete intrinsically into the bile. Biliary excretion of Cu (0.17 microgram/ml) in LEC rats was significantly lower than that (0.57 microgram/ml) in Fischer rats. The difference in biliary excretion of GSH between the two groups was significant but slight. The reduced excretion of GSH into bile in LEC rats may be due to increased hepatic gamma-glutamyltransferase but not to hepatic GSH levels. There were no differences in biliary potassium and inorganic phosphorous between the two groups. On the other hand, excretion of lysosomal enzymes such as beta-N-acetylglucosaminidase into bile was much lower in LEC rats (15.6 units/liter) than in controls (42.5 units/liter). The defective biliary excretion of Cu may be due to impaired lysosomal exocytosis, rather than canalicular membrane impairment. The LEC rat is very useful for research into the dynamics of metal excretion via the hepatobiliary system.
Biochem Mol Med 1995 Jun
PMID:Biliary excretion of copper, metallothionein, and glutathione into Long-Evans Cinnamon rats: a convincing animal model for Wilson disease. 755 24

The use of nucleic acid amplification techniques within the medical microbiology laboratory is becoming more and more accepted. Polymerase chain reaction (PCR) tests or nucleic acid sequence based amplification (NASBA) assays are already available in the form of commercial kits. Although the technology has been adapted for application in a routine diagnostic setting, some of the systems' characteristics are still amenable to improvement. In this communication several of these aspects will be discussed. Reproducibility of DNA amplification mediated diagnostics and quality control of tests aiming at detection or genetic typing of both viral and bacterial microorganisms, will be discussed. This will be exemplified by the results obtained in multicenter studies on PCR diagnostics of the hepatitis viruses HBV and HCV and by data gathered in the course of PCR mediated DNA fingerprinting of Staphylococcus aureus strains, also performed in different institutes. Application of related techniques such as direct sequencing of amplified (c)DNA or the development of species-specific DNA probes will be described.
Cell Mol Biol (Noisy-le-grand) 1995 Jul
PMID:Nucleic acid amplification and related techniques in microbiological diagnostics and epidemiology. 758 Aug 42

The decision about what operators to allow and how to charge for these operations when aligning strings that arise in a biological context is the decision about what model of evolution to assume. Frequently the operators used to construct an alignment between biological sequences are limited to deletion, insertion, or replacement of a character or block of characters, but there is biological evidence for the evolutionary operations of exchanging the positions of two segments in a sequence and the replacement of a segment by its reversed complement. In this paper we describe a family of heuristics designed to compute alignments of biological sequences assuming a model of evolution with swaps and inversions. The heuristics will necessarily be approximate since the appropriate way to charge for the evolutionary events (delete, insert, substitute, swap, and invert) is not known. The paper concludes with a pairwise comparison of 20 Picornavirus genomes, and a detailed comparison of the hepatitis delta virus with the citrus exocortis viroid.
Proc Int Conf Intell Syst Mol Biol 1994
PMID:Aligning genomes with inversions and swaps. 758 91

Nitric oxide is now established as a biological mediator of clinical relevance. The present study investigated the production of nitric oxide by lympho-mononuclear leukocytes from alcoholic patients with either hepatitis or cirrhosis. The study included 42 patients, 12 without any liver disease and 30 alcoholic patients, 13 of whom had histologically confirmed cirrhosis and 17 alcoholic hepatitis. Cells were obtained from peripheral blood by density gradient and incubated in sterile conditions in RPMI 1640 for 6 h at 37 degrees C. Culture supernatants were assayed for nitrite concentration using the Griess reaction. Cells from cirrhotic but not from hepatopathic patients showed significantly higher nitrite production than controls (cirrhotic, 0.36 +/- 0.07; hepatopathic, 0.13 +/- 0.02; control: 0.25 +/- 0.05 nmol/10(6) cells/6 h). In cirrhotic patients L-Nitro-arginine methylester inhibited nitrite production (0.18 +/- 0.05). These data suggest that alcoholic cirrhotic but nonhepatopathic patients show an increased nitric oxide production by blood lymphomononuclear cells. This production could be involved in the systemic vasodilation in cirrhotic patients.
J Mol Med (Berl) 1995 Jan
PMID:Nitric oxide production by mononuclear leukocytes in alcoholic cirrhosis. 763 39

Particulate and denatured core protein as well as e-antigen (HBe) of hepatitis B virus (HBV) differ in part immunologically but this has not been studied in sufficient detail. Therefore, in this study the B-cell immune response to native and denatured HBV core protein which both can exhibit HBe-specific epitopes was examined using a panel of mouse MABs and rabbit polyclonal antibodies to native and denatured core protein and polyclonal anti-HBe/anti-HBc antibodies from sera of infected patients. Epitope mapping was performed using a set of partially overlapping synthetic HBc peptides, carboxy-terminally truncated HBc proteins and various HBc fusion proteins. A major immunogenic region between amino acids 134-140 and two less immunogenic regions, one spanning amino acids 2-10 and one with three partially overlapping epitopes between amino acid positions 138 and 154, were defined by mouse MABs. Polyclonal rabbit antibodies to denatured HBc, woodchuck and ground squirrel hepatitis core proteins (WHc and GSHc) recognized similar epitopes but in addition occasionally region 61-85, and the latter was also recognized on particulate HBc. Two antigenic regions (amino acid positions 2-10 and 138-145) were found to be exposed on HBe from human serum, and were recognized by mouse anti-HBe but not by anti-HBc antibodies from sera of infected patients. This study demonstrates a more complex pattern of HBc and HBe epitopes than detected previously and provides tools to study conformational changes which may take place during HBc/HBe processing, transport and core particle assembly.
Mol Immunol 1993 Feb
PMID:Epitopes recognized by antibodies to denatured core protein of hepatitis B virus. 767 66

The aim of the present study was to determine, in a population of 70 HIV-1 infected patients with antibodies to HCV, the percentages of individuals with an active replication of HIV-1, HCV or both. During a one year follow-up of these patients at different stages of disease, blood samples were regularly collected for determination of transaminase, beta 2 microglobulin and CD4+ lymphocytes. Total RNAs were extracted from the sera, retrotranscribed with MoMuLV reverse transcriptase and nested PCR assays were carried out separately with sets of primers homologous to the 5' non-translated region of HCV and in HIV-1 gag. The amplified products were subjected to electrophoresis and observed under u.v. illumination after staining with ethidium bromide. For some samples, the identity of the amplified products was confirmed by Southern blotting by hybridization with enzyme-labelled probes. A total of 57% of the patients were found to produce HIV-1 RNA and 62% HCV RNA, while 34% produced both. HIV-1 RNA production was correlated with beta 2 microglobulin and CD4+ levels; active replication of HCV was correlated with hepatitis but not with CD4+ levels nor with HIV-1 RNA synthesis.
Mol Cell Probes 1993 Oct
PMID:HIV-1 and HCV co-infected patients: detection of active viral expression using a nested polymerase chain reaction. 790 23

Synergy between exposure to chemical carcinogens (nitrosamines) and infestation with the liver fluke Opisthorchis viverrini has been demonstrated in a hamster model of hepatocarcinogenesis (Flavell et al., Carcinogenesis 4:927-930, 1983; Thamavit et al., Carcinogenesis 8:1351-1353, 1987). To elucidate the mechanisms of this interaction we tested the hypothesis that liver parasitism might influence the expression and activity of carcinogen metabolizing enzymes. We found that one, and perhaps more, hamster liver cytochrome P450 (CYP) isozymes immunorelated to mouse CYP2A5 contributed up to 50 or 60% of the hepatic aflatoxin B1 (AFB) and N-nitrosodiethylamine (NDEA) metabolism, respectively. As inferred from average enzyme activities and from western blot, immunoinhibition, and substrate (coumarin) inhibition analyses, O. viverrini infestation increased the expression of enzymes detectable by anti-CYP2A5 antibody as well as NDEA metabolism in male but not in female hamsters. Immunohistochemical analysis of CYP2A expression by anti-mouse CYP2A5 antibody demonstrated that the O. viverrini-associated increase was not uniformly distributed throughout the liver but occurred in hepatocytes immediately adjacent to areas of inflammation. Immunohistochemical analysis of AFB-DNA adducts in the livers of O. viverrini-infested hamsters treated with AFB showed that the highest levels of adducts were found in the regions of liver where hepatocellular expression of enzymes detectable by anti-CYP2A5 antibody is induced. These results suggest that a high local expression of CYP isozymes in O. viverrini-infested livers could be a contributing risk factor in the development of liver cancers associated with parasitic hepatitis.
Mol Carcinog 1994 Oct
PMID:Association of liver fluke (Opisthorchis viverrini) infestation with increased expression of cytochrome P450 and carcinogen metabolism in male hamster liver. 791 96

Long Evans Cinnamon (LEC) rats, which spontaneously develop hepatitis, produce an autoantibody to protein disulfide isomerase (PDI) before the development of clinical signs of hepatitis. Anti-PDI antibody may be associated with immunological hepatitis. Thus, the purpose of this study was to investigate the effects of some drugs on the development of hepatitis and the occurrence of the antibody in LEC rats. Cyclosporin-A, an immunosuppressant, and D-penicillamine, which promotes copper excretion, were orally administered to LEC rats for 23 weeks. Mortality, blood biochemical parameters and the titer of serum anti-PDI antibody were measured. In control LEC rats, four of eight rats died before 20-weeks-old. Only one of seven rats in the cyclosporin-A-treated group died at the age of 20 weeks. When rats were treated with D-penicillamine, the development of clinical signs of hepatitis was inhibited, and all rats survived. Cyclosporin-A-treated rats showed increases in blood biochemical parameters similar to those in control rats. The titer of anti-PDI antibody in control rats was higher the non-survivors than survivors. These findings suggest the association of the anti-PDI antibody with lethality, but not with the apparent development and progression of hepatitis as measured by blood biochemical parameters in LEC rats.
Res Commun Mol Pathol Pharmacol 1994 Jul
PMID:Effects of cyclosporin-A and D-penicillamine on the development of hepatitis and the production of antibody to protein disulfide isomerase in LEC rats. 795 97

The antihypertensive drug dihydralazine may, on rare occasions, cause immunoallergic hepatitis characterized by anti-cytochrome P450 (P450)1A2 autoantibodies. To understand the first steps leading to this immune reaction, we studied the covalent binding fo dihydralazine metabolites to microsomes from rat and human livers. Upon incubation with NADPH and microsomes, dihydralazine formed metabolites that reacted with heme (as evidenced by destruction of heme, formation of 445-nm light-absorbing complexes, and covalent binding of heme to P450 apoprotein) and covalently bound to microsomal proteins. Formation of these metabolites was shown (by NADPH dependence, induction by beta-naphthoflavone, and immunoinhibition by anti-P4501A antibodies) to be mediated by P4501A. Finally, these metabolites appeared to bind to P4501A2, which produced them. These results support the following scheme for the first steps of this autoimmune reaction: P4501A2 metabolizes dihydralazine into reactive metabolites that then bind to it, forming a neoantigen that triggers an immune response characterized by autoantibodies against P4501A2.
Mol Pharmacol 1994 Jun
PMID:Interactions of dihydralazine with cytochromes P4501A: a possible explanation for the appearance of anti-cytochrome P4501A2 autoantibodies. 802 22

From a blood serum of patients with chronic posttransfusional non-A, non-B hepatitis the genomic RNA of hepatitis C virus (HCV) was isolated. Using RT-PCR (reverse transcription-polymerase chain reaction) there were synthesized and cloned cDNA fragments, representing 3 regions of the genome of a new virus isolate (HCV-R): 5'-nontranslating region, a core gene and a part of the nonstructural region NS3/NS4. Analysis of the nucleotide and of the amino acid sequences of a core and NS3/NS4 regions revealed significant difference between isolates from Russia (HCV-R) and from Japan (HCV-J). Nucleotide sequence homology between them was 90.0-90.87%, while homology between Russian and American isolates (USA-PT) complised 95.27-97.32%. No essential variations were found in the nucleotide sequences of 5'-nontranslating region of all three HCV isolates.
Mol Gen Mikrobiol Virusol
PMID:[Determination of the nucleotide sequence of the Russian variant of the hepatitis C virus]. 813 50


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