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)

Type-8 avian adenoviruses were isolated from chickens in a commerical flock suffering an outbreak of inclusion body hepatitis. Serum-neutralizing titer to this type, but not to 7 other types of avian adenovirus, was more than 4 times as high in convalescing chickens as in chickens from the flock bled 2 weeks previously, during the disease outbreak. A disease similar to that in the commercial flock and to inclusion body hepatitis as described in the literature was produced by intra-abdominal inoculation of a type-8 isolant, AMG 5 (2a), into 1-day-old specific-pathogen-free chicks. Pathologic features of the disease included necrotizing hepatitis, pancreatitis, and severe lymphoid depletion of the bursa of Fabricius, thymus, and spleen. It was concluded that type-8 avian adenoviruses were involved in the etiology of the naturally occurring outbreak of inclusion body hepatitis.
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PMID:Involvement of a type-8 avian adenovirus in the etiology of inclusion body hepatitis. 19 Sep 94

Mortality was 60% when chickens without detectable maternal antibody to avian adenoviruses were inoculated intra-abdominally with 10(6) plaque-forming units of AMG 5(2a), a type-8 avian adenovirus. Other results were macroscopic and microscopic lesions in a wide range of organs, statistically significant depression of body weights, AMG 5(2a) virus in the liver and feces, and high virus-neutralizing antibody titers to AMG 5(2a). The disease produced was similar to that described in a previous report of AMG 5(2a) infection of chickens, and similar to inclusion body hepatitis as described in the literature. In contrast, similar inoculation of chickens with maternal antibody to type-8 avian adenovirus resulted in no mortality, lesions in the liver only, no depression of body weight, AMG 5(2a) virus in the feces only, and relatively low virus-neutralizing antibody titers. During this study a hemorrhagic-aplastic anemia syndrome occurred in both AMG 5(2a)-inoculated and control chickens in one trial. Pathologic, virologic, and serologic findings indicated that the spontaneously occurring disease was not caused by an avian adenovirus.
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PMID:Effect of maternal antibody on experimental infections of chickens with a type-8 avian adenovirus. 19 Sep 97

Twenty 1-day-old specific-pathogen-free chickens each were given an intraabdominal inoculation of either a type-8 avian adenovirus, [AMG 5 (2a], or a type-5 avian adenovirus, inclusion body hepatitis virus (IBHV). The diseases produced were similar. High (60-100%) mortality and statistically significant depression of body weights occurred in both infections. There were necrotizing hepatitis and pancreatitis, lymphoid depletion in the spleen, bursa of Fabricius and thymus, hydropericardium, nephritis and enteritis. Intranuclear inclusions occurred in affected organs. Fluorescent-antibody staining, the Feulgen reaction for deoxyribonucleic acid and electron microscopic studies, as well as studies from the literature, indicated that basophilic inclusions consisted of assembled adenovirions.
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PMID:Comparative study of experimental inclusion body hepatitis of chickens caused by two serotypes of avian adenovirus. 20 21

Our aim was to characterize antinuclear antibody (ANA) targets in type 1 autoimmune hepatitis (AIH1) using a proteomic tool. ANA-positive sera from 29 patients with AIH1 and 14 negative controls were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. The principal antigens identified were a 30 kDa triplet band which was recognized by 79% of patient sera and 14% of control sera, and a 36 kDa antigen which was recognized by 52% and 14% of sera, respectively. The latter antigen was studied in more detail using two-dimensional electrophoresis (2-DE) and mass spectrometry (MS). Its identification corresponded to heterogeneous nuclear ribonucleoprotein A2/B1. This paper presents the first description of this protein as an antigen in AIH1.
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PMID:Heterogeneous nuclear ribonucleoprotein A2/B1 identified as an autoantigen in autoimmune hepatitis by proteome analysis. 1518 1

Sclerostin, an osteocyte-secreted protein, negatively regulates osteoblasts and inhibits bone formation. In this first-in-human study, a sclerostin monoclonal antibody (AMG 785) was administered to healthy men and postmenopausal women. In this phase I, randomized, double-blind, placebo-controlled, ascending, single-dose study, 72 healthy subjects received AMG 785 or placebo (3:1) subcutaneously (0.1, 0.3, 1, 3, 5, or 10 mg/kg) or intravenously (1 or 5 mg/kg). Depending on dose, subjects were followed for up to 85 days. The effects of AMG 785 on safety and tolerability (primary objectives) and pharmacokinetics, bone turnover markers, and bone mineral density (secondary objectives) were evaluated. AMG 785 generally was well tolerated. One treatment-related serious adverse event of nonspecific hepatitis was reported and was resolved. No deaths or study discontinuations occurred. AMG 785 pharmacokinetics were nonlinear with dose. Dose-related increases in the bone-formation markers procollagen type 1 N-propeptide (P1NP), bone-specific alkaline phosphatase (BAP), and osteocalcin were observed, along with a dose-related decrease in the bone-resorption marker serum C-telopeptide (sCTx), resulting in a large anabolic window. In addition, statistically significant increases in bone mineral density of up to 5.3% at the lumbar spine and 2.8% at the total hip compared with placebo were observed on day 85. Six subjects in the higher-dose groups developed anti-AMG 785 antibodies, 2 of which were neutralizing, with no discernible effect on the pharmacokinetics or pharmacodynamics. In summary, single doses of AMG 785 generally were well tolerated, and the data support further clinical investigation of sclerostin inhibition as a potential therapeutic strategy for conditions that could benefit from increased bone formation.
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PMID:Single-dose, placebo-controlled, randomized study of AMG 785, a sclerostin monoclonal antibody. 2059 11