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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have provided physicochemical and electron microscopic evidence for the existence of two distinct agents of posttransfusion non-A, non-B (NANB) hepatitis. One of these agents is chloroform-resistant and is not associated with the formation of unique ultrastructural structures in infected liver. The other agent is CHCl3-sensitive, induces the formation of characteristic hepatocyte cytoplasmic tubules, and interferes with concurrent HAV or HBV infection in experimentally inoculated chimpanzees. The tubuleforming agent (TFA) has also been shown to pass through an 80 nm capillary pore membrane filter, suggesting that it is a small enveloped (or lipid-containing) virus. The TFA can also be recovered from low titer (less than or equal to 10(5) infectious doses/ml) chronic-phase chimpanzee plasma by use of a multi-step purification procedure that assumes the agent is a small enveloped RNA virus with an approximate buoyant density of 1.24 g/cm3 and a sedimentation coefficient of 200-280 S. The apparent lack of nucleic acid homology between the NANB-TFA and HBV further suggests that the NANB-TFA is either Togavirus-like or belongs to another or as yet undefined class of RNA or DNA virus.
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PMID:The agents of non-A, non-B viral hepatitis. 392 11

A membrane-coated virus having a diameter of 85-90 nm and containing a 40-45 nm core was found to replicate in cell cultures derived from chimpanzee liver after inoculation of serum containing infective non-A, non-B (NANB) hepatitis viruses from two independent sources. Replication of this agent was not observed when the same cells were inoculated with a chloroform-extracted inoculum or were left uninoculated. Replication involves assembly of virus cores on tubular structures similar to those seen in liver cells of chimpanzees infected with most isolates of NANB virus.
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PMID:Isolation of a virus from chimpanzee liver cell cultures inoculated with sera containing the agent of non-A, non-B hepatitis. 615 Jan 43

An enzyme-linked immunosorbent assay for an antigen (termed DS-Ag) related to non-A, non-B hepatitis has recently been developed in our laboratory. The DS-Ag was derived from a proven infectious serum obtained from a patient with haemophilia and it was also detected in the acute phase serum of an experimentally infected chimpanzee. The DS-Ag has now been shown to have a buoyant density in CsCl of 1.32 g/cm2 and a sedimentation coefficient of 20 S. The mean molecular weight, determined by gel chromatography on 4% agarose columns, was found to be 0.9 x 10(6). The DS-Ag recovered from acute-phase chimpanzee serum has identical characteristics. The DS-Ag is stable for 1 h at 56 degrees C, at pH 3, in high concentration of CsCl or Nal and in 20% ether. Complete inactivation occurred after 1 min at 98 degrees C, at pH 2, in chloroform (1:1 mixture), in 1 ppm chlorine and in formalin (1:4000, 72 h 37 degrees C). Our studies showed that DS-Ag bears no resemblance to particles related to well-documented forms of viral hepatitis types A and B or other known pathogens. The DS-Ag is a complex substance which forms an antigenic entity related to non-A, non-B hepatitis.
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PMID:Characterization of DS-antigen, an antigen related to non-A, non-B hepatitis. I. Physico-chemical properties. 640 7

To determine whether a non-A, non-B hepatitis agent contained essential lipids, we extracted with chloroform a dilution of human plasma that contained approximately 10(4) chimpanzee infectious doses of non-A, non-B hepatitis virus and then tested for infectivity in chimpanzees. In addition, we treated a serum containing hepatitis B virus in the same way. Both of these samples were also sham extracted as controls. Known chloroform-sensitive and chloroform-resistant viruses were added directly to the hepatitis-containing serum or plasma as internal controls or to fetal calf serum as external controls and were assayed for infectivity in vitro after chloroform extraction or sham extraction. All infectivity of the diluted plasma that contained at least 10(4) chimpanzee infective doses of non-A, non-B hepatitis agent and all infectivity of the serum that contained 10(3.5) chimpanzee infective doses of hepatitis B virus were destroyed by chloroform. The chloroform-sensitive control viruses were completely inactivated, but the chloroform-resistant control viruses lost less than 0.5 log10 of infectivity. Sham-extracted non-A, non-B hepatitis agent-containing plasma was shown to maintain its infectivity in chimpanzees that had initially been inoculated with the chloroform-extracted plasma. Thus, both hepatitis type B and non-A, non-B hepatitis appear to be caused by viruses that can be inactivated by a lipid solvent.
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PMID:Inactivation of hepatitis B virus and non-A, non-B hepatitis by chloroform. 640 13

Two separate and distinct episodes of non-A, non-B hepatitis were induced in each of two chimpanzees by two inocula: one containing a chloroform-resistant agent and the other containing a chloroform-sensitive agent. Both agents were recovered from liver tissue and plasma obtained from a single chimpanzee during the acute and chronic phases of infection with a factor VIII concentrate, respectively. The chloroform-resistant agent did not cause unique changes in hepatocytes; in contrast, the chloroform-sensitive agent did induce the formation of cytoplasmic tubules, convoluted endoplasmic reticulum, and dense reticular inclusion bodies. The latter changes are similar in character to those induced in infected cells by some enveloped mammalian RNA viruses.
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PMID:Posttransfusion non-A, non-B hepatitis: physicochemical properties of two distinct agents. 641 32

Although aflatoxicosis in Coturnix coturnix japonica has been described, the histochemical localization of liver chemicals and the occurrence of ingested aflatoxins within blood, feces, and liver have not been described. Six to 8-week-old quail, which were intubated with a carrier with or without .3 mg mixed aflatoxins (AFB1, AFB2, AFG1, AFG2)/kg body weight were sacrificed within .25 to 5 days of intubation. Deparaffinized sections of livers were stained for lipids, nucleic acids, polysaccharides, and proteins. Other livers and excrement were homogenized and filtered homogenates as well as blood partitioned against chloroform. The aqueous phase was treated with pepsin and then partitioned, but the organic phase was analyzed directly. Organic phases of .25 to 5 day blood, feces, and liver lacked aflatoxins. Pepsin digesta of blood from males and females dosed 6 hr appeared to contain aflatoxicol (disappeared by 24 hr) and an unknown fluorescent compound, respectively. Whereas an unidentified fluorescent compound was observed within excrement of males dosed 6 hr, female excrement contained a fluorescent compound with an AFB1 Rf (disappeared by 24 hr). Although the liver of males dosed 6 hr had three fluorescent compounds (Rfs for AFB1 and AFB2a), only one was seen within dosed females. Ultra violet absorption spectra of presumed AFB2a and aflatoxicol failed to yield their reported absorption maxima. Livers from dosed quail exhibited bile duct proliferation, cellular necrosis, vacuolization, congestion, fatty changes and mild hepatitis. Sinusoidal membranes were thickened and contained abundant periodic acid-Schiff's (PAS)-positive substances. Although livers of nondosed quail abounded with regularly shaped and uniformly distributed, Sudan IV-positive droplets, livers of dosed quail accommodated few, irregularly-shaped and positioned droplets. Hepatocyte nuclei and nucleoli of dosed quail displayed marked affinities for the Feulgen reagent and toluidine blue O, respectively. Lobules of dosed quail possessed concentrations of cells in which their entire cytoplasm was PAS positive. Treatment of sections with alpha-amylase reduced staining suggesting the presence of glycogen. Ninhydrin-positive substances were distributed throughout the liver in both DQ and non DQ with no apparent difference in intensities between the two livers. Generally the DQ showed mild hepatitis due to aflatoxicosis and the toxin altered liver histochemistry for the major classes of cellular chemicals.
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PMID:Histochemical analysis of liver cells from short term, aflatoxin-dosed and nondosed Coturnix coturnix japonica. 1. Aflatoxin-sensitive quail. 666 1

The survival rate for acute hepatic failure induced by Propionibacterium acnes and lipopolysaccharide (LPS) was increased when a hot water extract from the flowers of Inula britannica L. subsp. japonica Kitam. was injected into the experimental hepatitis mice, and anti-hepatitis substances could be extracted with CHCl3. The CHCl3 extract from I.britannica was fractionated and anti-hepatitis fractions IB-3-2 and IB-3-3 were obtained. IB-3-3 had the most potent anti-hepatitis activity among the fractions but further purification of the active compound was not achieved because of the low yield. IB-3-2 contained only one substance which was identified to be taraxasteryl acetate by 1H- and 13C-NMR and MS. Taraxasteryl acetate showed potent preventive activity against acute hepatic failure induced by P.acnes and LPS in a dose-dependent manner, however deacetylation and modification of the olefinic bonds significantly decreased the anti-hepatitis activity of taraxasteryl acetate. Taraxasteryl acetate also inhibited the increment of plasma transaminase on acute hepatic failure induced by carbon tetrachloride (CCl4) or D-galactosamine. From a histological study it appeared that degeneration and necrosis, which were observed in the liver from CCl4 mice, were not found in the liver cells from taraxasteryl acetate treated mice. These results indicates that taraxasteryl acetate shows preventive effects on experimental hepatitis caused by either immunologically induced injuries or hepatotoxic chemicals.
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PMID:Preventive effect of taraxasteryl acetate from Inula britannica subsp. japonica on experimental hepatitis in vivo. 1725 90

Mycotoxin hepatitis which develops in pigs when they eat fodder contaminated by mycotoxin (sterigmatocystin) is registered at large pig breeding farms of Ukraine. Diagnostics of mycotoxin hepatitis of pigs induced by sterigmatocystin is based on clinical-epizootiological studies and mycotoxin analysis of the fodder including detection of fungi, producers of sterigmatocystin and determination of the content of mycotoxin itself. The authors have suggested a method based on extraction of mycotoxin from the fodder by means of the mixture of chloroform and 4% water solution of potassium chloride, on concentration of the chloroform residue, its separation in a thin layer of silicagel, and UV examination of chromatograms. The method sensitivity is 30 micrograms per 1 kg of the product. This method will permit diagnosis of mycotoxin hepatitis in animals and will promote timely prophylactic measures. The method is easy to be applied in veterinary laboratories.
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PMID:[The diagnosis of mycotoxin hepatitis in swine]. 783 1

In order to better understand the first steps leading to drug-induced immunoallergic hepatitis, we studied the target of anti-LKM2 autoantibodies appearing in tienilic acid-induced hepatitis, and the target of tienilic acid-reactive metabolites. It was identified as cytochrome P450 2C9, (P450 2C9): indeed, anti-LKM2 specifically recognized P450 2C9, but none of the other P450s tested (including other 2C subfamily members, 2C8 and 2C18). Tienilic acid-reactive metabolite(s) specifically bound to P450 2C9, and experiments with yeast expressing active isolated P450s showed that P450 2C9 was responsible for tienilic acid-reactive metabolite(s) production. Results of qualitative and quantitative covalent binding of tienilic acid metabolite(s) to human liver microsomes were then compared to those obtained with two drugs leading to direct toxic hepatitis, namely, acetaminophen and chloroform. Kinetic constants (Km and Vmax) were measured, and the covalent binding profile of the metabolites to human liver microsomal proteins was studied. Tienilic acid had both the lowest Km and the highest covalent binding rate at pharmacological doses. For acetaminophen and chloroform, several microsomal proteins were covalently bound, while covalent binding was highly specific for tienilic acid and dihydralazine, another drug leading to immunoallergic hepatitis. Although low numbers of drugs were tested, these results led us to think that there may exist a relationship between the specificity of covalent binding and the type of hepatotoxicity.
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PMID:Specificity of in vitro covalent binding of tienilic acid metabolites to human liver microsomes in relationship to the type of hepatotoxicity: comparison with two directly hepatotoxic drugs. 807 77

Chemical hepatic injury is not rare in Taiwan. We here report such an injury induced by chloroform. A previously healthy 26-year-old married woman was admitted under the impression of acute chemical hepatitis in December, 1991. Two weeks before, she had used chloroform as glue to unite two pieces of plastic pencil sharpener at home. Nasty odor was sensed while working. After series of hepatitis workup, liver echo, site visit, survey of coworkers and gas chromatography for the "glue", the diagnosis of chloroform-induced hepatic injury was confirmed. This case found that neither employer nor employee was aware of the toxicity of chloroform. No ventilation system or personal respiratory protection equipment was provided. Preemployment training and Material Safety Data Sheet were obviously insufficient, also. The diagnostic criteria of chemical hepatic injury were therefore proposed to alert medical professionals, industrial hygienist, safety personnel and factory inspectors, not to prompt an early diagnosis but also hopefully to prevent the occurrence of occupational liver diseases.
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PMID:[Chloroform-induced hepatic injury: a case report]. 840 69


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