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)

A case is described in which a patient developed TT prolongation and bleeding during CMV hepatitis following successful renal transplantation. Bence-Jones proteinuria was noted, but there was no other evidence of myeloma. Bence-Jones proteinuria, TT prolongation, and bleeding abated as hepatitis resolved. In vitro, a protein isolated from the patient's urine was capable of prolonging the TT markedly, but it did not impair thrombin esterase activity. The effect of the protein seemed to be inhibition of fibrin polymerization. Sephadex gel filtration revealed a single TT-prolonging peak at 11,000 daltons, containing kappa, lambda, and delta antigens. By radioimmunoassay, virtually all the protein present reacted as beta2-microglobulin. Incubation with anti-beta2-microglobulin antiserum markedly attenuated anticoagulant activity. The paraprotein observed transiently in this patient's urine during hepatitis had potent anticoagulant activity and may well have accounted for his abnormal TT and bleeding diathesis; this paraprotein was not distinguishable from beta2-microglobulin.
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PMID:Impaired fibrin polymerization in viral hepatitis. Report of a case: probable identity of the inhibitor with beta2-microglobulin. 21 57

The plasma lecithin: cholesterol acyltransferase was determined in patients with various liver diseases and the relationship between this enzyme activity and the other liver function tests were studied including long term observations. Lecithin: cholesterol acyltransferase activity in fulminant hepatitis and liver cirrhosis showed a significant decrease in comparison with normal volunteers. Although the enzyme activity of hepatoma showed significant decrease, they were ascribed to the influence of concomitant liver cirrhosis. The enzyme activity showed insignificant changes in the acute and chronic hepatitis and alcoholic liver disease. Lecithin: cholesterol acyltransferase activity was correlated with the concentration of cholesterolester rather than with the ratio of esters to cholesterol. In addition, it was well correlated with pseudocholine esterase and serum albumin. The lecithin: cholesterol acyltransferase activity in the cases during follow-up period varied in good parallel with cholesterol-esters concentration and pseudocholine esterase in the cases with acute hepatitis; with serum albumin in the cases with liver cirrhosis. Furthermore, it varied inversely with SGPT in the cases with acute hepatitis. In a case with hepatoma, lecithin: cholesterol acyltransferase activity decreased more sharply than the cholesterolesters concentration and serum albumin immediately before death.
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PMID:Plasma lecithin: cholesterol acyltransferase activity in liver disease. 23 Sep 93

Plasma prekallikrein (kallikreinogen) and kallikrein inhibitor, assayed with the kaolin activable esterase method, have been evaluated in 20 patients with hepatic cirrhosis, in 12 cases with jaundice from acute viral hepatitis, and in 9 normal. A significant reduction of the plasma prekallikrein in cirrhosis has been found. A lowering of plasma prekallikrein has also been observed in viral hepatitis; in this condition, however, the modifications were less important than those obtained in cirrhosis. In three cases of hepatitis, the behaviour of the plasma prekallikrein and kallikrein inhibitor have been controlled during the period of the disease and compared with the behaviour of some conventional parameters, such as serum transaminases and bilirubin. An important increase of the prekallikrein level has been observed during the improvement of hepatitis. These data confirm the implication of the prekallikrein-kallikrein system in severe liver diseases, and indirectly points out the role of the liver in maintaining the physiological balance of the kallikrein system.
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PMID:Prekallikein and kallikrein inhibitor in liver cirrhosis and hepatitis. 108 79

Two groups of experimental animals, each consisting of 12 rabbits, were subjected to local fractional irradiation with cobalt 60. Group I received the total dose of 2580 R during 13 days, group II - 5100 R during 24 days. The effects of irradiation were estimated on the strength of histological examination of the liver immediately and after 7, 15, 30, 60 and 90 days after the last exposition. The histological sections were stained with haematoxylin and eosin, and colour reactions were performed for argentaffine and collagen fibres and for glycogen, neutral fats, alkaline and acid phosphatase, ATP-ase, glycose-6-phosphatase, non-specific esterase and succinic acid dehydrogenase. It was found that the dose of 2580 R is safe for the liver. The effects of irradiation were slight and limited to weak catabolic disturbances in the form of mild steatosis of the liver and of a transient and short-lived fall of glycogen and rise of hydrolytic enzymes. More pronounced and intense changes were observed in the other group of animals. During the early period, the changes were of a retrograde character and were typical of the acute post-irradiation effect. There was necrosis of the walls of the blood vessels, of the epithelium of the bile ducts and of the liver cells, accompanied by a rise in the hydrolytic enzymes and by a considerable fall of the level of glycogen and succinic acid dehydrogenase. During the late period (30-90 days), changes typical of the so-called post-irradiation hepatitis were found histologically.
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PMID:[Pathomorphological and histochemical changes in the liver of rabbits following fractional irradiation with Co-60]. 118 53

The gene encoding the membrane (M) protein of the OC43 strain of human coronavirus (HCV-OC43) was amplified by a reverse transcription-polymerase chain reaction of viral RNA with HCV-OC43- and bovine coronavirus (BCV)-specific primers. The nucleotide sequence of the cloned 1.5 kb fragment revealed an open reading frame (ORF) of 690 nucleotides which was identified as the M protein gene from its homology to BCV. This ORF encodes a protein of 230 amino acids with an M(r) of 26416. The gene is preceded by the motif UCCAAAC, analogous to the consensus coronavirus transcription initiation sequence. The M protein of HCV-OC43 shows features typical of all coronavirus M proteins studied: a hydrophilic, presumably external N terminus including about 10% of the protein, and a potential N-glycosylation site followed by three major hydrophobic transmembrane domains. The amino acid sequence of the M protein of HCV-OC43 has 94% identity with that of the Mebus strain of BCV, and also contains six potential O-glycosylation sites in the exposed N-terminal domain. Indeed, the glycosylation of the M protein was not inhibited in the presence of tunicamycin, which is indicative of O-glycosylation, as previously reported for BCV and murine hepatitis virus. Virions released from tunicamycin-treated cells contained the M glycoprotein but were devoid of both peplomer (S) and haemagglutinin-esterase (HE) proteins. Thus, inhibition of the N-glycosylation of the S and HE structural proteins prevented their incorporation into progeny virions, an indication that they are dispensable for virion morphogenesis, unlike the M protein.
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PMID:Sequence analysis of the membrane protein gene of human coronavirus OC43 and evidence for O-glycosylation. 140 6

Overall 180 children aged 3 months to 12 years with acute and chronic hepatitis B and delta were examined for macrophagal function. Chemotaxis, saturation with esterase, the content of nuclear RNA were estimated, antigens of HB virus in these cells were identified as well. The data obtained attest to the correlation between the degree of macrophagal function disorders and the gravity of acute virus hepatitis. The chronic disease is characterized by stable depression of mononuclear cells with a tendency toward deeper depression of their function in patients with virus hepatitis delta as well as a higher rate of HBsAg and HBeAg demonstration in these cells. The authors provide evidence for advisability of the use of BCG vaccine and tactivin in patients with the chronic disease, since they improve macrophagal function, promote the inhibition of HB-virus replication and the onset of a stable remission in patients with chronic hepatitis B and delta.
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PMID:[The pathogenetic significance of disorders in macrophage function in viral hepatitis B and delta in children]. 147 35

Some of mouse hepatitis virus strains contain an optional envelope glycoprotein, hemagglutinin-esterase (HE) protein. To understand the functional significance of this protein, monoclonal antibodies (MAbs) specific for this protein were generated and used for passive immunization of mice. None of these MAbs showed any virus-neutralizing activity in vitro; however, mice passively immunized with the purified MAbs were protected from lethal infection by the JHM strain of mouse hepatitis virus. Passive immunization altered the pathogenicity such that the virus caused subacute and chronic demyelination instead of acute lethal encephalitis. Virus titers in the brains of the immunized mice were significantly lower than those for the nonimmunized control mice, suggesting that the virus replication or spread was inhibited. In addition, histopathological analysis indicated that the spread of virus in the brain and spinal cord was significantly inhibited in the immunized mice. Furthermore, the mononuclear cell infiltration in the immunized mice appeared earlier than in the nonimmunized mice, suggesting that the exogenous antibody might have activated host immune responses, and thus facilitated clearance of the virus or virus-infected cells. The same protective effects were observed for both JHM(2) and JHM(3) viruses, which expressed different amounts of the HE protein. In contrast, mice infected with At11f, a variant of JHM which does not express the HE protein, were not protected by these MAbs, suggesting that protection was mediated by the specific interaction between the MAb and the HE protein. Thus, the mechanism of protection by the exogenous HE-specific MAbs may represent the early activation of innate immune mechanisms in response to the interaction between the MAbs and the HE protein.
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PMID:Hemagglutinin-esterase-specific monoclonal antibodies alter the neuropathogenicity of mouse hepatitis virus. 156 May 31

The hemagglutinin-esterase (HE) membrane glycoprotein is present only in some members of the coronavirus family, including some strains of mouse hepatitis virus (MHV). In the JHM strain of MHV, expression of the HE gene is variable and corresponds to the number of copies of a UCUAA pentanucleotide sequence present at the 3'-end of the leader RNA. This copy number varies among MHV strains, depending on their passage history. The JHM isolates with two copies of UCUAA in their leader RNA showed a high level of HE expression, whereas the JHM isolate with three copies had a low-level expression. In this study, the analysis of HE gene expression was extended to other MHV strains. The synthesis of HE mRNA in these viruses also correlates with the copy number of UCUAA in the leader RNA and the particular intergenic sequence preceding the HE gene. In one MHV strain, MHV-1, no detectable HE mRNA was synthesized, despite the presence of a proper transcription initiation signal. This lack of HE mRNA expression was consistent with a leader RNA containing three UCUAA copies. However, mutations and deletions within the coding region of the MHV-1 HE gene have generated a stretch of sequence which resembled the transcriptional initiation motif, and was shown to initiate the synthesis of a novel smaller mRNA. These findings strengthened the theory that interactions between leader RNA and transcriptional initiation sequences regulate MHV subgenomic mRNA transcription. Sequence analysis revealed that most MHV strains, through extensive mutations, deletions, or insertions, have lost the complete HE open reading frame, thus turning HE into a pseudogene. This high degree of variation is unusual as the other three structural proteins (spike, membrane, and nucleocapsid) are well-maintained. In contrast to bovine coronavirus, which apparently requires HE for viral replication, the HE protein in MHV may be only an accessory protein which is not necessary for viral replication. JHM and MHV-S, however, have preserved the expression of HE protein.
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PMID:Heterogeneity of gene expression of the hemagglutinin-esterase (HE) protein of murine coronaviruses. 164 5

Genes 4 and 5 of mouse hepatitis virus (MHV) are known to encode nonstructural proteins ns4, ns5a, and ns5b, whose function is unknown. In this study, we demonstrated that one of the MHV strains, MHV-S, did not synthesize mRNA 4 and made a smaller mRNA 5. Sequence analysis showed that the transcription initiation site for gene 4 of MHV-S was mutated from the consensus UCUAAAC to UUUAAAC, consistent with the idea that mutations in this region abolish mRNA synthesis. Furthermore, within gene 5 there were deletions totaling 307 nucleotides which deleted almost all of open reading frame 5a, but preserved open reading frame 5b of gene 5. Comparison of the growth of MHV-S with other MHV strains in DBT cells revealed no significant growth defect in MHV-S. These results suggest that ns4 and ns5a are not essential for viral replication in tissue culture cells, and thus join gene 2 and the hemagglutinin-esterase (HE) gene as nonessential viral genes in MHV.
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PMID:Mouse hepatitis virus S RNA sequence reveals that nonstructural proteins ns4 and ns5a are not essential for murine coronavirus replication. 165 56

The incidence and phenotype of preneoplastic and neoplastic liver lesions appearing in LEC rats after recovery from severe hereditary hepatitis were studied in comparison with the liver lesions appearing in chemical liver carcinogenesis. The livers of 168 rats (90 male, 78 female) were stained for seven histochemical markers at different time periods from the 20th week to the 122nd week of life. Glucose-6-phosphatase (G6Pase), adenosine triphosphatase (ATPase) and non-specific esterase (ES) were used as negative markers. Gamma-glutamyltransferase (GGT), glutathione S-transferase placental form (GSTP), esterase isozyme L-1 (L1) and alpha-fetoprotein (AFP) were used as positive markers. The study on the incidence of liver lesions in the LEC rats revealed sequential development of liver foci, nodules and hepatocellular carcinomas (HCCs) similar to those seen in chemically induced liver carcinogenesis. These lesions appeared earlier and more frequently in male LEC rats than in female ones, suggesting the importance of hormonal environment in spontaneous HCC development. The histochemical analysis of spontaneous liver lesions in LEC rats showed that GSTP was the most reliable positive marker as previously reported in chemical liver carcinogenesis. There was no essential difference in the expression of the markers in spontaneous and chemically induced liver lesions except for L1, which is considered to be related to xenobiotic metabolism. The results of this study suggest that both spontaneous and chemically induced liver cancer may develop by passing through phenotypically similar preneoplastic processes. In addition, the LEC rat uniquely showed chronic liver damage (hepatocyte death and regeneration) at the promotion stage of carcinogenesis. Such a natural history of HCC development in LEC rats is similar to that of human HCC which is frequently associated with chronic liver damage. Thus, the LEC rat provides a useful model for studying the process and underlying mechanisms of human liver cancer development.
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PMID:Phenotype of preneoplastic and neoplastic liver lesions during spontaneous liver carcinogenesis of LEC rats. 169 69


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