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

A decrease in sodium, potassium and anion (HCO3)-activated erythrocyte ATPases is noted in patients with acute viral hepatitides A and B, chronic persisting hepatitis, liver cirrhosis, chronic cholecystitis and in HBs-antigen carriers, the reduction of HCO8-ATPase being more noticeable. A degree of expression of the above changes depends on the severity of a pathological process in the liver. The most serious changes are noted in liver cirrhosis. In this disease calcium ATPase activity is also on a decrease. Erythrocyte ATPase activity is lowered in chronic cholecystitis to a lesser degree. In patients with chronic persisting hepatitis and liver cirrhosis erythrocyte ATPase activity slightly increases, however it remains significantly lowered as compared to the control level. The determination of erythrocyte ATPase activity can be used for assessment of the status of patients with acute and chronic liver diseases.
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PMID:[Comparative characteristics of adenosine triphosphatase activity in the erythrocytes of patients with acute and chronic liver diseases, chronic cholecystitis and in HBs antigen carriers]. 295 84

In the murine coronavirus mouse hepatitis virus, a single glycoprotein, E2, is required both for attachment to cells and for cell fusion. Cell fusion induced by infection with mouse hepatitis virus strain A59 was inhibited by the addition of monospecific anti-E2 antibody after virus adsorption and penetration. Adsorption of concentrated coronavirions to uninfected cells did not cause cell fusion in the presence of cycloheximide. Thus, cell fusion was induced by E2 on the plasma membrane of infected 17 Cl 1 cells but not by E2 on virions grown in these cells. Trypsin treatment of virions purified from 17 Cl 1 cells quantitatively cleaved 180K E2 to 90K E2 and activated cell-fusing activity of the virions. This proteolytic cleavage yielded two different 90K species which were separable by sodium dodecyl sulfate-hydroxyapatite chromatography. One of the trypsin cleavage products, 90A, was acylated and may be associated with the lipid bilayer. The other, 90B, was not acylated and yielded different peptides than did 90A upon limited digestion with thermolysin or staphylococcal V8 protease. Thus, the cell-fusing activity of a coronavirus required proteolytic cleavage of the E2 glycoprotein, either by the addition of a protease to virions or by cellular proteases acting on E2, which was transported to the plasma membrane during virus maturation. There is a striking functional similarity between the E2 glycoprotein of coronavirus, which is a positive-strand RNA virus, and the hemagglutinin glycoprotein of negative-strand orthomyxoviruses, in that a single glycoprotein has both attachment and protease-activated cell-fusing activities.
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PMID:Proteolytic cleavage of the E2 glycoprotein of murine coronavirus: activation of cell-fusing activity of virions by trypsin and separation of two different 90K cleavage fragments. 299 43

Ten Kenyan patients with visceral leishmaniasis unresponsive to sodium stibogluconate, at a dose of 16 to 20 mg Sb/kg body-weight/day given for 30 to 98 days, were treated with 20 mg Sb/kg bw given every eight hours. This regimen was modified or abandoned in six patients because of suspected toxicity, although toxicity was difficult to assess because of intercurrent illness. Toxic effects included lethargy, anorexia, vomiting, electrocardiographic changes, fall in haemoglobin and rise in liver enzymes. One patient died, probably from a cardiac arrhythmia. Two patients were cured, four responded partially and four showed no response. Pentamidine, at a dose of 4 mg/kg body-weight given one to 3 times per week for 5 to 39 weeks, was given as initial treatment in one patient and after failure of sodium stibogluconate in seven. Toxic effects included nephritis, hepatitis, transient diabetes and subcutaneous abscesses. Two patients were cured, two responded partially, three showed no response and one, after apparent cure, relapsed and was unresponsive to additional pentamidine treatment. Low-frequency, long-duration pentamidine was often useful in maintaining any improvement made during treatment with the less well tolerated high-dose, high frequency sodium stibogluconate. We observed the step-wise development of resistance to both sodium stibogluconate and pentamidine. The problems of managing patients with visceral leishmaniasis which is unresponsive to conventional doses of pentavalent antimonials are discussed and some tentative suggestions put forward.
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PMID:Visceral leishmaniasis unresponsive to antimonial drugs. II. Response to high dosage sodium stibogluconate or prolonged treatment with pentamidine. 300 95

The molecular mechanism of genetic resistance of inbred mouse strains to mouse hepatitis virus, a murine coronavirus, was studied by comparing virus binding to plasma membranes of intestinal epithelium or liver from susceptible BALB/c and resistant SJL/J mice with a new solid-phase assay for virus-binding activity. Virus bound to isolated membranes from susceptible mice, but not to membranes from resistant mice. F1 progeny of SJL/J X BALB/c mice had an intermediate level of virus-binding activity on their enterocyte and hepatocyte membranes. This correlated well with previous studies showing that susceptibility to mouse hepatitis virus strain A59 is controlled by a single autosomal dominant gene (M. S. Smith, R. E. Click, and P. G. W. Plagemann, J. Immunol. 133:428-432). Because virus binding was not prevented by treating membranes with sodium dodecyl sulfate, the virus-binding molecule could be identified by a virus overlay protein blot assay. Virus bound to a single broad band of Mr 100,000 to 110,000 in membranes from hepatocytes or enterocytes of susceptible BALB/c and semisusceptible C3H mice, but no virus-binding band was detected in comparable preparations of resistant SJL/J mouse membranes. Therefore, SJL/J mice may be resistant to mouse hepatitis virus A59 infection because they lack a specific virus receptor which is present on the plasma membranes of target cells from genetically susceptible BALB/c and semisusceptible C3H mice.
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PMID:Genetic resistance to mouse hepatitis virus correlates with absence of virus-binding activity on target tissues. 302 96

Infection of mouse L-2 fibroblasts with mouse hepatitis virus (MHV) results in strong inhibition of host cell protein synthesis. Since it has been suggested in other virus systems that translational control is modulated by changes in the intracellular ionic environment, we investigated the possible occurrence of similar changes during MHV infection. Membrane permeability to extracellular sodium ions was measured by culturing MHV-infected cells in the presence of 22Na+. Sodium influx into MHV-infected cells rose dramatically from 4 to 6 h post-infection. This influx correlated chronologically with the expression of MHV-mediated cell fusion. Cell fusion was blocked by the addition of a monoclonal antibody against the MHV E2 glycoprotein. This addition also resulted in a reduction in the normal influx of 22Na+, suggesting that E2 expression was responsible, directly or indirectly, for the increased permeability to sodium ions in infected cells. Cultures of MHV-infected cells were labelled with [35S]methionine in the presence of medium supplemented with sodium chloride at final concentrations ranging from 150 mM to 350 mM. Incorporation of radiolabel into proteins decreased with increasing NaCl concentration; however, the ratio of viral to cellular protein synthesis remained relatively constant. Similarly, alteration of intracellular Na+ and K+ levels by treatment of infected cells with ouabain had little effect on the pattern of viral/cellular protein synthesis. Using monoclonal anti-E2 antibody to inhibit Na+ influx, we demonstrated normal inhibition of host cell protein synthesis. We therefore conclude that MHV-induced shut-off of host translation is not mediated by changes in intracellular Na+ concentrations.
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PMID:Translational regulation in mouse hepatitis virus infection is not mediated by altered intracellular ion concentrations. 303 44

A 37 year old female with rheumatoid arthritis developed clinical and biochemical evidence of hepatitis after receiving 80 mg of sodium aurothiomalate. Inadvertent rechallenge with sodium aurothiomalate led to recurrence of the biochemical abnormalities and a profound neutropenia and eosinophilia.
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PMID:Hepatitis and neutropenia secondary to gold thiomalate therapy for rheumatoid arthritis. 308 48

Acute ergotamine intoxication in a 29-year-old man was complicated by peripheral ischemia, pancreatitis, and hepatitis. The patient was treated with sodium nitroprusside infusion. Complications and treatment of ergotamine poisoning are discussed.
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PMID:Ischemic pancreatitis and hepatitis secondary to ergotamine poisoning. 311 14

Pharmacokinetic and clinical studies on imipenem/cilastatin sodium (IPM/CS) in pediatric surgery were performed and the results obtained are summarized below. 1. Plasma and urinary levels of IPM/CS were measured in 9 neonate patients following drip-infusion for 1 hour of IPM/CS (dose of IPM 10 mg/kg for 5 patients, 20 mg/kg for 4 patients). In the 10 mg/kg group, peak plasma levels were observed at the end of infusion or after 1 hour of it. IPM 9.95-14.2 micrograms/ml, CS 7.7-30.1 micrograms/ml. In the 20 mg/kg group, peak levels were found at the end of the infusion, IPM 39.2-41.7 micrograms/ml, CS 48.1-58.8 micrograms/ml. In both groups, plasma levels of IPM/CS decreased rapidly, and plasma half-lives (T 1/2) in the 20 mg/kg group were 0.9-1.2 hours (IPM) and 0.8-1.1 hours (CS). Urinary recovery rates were 17.7-28.7% (10 mg/kg), 21.1-36.9% (20 mg/kg) for IPM and 27.1-43.8% (10 mg/kg) and 21.5-76.5% (20 mg/kg) for CS. 2. Bile levels of IPM/CS were measured in 3 patients with congenital biliary atresia and 1 patient with neonatal hepatitis. Peak levels of IPM/CS in bile were noted 1 hour after the end of infusion, and they were 3.01-12.3 micrograms/ml for IPM, and 2.5-13.1 micrograms/ml for CS. Recovery rates in bile in 7 hours after the end of infusion were 0.03-0.12% (IPM), 0.01-0.12% (CS). 3. IPM/CS was administered to 9 patients as prophylaxis against postoperative infections and to 2 patients with postoperative cholangitis. No infectious complications were observed in patients after the prophylactic use. In 1 patient with cholangitis, clinical effect was good and organisms were eradicated. No clinical or laboratory adverse reactions due to the administration of IPM/CS were noted. It is concluded that IPM/CS is an effective and safe antibiotic in pediatric surgery.
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PMID:[Pharmacokinetics and clinical evaluation of imipenem/cilastatin sodium in pediatric surgery]. 321 Mar 4

The extent of association between woodchuck hepatitis virus surface antigen and host hepatocyte plasma membrane in chronic hepatitis was studied. Purified membranes containing the antigen were treated with various agents which perturb plasma membrane constituents to elute woodchuck hepatitis virus surface antigen. The products from disrupted membranes were analyzed by sedimentation in sucrose gradients and tested to identify the antigen reactivity. The results indicated that membrane-bound woodchuck hepatitis virus surface antigen was partially released by 4 M potassium chloride, potassium thiocyanate and guanidine, 6 M urea or 0.1 N sodium hydroxide (pH 13.5), but not in the presence of low concentrations of these reagents or by 10% 2-mercaptoethanol and 1% sodium dodecyl sulfate. No more than 15% of the total membrane-associated woodchuck hepatitis virus surface antigen was eluted by 0.1 N NaOH, which was found to be the most effective eluent among tested agents at the antigen removal. The remaining woodchuck hepatitis virus surface antigen was resistant to further extraction with sodium hydroxide, as expected for an integral membrane protein. Treatment of the infected membranes with 1% Triton X-100 or 50 mM deoxycholic acid, that solubilize the membrane lipid bilayer releasing most of the integral membrane proteins, resulted in the sedimentation of almost all detectable woodchuck hepatitis virus surface antigen reactivity with the detergent-insoluble membrane residues, suggesting a firm interaction of the antigen with the plasma membrane matrix.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interaction of woodchuck hepatitis virus surface antigen with hepatocyte plasma membrane in woodchuck chronic hepatitis. 328 58

Virucidal efficacy of chemical disinfectants, heating and ultraviolet radiation against mouse hepatitis virus (MHV), canine coronavirus (CCV), Kilham rat virus (KRV) and canine parvovirus (CPV) were examined. Coronaviruses (MHV and CCV) were inactivated by ethanol, isopropanol, benzalkonium chloride, iodophor, sodium hypochlorite, sodium chlorite, cresol soap and formaldehyde as well as by heating at 60 degrees C for 15 minutes, whereas parvoviruses (KRV and CPV) appeared to be inactivated by disinfectants such as formaldehyde, iodophor, sodium hypochlorite and sodium chlorite. Parvoviruses were stable under heating of up to 80 degrees C for 30 minutes. Ultraviolet radiation inactivated all viruses within 15 minutes. No significant differences in stability against physico-chemical treatments were seen between viruses in the same group.
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PMID:Virucidal efficacy of physico-chemical treatments against coronaviruses and parvoviruses of laboratory animals. 341 41


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