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)

Amplification by the polymerase chain reaction (PCR) of hepatitis B virus (HBV) DNA extracted from parallel samples of serum and heparinized plasma gave contradictory results, indicating that heparin inhibits virus detection. Similarly, analysis of PCR products of woodchuck hepatitis virus (WHV) DNA showed that heparinization of blood abolished WHV DNA amplification, while anticoagulation with sodium EDTA or acid citrate dextrose did not. Amplification of recombinant WHV and HBV DNA in the presence of increasing concentrations of sodium heparin progressively inhibited and finally abolished virus genome detection. The inhibitory effect of heparin was reversed by treatment of either plasma or isolated DNA with heparinase (5 U/reaction, 1 h at 28 degrees C) prior to PCR. In contrast, heparin did not influence the detection of hepadnavirus in peripheral blood mononuclear cells (PBMC), even after prolonged incubation of the cells with heparin in culture. These findings confirm that heparin exerts a dramatic inhibitory effect on hepadnaviral DNA detection by PCR and they demonstrate that this effect can be reversed by heparinase. The findings also show that extensively washed PBMC derived from heparinized blood can be a reliable source of nucleic acids for amplification of hepadnavirus genome. These results imply that previous data should be reassessed if samples of heparinized plasma were found hepadnavirus DNA nonreactive by PCR or when these samples were used as a starting material for PCR quantitation of viral genome.
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PMID:Detection of hepatitis B and woodchuck hepatitis viral DNA in plasma and mononuclear cells from heparinized blood by the polymerase chain reaction. 773 48

The mannose 6-phosphate/insulin-like growth factor II receptor (M6P/IGFIIr) is required for the activation of transforming growth factor beta, and previously we have found its expression to be significantly reduced in both rat and human hepatocellular carcinomas (HCCs). Therefore, we have postulated that loss of the M6P/IGFIIr gene may be mechanistically involved in liver carcinogenesis. Using the polymerase chain reaction, we utilized two polymorphisms in the 3' untranslated region of the M6P/IGFIIr gene to screen non-cirrhotic, hepatitis virus negative patients with hepatocellular tumors for LOH. Twenty-two of 36 (61%) patients were informative (heterozygous), and 14/22 (64%) liver tumors had LOH; 11/16 (69%) carcinomas, 1/3 (33%) fibrolamellar tumors and 2/3 (67%) adenomas. This is the first report of LOH at the M6P/IGFIIr locus in human hepatocellular tumors, and the presence of LOH in adenomas suggests that allelic loss may be an early event in the etiology of HCCs. These results support the hypothesis that the M6P/IGFIIr gene may function as a tumor suppressor gene in the liver.
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PMID:Frequent loss of heterozygosity on 6q at the mannose 6-phosphate/insulin-like growth factor II receptor locus in human hepatocellular tumors. 775 49

Cefoperazone is a semisynthetic cephalosporin antibiotic containing a piperazine side chain, which results in antipseudomonal activity. Unlike the other cephalosporins, it is mainly cleared by the liver (60-80%) and it may be more sensitive to changes in the liver function and/or plasma protein binding than other cephalosporins, which are not primarily cleared by the liver. In order to study the influence of chronic lobular hepatitis on the pharmacokinetics of cefoperazone, a dose of 1 g of cefoperazone was administered to 11 normal, healthy volunteers and 16 subjects with chronic lobular hepatitis. In each volunteer or patient, a novel galactose single-point (GSP) method, the galactose elimination capacity (GEC) test, and the modified galactose elimination capacity (MGEC) test were also performed as a measure of residual liver function. Cefoperazone was administered intravenously over a period of 3-5 min. Blood and urine samples were collected at appropriate intervals after drug administration and stored at -30 degrees C until high-pressure liquid chromatographic (HPLC) analysis. The cefoperazone hepatic clearance, mean residence time, and renal clearance in hepatitis patients were significantly different from those of normal healthy volunteers, whereas the plasma protein binding was unaltered between the two groups. Urinary excretion of cefoperazone showed a highly significant increase in patients, 23.95 +/- 5.06% and 37.54 +/- 13.61% for normal men and hepatitis patients respectively. Hepatic clearance and fraction excreted in urine significantly correlated with values of GSP and MGEC respectively (p < 0.05). These results suggest (i) cefoperazone kinetics was significantly altered in patients with chronic lobular hepatitis; (ii) GSP, a novel simple, clinically useful quantitative liver function test, can predict the cefoperazone hepatic clearance in patients with liver dysfunction.
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PMID:The influence of chronic lobular hepatitis on pharmacokinetics of cefoperazone--a novel galactose single-point method as a measure of residual liver function. 784 32

The incidence of hypoxic hepatitis was prospectively studied for 1 year in a group of high-risk patients suffering from low cardiac output in a coronary care unit. Hypoxic hepatitis, defined as an increase in serum aminotransferase activity of at least 20 times the upper limit of normal without any other cause for hepatic necrosis, was observed in 20 patients. This represents 2.6% of the 766 patients admitted to the unit during this period and 21.9% of the 91 patients suffering from low cardiac output. Clinical, biological and hemodynamic data were compared between 20 patients with low cardiac output and hypoxic hepatitis, and 48 patients with low cardiac output but without hypoxic hepatitis who survived more than 24 h. In these two groups of patients, hepatic blood flow was measured by galactose clearance at low concentration. Patients with hypoxic hepatitis exhibited a higher central venous pressure (90% versus 38%-p < 0.001) as well as a lower hepatic blood flow (867 +/- 377 ml/min versus 1429 +/- 644 ml/min-p = 0.001). In conclusion, although it is considered a rare hepatic disorder, hypoxic hepatitis is frequent in patients with low cardiac output admitted to the coronary care unit, and is associated with a decrease in hepatic blood flow and passive hepatic venous congestion.
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PMID:Hypoxic hepatitis in patients with cardiac failure: incidence in a coronary care unit and measurement of hepatic blood flow. 789 Aug 81

Acute (hepatitis) and chronic (cirrhosis) liver injuries were experimentally induced in BALB/c-mice by administration of D-galactosamine and carbon tetrachloride, respectively. In both experimental liver diseases the incidence of hepatic tumor colonization of sarcoma L-1 was significantly reduced as compared to non-treated control animals. Thus, it seems that either dysfunction or loss of organ-characteristic lectins (galactosyl-specific hepatic lectins) prevented liver colonization. Histochemical staining of liver sections from D-galactosamine or carbon tetrachloride-treated mice with appropriate galactose-containing (neo)glycoproteins supported this hypothesis, since the lectin-dependent binding was greatly reduced as compared to sections from non-treated animals.
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PMID:Hepatocellular injury inhibits lectin-mediated tumor colonization into BALB/c-mice livers. 833 80

CD4+ T lymphocytes have been identified as being responsible for organ damage in the murine model of experimental liver injury induced by intravenous injection of concanavalin A (Con A). Liver sinusoidal endothelial cells (SEC) and Kupffer's cells (KC) are among the first cells that come into contact with lymphocytes in the liver sinusoid. We aimed to investigate the respective role of these cell populations in the initial steps of T-cell-mediated liver injury in Con A-induced hepatitis. By electron microscopy, we could show that intravenously applied Con A bound predominantly to SEC but not to KC. KC depletion by gadolinium chloride treatment of mice did not result in protection from liver injury, indicating that KCs are not primarily involved in the generation of liver injury. We could show that a CD4+ T-cell line (LNC.2) displayed selective cytotoxicity toward SEC (>50%) but not KC (12%) or fibroblasts (5%) in the presence of Con A in vitro. Microscopic observation revealed that the SEC monolayer was rapidly destroyed by LnC2 in the presence of Con A. Specificity of the Con A-induced cytotoxicity was shown by the ability of a competitive ligand, methyl-alpha-D-mannopyranoside, to reduce T-cell-mediated cytotoxicity to SEC by more than 50%. Tumor necrosis factor alpha (TNF-alpha) was produced by LnC2 in high amounts after Con A stimulation (>6 ng/mL), but antiserum to TNF-alpha did not reduce LnC2-mediated cytotoxicity toward SEC. In conclusion, we could show for the first time that liver SECs have accessory function and are selectively destroyed by CD4+ T lymphocytes in the presence of Con A. We speculate that SEC damage is an early event in T-cell-mediated liver injury recruiting T lymphocytes from the sinusoidal circulation. Loss of the SEC barrier function then exposes underlying hepatocytes to further attack by activated T lymphocytes. These results offer a model of initiating events in T-cell-mediated liver diseases, such as viral or autoimmune hepatitis, and suggest an important role for sinusoidal endothelial cells.
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PMID:Role of sinusoidal endothelial cells of the liver in concanavalin A-induced hepatic injury in mice. 885 84

Recently it has been reported that Shosaiko-to (SHO), a traditional Chinese medicine used for treating gastritis and hepatitis, also has been found useful for treating gastric ulcers, although no pharmacological study has yet investigated the precise antiulcer properties of SHO. Herein, the authors report on the results of a rat study in which the effects of SHO on gastric ulcers, acid secretions and potential difference of gastric mucosa (PD) were studied. SHO (100, 250 or 500 mg /kg, p.o.) significantly inhibited the development of ethanol-induced gastric lesions in a dose-dependent manner. SHO (500 mg/kg, p.o.) significantly inhibited the development of aspirin-,indomethacin- or water-immersion-stress induced gastric lesions. Sucralfate (500 mg/kg, p.o.) inhibited both ethanol- and aspirin-induced gastric lesions, and cimetidine (10 mg/kg, p.o.) inhibited aspirin-, indomethacin- or stress-induced gastric lesions. SHO (10, 30 and 100 mg/kg, i.p.) also significantly inhibited pentagastrin- and 2-deoxy-D-glucose (2-DG)-induced gastric acid secretions in a dose-dependent manner, whereas cimetidine (1 mg/kg, i.p.) inhibited a pentagastrin-induced secretion and atropine (0.05 mg/kg, i.p.) inhibited pentagastrin- or 2-DG-induced acid secretions. SHO (250, 500 or 1000 mg/kg, i.g.) significantly inhibited ethanol-induced PD reduction. Sucralfate (500 mg/kg, i.g.) inhibited the reduction, and cimetidine (250 mg/kg, i.g.) didn't inhibit it. These results indicate that SHO not only possesses the capability of protecting the rat gastric mucosa as well as sucralfate, but also is able to inhibit gastric acid secretions like cimetidine or atropine.
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PMID:[Antiulcer properties of shosaiko-to]. 894 Jul 3

This report shows that loss of heterozygosity at the mannose 6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) locus occurred in 5/8 (63%) dysplastic liver lesions and 11/18 (61%) hepatocellular carcinomas (HCCs) associated with the high risk factors of hepatitis virus infection and liver cirrhosis. Mutations in the remaining allele were detected in 6/11 (55%) HCCs, including deletions in a polydeoxyguanosine region known to be a target of microsatellite instability. M6P/IGF2R allele loss was also found in cirrhotic tissue of clonal origin adjacent to these dysplastic lesions and HCCs, demonstrating that M6P/IGF2R inactivation occurs early in liver carcinogenesis. In conclusion, HCCs frequently develop from clonal expansions of phenotypically normal, M6P/IGF2R-mutated hepatocytes, providing further support for the idea that M6P/IGF2R functions as a liver tumor-suppressor gene.
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PMID:Loss of the gene encoding mannose 6-phosphate/insulin-like growth factor II receptor is an early event in liver carcinogenesis. 929 14

Small-diameter H-graft portacaval shunts (HGPCSs) effectively treat bleeding varices due to cirrhosis, although the effects of such shunts on hepatic blood flow are not well established. Proponents of HGPCS believe that portal flow diverted through the shunt is regained through increased hepatic arterial inflow while others argue that this flow is never recovered; resulting in compromised nutrient flow. In this study, we sought to determine the effects of HGPCS on effective hepatic and portal blood flow. Patients undergoing HGPCS had portal pressures and flow (via color-flow Doppler ultrasound) measured intraoperatively before and after placement of HGPCS. Effective hepatic blood flow was determined utilizing low-dose galactose clearance 1 day preoperatively and 5 days postoperatively. Over a 7-year period, 64 patients (42 male and 22 female), average age 54 +/- 13.6 years (SD), were studied. Cirrhosis was due to alcohol in 37 patients, hepatitis in 9, alcohol and hepatitis in 5, and assorted other causes in 13. Child's class was A in 11 patients, B in 35, and C in 18. Both portal flow and pressures decreased significantly postoperatively (15 +/- 14.2 to 10 +/- 15.1 mL/min [P < 0.05] and 29 +/- 13.0 to 18 + 6.2 mm/Hg [P < 0.05]), whereas effective hepatic blood flow decreased insignificantly (1441 +/- 1719 to 1332 +/- 863 mL/min). Small-diameter HGPCS significantly reduce portal pressures and portal blood flow while maintaining effective hepatic flow. These findings suggest that hepatic arterialization occurs as early as 5 days after shunting and thus support the application of HGPCS.
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PMID:Small-diameter H-graft portacaval shunt reduces portal flow yet maintains effective hepatic blood flow. 945 41

Three fractions of polysaccharides that have high biological activity were extracted from Chinese bamboo leaves (Indocalamus Tesselatus) with 0.9% sodium chloride, 1% ammonium oxalate and 85% ethanol. Their component sugars were investigated by paper chromatography developed with n-butanol-pyridine-water (6:4:3 by vol), and by gas chromatography with crown ester stationary-phase-fused silica capillary column. Their monosaccharide compositions are different from each other with glucuronic acid, galactose, arabinose, mannose, glucose, and xylose (52, 18, 9, 7 and 6%, respectively) in one fraction, only glucuronic acid in another and glucuronic acid, fucose, arabinose and xylose (36, 31, 24 and 9%, respectively) in the third fraction. The protection effect of two polysaccharides against experimental hepatitis was studied in mice.
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PMID:Chromatographic analysis of polysaccharides extracted from Chinese Indocalamus tesselatus. 956 76


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