Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary sclerosing cholangitis, a chronic cholestatic liver disease, frequently leads to an impairment of liver function. In nine men and two women, aged 23 to 57 years, we prospectively studied for three to six years the effect of treatment with ursodeoxycholic acid (UDCA) on liver function. 10 mg UDCA/kg bw significantly reduced serum activities of AP, gamma GT, AST and ALT for several years. After three years of treatment, however, serum concentration of bilirubin was higher than before therapy in eight out of eleven patients (1.8 +/- 0.8 versus 0.9 +/- 0.1 mg/dl; p = 0.01). Likewise, serum concentration of bilirubin was higher in eight out of nine patients after four years of treatment (1.3 +/- 0.3 versus 0.9 +/- 0.1 mg/dl; p = 0.03). In most cases, however, the increase was discrete. Parameters of synthetic liver function (coagulation, serum protein concentration, serum activity of cholinesterase) remained constant in the observation time. Quantitative liver function tests (galactose elimination capacity and indocyanine green half-life) also showed little variation in the observation time. We conclude that UDCA treatment significantly improves serum activities of liver enzymes for several years. Nevertheless, serum bilirubin concentration, believed to be of prognostic value in patients with PSC, seems to rise slowly over time. Serial determinations of galactose elimination capacity and indocyanine green halflife are not superior to conventional liver function tests in the timing of liver transplantation in the individual patient.
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PMID:[Primary sclerosing cholangitis: conventional and quantitative liver function tests during long-term therapy with ursodeoxycholic acid]. 865 87

Portal venous blood for rinsing out the University of Wisconsin solution (UWs) has the advantages of being a physiological fluid, removing acidotic mesenteric venous blood and perhaps resulting in more stable haemodynamic parameters during reperfusion. A group of 209 consecutive adult OLTs carried out between July 1993 and February 1995 were studied prospectively. The UWs was flushed out with 500 ml portal blood in 95 OLTs (group 1) and with 1.0 L 0.5% dextrose at 37 degrees C in 114 OLTs (group 2). The median day 1 and peak day 1-5 AST levels were significantly elevated in the 5% dextrose group: median 755 (118-11090) vs. 546 (121-6150) IU/I (P = 0.007, Wilcoxon); and median 1095 (159-11090) vs. 744 (157-7870) IU/l (p = 0.008, Wilcoxon), respectively. A median of 5 (0-27) units of blood were transfused in group 1 compared to 4 (0-54) units in group 2 (n.s.). There was no difference in peak bilirubin, lowest day 1-5 PT levels, primary nonfunction, median ITU stay, total inpatient stay and 1-month graft survival between the two groups (89% vs. 88%). Pre-reperfusion blood flush may be associated with less hepatocellular damage, without significant additional blood usage.
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PMID:Effect of pre-reperfusion portal venous blood flush on early liver transplant function. 895 23

In long-term survivors of liver transplantation, hepatic function is obviously of vital importance. Therefore, we prospectively performed conventional and quantitative liver function tests in patients who had survived a first transplantation for at least 4 years. Compared to 6 months after transplantation, serum bilirubin concentration and gamma GT activity were significantly lower after 3, 4, and 5 years (bilirubin 1.2 +/- 0.2 mg/dl at 6 months vs 1.0 +/- 0.1, 1.0 +/- 0.2, and 0.8 +/- 0.1 mg/dl respectively; gamma GT 106 +/- 0 33 U/l at 6 months vs 56 +/- 17, 67 +/- 35, 39 +/- 10 U/l respectively). At these points in time, blood levels of cyclosporin A were also significantly lower. Other parameters of liver cell function and liver cell integrity (AP, AST, ALT, GLDH, total protein, thromboplastin time, partial thromboplastin time) were unchanged over time. Serial quantitative liver function tests (indocyanine green half-life, galactose elimination capacity, lidocaine half-life, and MEGX formation) also remained stable. Thus, we conclude that hepatic function remains stable in long-term survivors of liver transplantation for at least several years.
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PMID:Conventional and quantitative liver function tests after hepatic transplantation: a prospective long-term follow-up. 916 62

Primary biliary cirrhosis (PBC) is a rare chronic cholestatic disorder of unknown origin that can now be treated effectively with ursodeoxycholic acid (UDCA). The clinical course of PBC is very variable, but a significant proportion of patients eventually die or undergo liver transplantation. In this single-center prospective long-term study, we analyzed the effect of UDCA therapy (10 mg/kg b.w./day) on conventional liver function tests and we also investigated whether serial quantitative liver function tests are useful in the clinical management of patients with PBC. Fifteen patients, most of them in an early disease stage, were followed up for either 4 (n = 7) or 5 (n = 8) years. In addition to regular conventional liver function tests, every 12 months quantitative liver function tests were performed. Thus we measured galactose elimination capacity, indocyanine green half-life and lidocaine half-life. Quantitative liver function tests were also performed once in healthy volunteers. Treatment with UDCA significantly improved conventional liver function tests, and this effect was maintained for several years (values in U/l before therapy and 4 years after therapy: AP = 1,346 +/- 317 vs. 516 +/- 93; gammaGT 378 +/- 80 vs. 144 +/- 30; LAP 122 +/- 10 vs. 71 +/- 9; AST 61 +/- 19 vs. 34 +/- 12; ALT 90 +/- 19 vs. 68 +/- 35; GLDH 14.3 +/- 1.9 vs. 8.2 +/- 1.9). Quantitative liver function tests were not significantly different between healthy volunteers and patients (GEC 6.8 +/- 0.3 vs. 7.0 +/- 0.3 mg/kg x min; ICG half-life 4.2 +/- 0.4 vs. 3.7 +/- 0.3 min; lidocaine half-life 75 +/- 8 vs. 79 +/- 6 min). In the patients, results of quantitative liver function tests (GEC, ICG and lidocaine half-lives) were not affected by UDCA therapy and remained constant over time. In the 1 patient who was transplanted, serial quantitative liver function tests did not indicate deteriorating liver function earlier than the patient's progressive symptoms or conventional liver function tests. Thus UDCA therapy markedly improved conventional liver function tests in patients with PBC, and this effect was maintained for at least 4-5 years. Possibly due to the fact that most of the patients were in an early disease stage, serial quantitative liver function tests provided little additional information that was relevant for planning therapy in the individual patient.
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PMID:Serial quantitative liver function tests in patients with primary biliary cirrhosis: a prospective long-term study. 932 69

The purpose of this study was to elucidate the interaction of cationic liposomes and plasmid cDNA by examining their ultrastructure, zeta potential, stability in aqueous media and protection from DNaseI digestion; their potential for hemolysis and platelet aggregation was evaluated as it may serve as an in vitro toxicity screen. Liposomes consisting of N-[1-(2,3-dioleyloxy)propyl]-N,N,N-trimethylammonium chloride (DOTMA) or 3 beta-[N-(N',N'-dimethylaminoethane)-carbamoyl]-cholesterol (DC-Chol) and dioleylphosphatidylethanolamine (DOPE) were complexed with plasmid constructs of ovine prostaglandin G/H synthase (pCMV4-PGH) or human alpha 1-antitrypsin (pCMV4-AAT) at lipid:plasmid (L/P) ratios of 3:1-8:1 (w/w). The electron micrographs showed bead-like attachment of liposomes to cDNA and coating of plasmid strands. The zeta potential showed isoelectric points at L/P ratios of 3.5-4 (DOTMA/DOPE) and 5.5-6.5, corresponding to a pKa of 6.45 (DC-Chol/DOPE). Liposome cDNA complexes were stable in water, saline and 5% dextrose for 48 h, but precipitated instantaneously in PBS. An increase in the L/P ratio corresponded with increased protection from DNaseI digestion. DOTMA/DOPE liposomes alone were highly hemolytic and DC-Chol/DOPE liposomes moderately hemolytic; hemolysis was abolished by cDNA complexation, with the exception of very high (> or = 7:1) L/P ratios. Both liposomes alone and cDNA complexes caused transient serum turbidity, while none caused platelet aggregation. It was concluded that current cationic lipid cDNA formulations are metastable and appear to have very little if any toxicity with respect to hemolytic potential and untoward interaction with other blood components.
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PMID:Physicochemical properties and in vitro toxicity of cationic liposome cDNA complexes. 937 44

In order to compare the nutritional effect of vitamin B6 derivatives, long-term feeding experiments with rats were carried out using pyridoxine-alpha-D-glucoside (PN-alpha-Glc), pyridoxine-beta-D-glucoside (PN-beta-Glc) or epsilon- (N-phosphopyridoxyl)lysine (PNP-Lys) with test diets consisting of basically the AIN-76 composition, except for the addition of 0.1 mg pyridoxine equivalent (PN eq.)/100 g diet. During 21 days of pair-feeding against the vitamin B6-deficient diet group, body weight gain, urinary excretion of xanthurenic acid and pyridoxic acid were measured. After the feeding experiment, rats were killed and examined in terms of liver kynureninase activity (EC 3.7.1.3) with and without adding exogenous pyridoxal 5'-phosphate (PLP), erythrocyte aspartate aminotransferase activity (EC 2.6.1.1), as well as PLP concentration in blood. Rats fed with PN-alpha-Glc grew well, relative to the PN group. On the contrary, PN-beta-Glc poorly served as vitamin B6 source, because average bioavailability was only about 22% in comparison to that of PN (100%). From this long-term feeding experiments, we have shown that PN-alpha-Glc (average bioavailability about 84%) is a good source of vitamin B6 similar to PN.
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PMID:Feeding experiments of pyridoxine derivatives as vitamin B6. 943 79

The effects of dietary oligosaccharides on the hepatotoxic action of D-galactosamine (GalN) were investigated in this study. Male Wistar rats fed with 20% casein diets containing 10% oligosaccharide or D-galactose (Gal) for 2 weeks were injected with GalN (1,900 mg/kg of body weight), and the plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and the hepatic glycogen concentration were examined 20 hours after the injection. The plasma AST and ALT activities in experiment 1 for the Gal + neomycin (NEO) group were significantly lower than those for the control (C), NEO, raffinose (RAF) + NEO and galacto-oligosaccharide (GA-LO) + NEO groups. In experiment 2, these activities were significantly lower in the Gal, Gal + NEO and RAF groups than in the RAF + NEO group when the groups were treated with GalN. On the other hand, in respect of the hepatic glycogen concentration in experiment 1, that of the Gal + NEO group was higher than that of the C, NEO, RAF + NEO or GALO + NEO groups. In experiment 2, this parameter was significantly higher in the Gal, Gal + NEO and RAF groups than in the RAF + NEO group after the GalN treatment. As a result, it is suggested that the GalN-hepatitis-suppressive effects of indigestible oligosaccharides such as RAF or GALO is mediated by the action of intestinal bacteria.
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PMID:Effect of indigestible oligosaccharides on the hepatotoxic action of D-galactosamine in rats. 975 56

The structure of the pneumococcal common antigen, C-polysaccharide, from a noncapsulated pneumococcal strain, CSR SCS2, was studied using 1H-NMR, 13C-NMR and 31P-NMR spectroscopy. The dependence of NMR chemical shifts on the variation in pD was also studied. It was established that the C-polysaccharide is composed of a backbone of tetrasaccharide-ribitol repeating units that are linked to each other by a phosphodiester linkage between position 5 of a D-ribitol residue and position 6 of a beta-D-glucopyranosyl residue. The polysaccharide is substituted with one residue of phosphocholine at position 6 of the 4-substituted 2-acetamido-2-deoxy-alpha-D-galactopyranosyl residue. Both galactosamine residues in the polysaccharide are N-acetylated. O)-P-Cho | 6 6)-beta-D-Glcp-(1-->3)-alpha-AATp-(1-->4)-alpha-D-GalpNAc-(1-->3)- bet a-D-GalpNAc-(1-->1)-D-ribitol-5-P-(O--> where AAT is 2-acetamido-4-amino-2,4,6-trideoxy-D-galactose and Cho is choline. This structure differs, concerning phosphocholine substituents and N-acetylation, from those reported previously for pneumococcal C-polysaccharide [Jennings, H.J., Lugowski, C. & Young, N.M. (1980) Biochemistry 19, 4712-4719; Fischer, W., Behr, T., Hartmann, R., Peter-Katalinic, J. & Egge, H. (1993) Eur. J. Biochem. 215, 851-857; Kulakowska, M., Brisson, J.-R., Griffith, D.W., Young, N.M. & Jennings, H.J. (1993) Can. J. Chem. 71, 644-648]. The structures of the C-polysaccharides present in three pneumococcal types were also examined. They contain one (in 18B) or two (in 32F and 32A) phosphocholine residues in the repeating unit. The degree of substitution was not determined. The backbone of all examined C-polysaccharides was identical and in all cases both galactosamine residues appeared to be N-acetylated.
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PMID:The pneumococcal common antigen C-polysaccharide occurs in different forms. Mono-substituted or di-substituted with phosphocholine. 1051 6

beta-1,4-galactosyltransferase 1 (beta1,4-GT 1) is localized both in the Golgi complex where it catalyzes the transfer of galactose from UDP-galactose to terminal N-acetylglucosamine forming Galbeta1 --> 4GlcNAc structure, and on the cell surface where it serves as an adhesion molecule. It has previously been reported that the expression of beta1,4-GT 1 was cell-cycle-specific, regulated by cell growth. Transforming growth factor-beta1 (TGF-beta1) could regulate cell G1/S phase transition and modulate cell growth in many types of cells. In this study, we introduced the antisense-TGF-beta1 into SMMC-7721 cell, a human hepatocarcinoma cell line, for blocking its intrinsic TGF-beta1 expression, and changing its cell-cycle, and then analyzed the gene expression of beta1,4-GT 1 together with the beta1,4-GT activity. The result showed that the antisense-TGF-beta1 transfected SMMC-7721 cells (AST/7721) were growth enhanced, with more cells in S phase and less cells in G2/M phase compared with the mock transfected cells (pcDNA3/7721). At the same time, it was found that the gene expression of beta1,4-GT 1 in AST/7721 was decreased to one fifth that of pcDNA3/7721, and the cell surface beta1,4-GT activity was reduced to one fifth of the control, while the total activity of beta1,4-GT was decreased to one half that of the control. The results indicate that suppression of TGF-beta1 expression resulted in change of cell-cycle together with the decreased gene expression of beta1,4-GT 1 and beta1,4-GT activity in human hepatocarcinoma cells.
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PMID:Effect of suppression of TGF-beta1 expression on cell-cycle and gene expression of beta-1,4-galactosyltransferase 1 in human hepatocarcinoma cells. 1089 33

The aim of this study was to develop an oviparous model suitable for studying the differential effects and mechanisms by which a high concentration of extracellular glucose and other sugars produce diabetes complications, particularly body growth retardation during development. Hence, we studied the experimental conditions necessary to obtain measurable effects of high sugar concentrations (5-mM glucose, mannitol, fructose and galactose) upon body growth and development of Bufo arenarum embryos and larvae, and upon the activity of aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), and alkaline phosphatase (APP). Unfed animals kept in glucose showed lower body weight than controls at all stages, a condition only observed at stage 26 for animals kept in galactose and fructose. All animals reached the same stage of development regardless of the solution in which they were kept. Glucose and fructose significantly decreased the activity of all enzymes tested, while galactose only affected GGT activity. The model provides the first experimental evidence for the deleterious effect exerted in vivo by different sugars upon developing embryos and larvaes of Bufo arenarum. The results prove that this model might help to elucidate the effects and the pathogenic mechanisms of hyperglycemia upon growth and development of embryos exposed to environments with high sugar concentrations. It might also become a useful tool for testing the effectiveness of drugs designed to prevent the deleterious effect of such exposure.
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PMID:A useful model to study the effect of high sugar concentrations upon growth and enzymic activities of toad embryos and larvae. 1104 75


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