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)

41 heterozygoes and 4 homozygotes with a deficiency of galactose 1-phosphate uridyl transferase and also 3 heterozygotes and 1 homozygous patient with galactokinase deficiency were subjected to intravenous galactose loading tests with a dose of 350 mg/kg body weight in order to answer the question whether it is possible to detect the heterozygotes of both types of galactosemia by this method. For comparison, 38 healthy children and adolescents, 24 children with epidemic hepatitis and 4 children with cirrhosis of the liver, which was verified by histology, were included in the study. The elimination half-life (and also the other pharmacokinetic parameters as inaugurated by Dost) was the same for all the heterozygotes for both types of galactosemia almost without exception, and for the healthy cs, children in the acute stages of hepatitis and patients with cirrhosis of the liver was prolonged 2 to 5 times the normal. In patients with hepatitis, however, the elimination half-life was normal before the transaminases. Accordingly, the galactose clearance was decreased to half and one-fourth of the normal. Hence, heterozygotes with galactosemia cannot be detected with galactose loading tests.
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PMID:Biokinetics of galactose in the homozygotes and heterozygotes of both forms of galactosemia. 18 90

One of the most sensitive and specific signs of the galactosamine effect upon the rat liver cell is the appearance of PAS-positive and diastase-resistant granules within the cytoplasm of hepatocytes. Light-microscopic, histochemical, biochemical, and electron-microscopic findings reveal that the appearance of these ADB (= atypical dense bodies) depends upon a working glycogen metabolism at the time of GalN treatment. The ADB are composed of particles resembling, due to shape and size, ribosomes and beta particles of glycogen. Most of them are surrounded by the rER, but they are never enclosed by a limiting membrane. Due to sequential changes they can be generally classified into three types; the early, the intermediate, and the late type. In seven experiments it can be shown, that the appearance of the ADB depends upon the time and dosage after GalN treatment. They occur even if an additional treatment with galactose or uridine prevents the liver from the features of a hepatitis, as also shown in the livers of newborn animals up to 3 weeks of age. The histochemical response against various glucosidases, hexosaminidases, pronase, and RNAse as well as against various fixatives indicates that ADB are composed of, at least, two different constituents, the former RNAse-sensitive and visible with routine light-microscopic staining procedures, the latter RNA-resistant, PAS-positive, and invisible after staining with H & E or toluidine blue. The latter is diastase-resistant, suggesting that this portion of ADB does not represent the usual glycoproteins but some abnormal metabolite of glycogen. The ADB can be detected with maximal accumulation in the cytoplasm of hepatocytes at that time when the glycogen content determined in the liver homogenate by biochemical methods is greatly reduced.
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PMID:The appearance and degradation of specific hepatocellular cytoplasmic inclusion bodies in rat liver due to D-galactosamine. I. The relation between the amount of liver glycogen and the appearance of the atypical dense bodies in the liver cell. 18 85

Re/coagulan was compared to the standard calcium chloride (CaCl2) method for effectiveness of recalcification of plasma and whole blood. The time required for clot formation was determined. The effect of Re/coagulan on the specificity of hepatitis tests, direct antiglobulin tests, indirect antiglobulin tests, and agglutination tests were investigated. Hepatitis testing was performed on untreated serum and Re/coagulan-treated ethylenediamine tetraacetic acid (EDTA) plasmas by radioimmunoassay, reversed passive latex agglutination, and reversed passive hemagglutination methods. Direct antiglobulin tests were performed on untreated, CaCl2 treated, and Re/coagulan treated EDTA, acid-citrate-dextrose (ACD), and citrate-phosphate-dextrose (CPD) samples of whole blood. Red cell antibody specificity and titer were determined before and after clot formation by both the CaCl2 and Re/coagulan methods. Examples of agglutinating and sensitizing antibodies were tested. Antibodies directed against antigens in the Rh, Kell, MNS, Lewis, P, Kidd, Duffy, and Lutheran blood groups systems were investigated. Re/coaglulan didnot have a detrimental effect on the tests performed and compared favorably to the standard recalcification method.
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PMID:An evaluation of Re/coagulan for blood center tests. 51 59

Different groups of rats suffering from galactosamine hepatitis or ANIT-cholestasis received 200 mg galactose either by 5 minutes intravenous infusion or via a gastric tube. Blood galactose concentrations were measured for a time period of 1.5 hrs. after intravenous administration and the galactose elimination capacity (GEC) was calculated. After oral administration the galactose blood concentrations were determined for a period of 3.5 hrs. and the oral galactose clearance was estimated. After termination of both types of galactose loading the activity of the galactokinase (EC 2.7.1.6.) was determined in total liver homogenate and compared either to the GEC or to the oral galactose clearance in vivo. Galactokinase activity in the liver increased in the group of animals with experimental cholestasis and was significantly reduced in the galactosamine treated group. In vivo these changes could be estimated much better by the GEC than by determination of the oral galactose clearance.
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PMID:[Intravenous and oral galactose loading of rats suffering from galactosamine hepatitis and ANIT-cholestasis; comparison of the kinetics in vivo and the galactose metabolism in the liver in vitro (author's transl)]. 52 47

Plasma azopigments derived from conjugated bilirubin were analyzed by thin-layer chromatography according to HEIRWEGH et al. in 14 cases of obstructive jaundice and in 11 of acute hepatitis. The chromatographic patterns were compared with those obtained from azopigments derived from 8 normal bile samples. The plasma pigment patterns did not differ from those of the bile in number and chromatographic mobility of the spots. However, the quantitative percentages of the plasma azopigments were significantly modified: the alpha 0 fraction (free azodipyrrolic pigment) increased in both icteric syndromes, while the delta fraction (mainly glucuronide azopigment) decreased. Moreover, the behavior of two closed components of the delta group showed significant differences in both icteric syndromes. It can be postulated that the synthesis of bilirubin diconjugates decreases both in hepatocellular and cholestatic jaundice, while monoglucuronidated as well as saccharide and glucoside conjugates increase. In cholestatic jaundice the conjugation with glucuronic acid mainly takes place in the normal way, whereas compounds with different features are formed in hepatitis.
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PMID:Plasma bile pigment conjugation modalities in icterus syndromes of various origin. 54 46

All previous experiences have shown that the application of blood, blood components and intravenous solutions presents an unreplaceable therapeutical measure in modern surgical-resuscitative management of war injuries. Together with the broad application of the whole blood, there have been also used other blood components (even such as cryoprecipitate and platelet rich plasma). Among intravenous solutions the most frequently mentioned were isotonic saline, Ringer's lactate solution, glucosaline, 5% dextrose solution, dextran solutions and, recently, human albumin solutions. Due to a high risk of transmission of hepatitis virus, the dried pooled human plasma is less frequently used. There is the generally accepted agreement that availability of the sufficient quantity of blood, blood components and intravenous solutions resulted in the decreased mortality of the wounded. The role of intravenous solutions is of particular importance in the initial phase of management of the wounded and in the situations when it is necessary to wait for blood.
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PMID:[Transfusion-infusion therapy in modern wars]. 75 89

Previous work from this laboratory has suggested that the plasma amino acid pattern, known to be deranged in hepatic encephalopathy, may be related causally. In order to test this hypothesis, 23% dextrose and a special amino acid solution whose components were calculated to normalize the plasma amino acid pattern were infused in 11 patients, eight with chronic cirrhosis and acute exacerbation (Group 1) and three patients with fulminant hepatitis (Group 2), in amounts of up to 120 Gm. of protein equivalent per 24 hours. Plasma amino acids were abnormal but different in both groups. In Group 1 (cirrhosis) changes in plasma amino acid pattern including elevated phenylalanine, tyrosine, glutamate, aspartate, and methionine and decreased valine, leucine, and isoleucine. In Group 2 all amino acids were elevated, with the exception of the branched chains which were normal. Hepatic encephalopathy improved in all patients in Group 1 and in one of three patients in Group 2 following the infusion. The ratio (see article) showed an excellent correlation with a grade of encephalopathy. When this ratio, previously 1.0 in the presence of encephalopathy, returned to the normal value near 3.0 to 3.5, encephalopathy improved. An excellent correlation was obtained between the ratio and the grade of encephalopathy and was dose related as well. The results suggest that different amino acid patterns in hepatic encephalopathy of differing etiologies require treatment modalities which may differ for the two types of encephalopathy. Whereas amino acid infusion appears to be a valuable, efficacious way of providing nutrition in treating hepatic encephalopathy in patients with cirrhosis and acute deterioration and coma, other means of therapy such as plasms "laundering" appear to be necessary in patients with fulminant hepatitis.
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PMID:The effect of normalization of plasma amino acids on hepatic encephalopathy in man. 81 29

Among 466 hospitalized patients with serologically verified acute hepatitis B, 440 individuals (94.4%) could be followed up until normalization of liver function had occured, or for at least one year. In 90.2% of the patients followed-up liver function including galactose tolerance) returned to normal within four months after onset of illness. Chronic persistent hepatitis B surface antigen (HB Ag) for at least one year in 14 patients (50%). Liver biopsy was performed in consistent with CPH in all cases. Histological signs of chronic aggressive hepatitis developed in 15 patients (3.4%) and persistence of HB Ag was observed in 11 of these patients (73%). No histological follow-up was performed in patients with normal liver function within four months after onset of illness. Cprticosteroid treatment in 56 patients with prolonged symptoms did not seem to predispose to persistence of HbsaG in the serum.
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PMID:The long-term outcome of hepatitis B. 94 48

In adrenalectomized female rats a single dose of 375 mg D-galactosamine.HCl per kg of body weight produces both hepatitis and generalized edema with ascites. These alterations depend upon the dose and the time interval after injection of the aminosugar. The effect is specific for D-galactosamine; 2-deoxy-galactose produces only edema and no hepatitis, whereas D-glucosamine and D-galactose are without any measurable effect. In male adrenalectomized animals D-galactosamine produced hepatitis alone; fluid extravasation occurs only after additional orchiectomy. Glucocorticoids given before or simultaneously with D-galactosamine are able to prevent the animals from gettin edema and to ameliorate hepatitis, while mineralcorticoids do not show any effect on these alterations. It is evident that the effects of D-galactosamine on the hepatocyte and on the endothelial cells are independent from each other. This leads to the conclusion that D-galactosamine acts at least upon two different target organs, the liver and the reticulo-endothelial system in general.
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PMID:The appearance of D-galactosamine-induced hepatitis and generalized edema in adrenalectomized rats. 118 Aug 18

It has previously been shown that the M (E1) glycoprotein of mouse hepatitis virus strain A59 (MHV-A59) contains only O-linked oligosaccharides and localizes to the Golgi region when expressed independently. A detailed pulse-chase analysis was made of the addition of O-linked sugars to the M protein; upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis, three different electrophoretic forms could be distinguished that corresponded to the sequential acquisition of N-acetylgalactosamine (GalNAc), galactose (Gal), and sialic acid (SA). A fourth and fifth form could also be detected which we were unable to identify. Following Brefeldin A treatment, the M protein still acquired GalNAc, Gal, and SA, but the fourth and fifth forms were absent, suggesting that these modifications occur in the trans-Golgi network (TGN). In contrast, in the presence of BFA, the G protein of vesicular stomatitis virus (VSV), which contains N-linked oligosaccharides, acquired Gal and fucose but not SA. These results are consistent with earlier published data showing that Golgi compartments proximal to the TGN, but not the TGN itself, relocate to the endoplasmatic reticulum/intermediate compartment. More importantly, our data argue that, whereas addition of SA to N-linked sugars occurs in the TGN the acquisition of both SA on O-linked sugars and the addition of fucose to N-linked oligosaccharides must occur in Golgi compartments proximal to the TGN. The glycosylation of the M protein moreover indicates that it is transported to trans-Golgi and TGN. This was confirmed by electron microscopy immunocytochemistry, showing that the protein is targeted to cisternae on the trans side of the Golgi and co-localizes, at least in part, with TGN 38, a marker of the TGN, as well as with a lectin specific for sialic acid.
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PMID:O-glycosylation of the coronavirus M protein. Differential localization of sialyltransferases in N- and O-linked glycosylation. 162 9


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