Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

I evaluated the diagnostic value of routinely ordered liver-function tests in 175 biopsy-proven cases of hepatic disease by use of stepwise discriminant analysis. The tests studied-total and "direct" bilirubin, alkaline phosphatase, lactate dehydrogenase, and aspartate aminotransferase-correctly classified 45-73% of cases, depending on the homogeneity of the diagnostic groups. Aspartate aminotransferase and alkaline phosphatase were the best discriminators. When all tests were used in the most homogeneous groups (tumors, cirrhosis, and hepatitis), there was a stepwise improvement in diagnostic accuracy from 51 to 73%.
 ...
PMID:Diagnostic effectiveness of biochemical liver-function tests, as evaluated by discriminant function analysis. 84 56

Orthotopic allogenic liver transplantations were carried out on 39 pigs. The length of survival time ranged from a few hours until 179 days. The clinical and biochemical laboratory findings as well as the macroscopical, light microscopical and electron microscopical findings established by biopsy and autopsy in the period after the transplantation are described and discussed with regard to their diagnostic significance and pathogenesis. The causes of death are generalized haemorrhages (15 cases), post-operatively bleeding gastric ulcers (12 cases), infections (7 cases), and early or late complications connected with the surgical interventions (5 cases). Observations of liver homografts over a long period after healing-in without complications and during sufficient function of the transplant show (without immunosuppressive treatment) the development of alterations in accordance with the features of chronic aggressive hepatitis and subsequent liver cirrhosis. Complications resulting from this account for some of the established causes of death. According to the results of experiments in animals surviving for a longer time after transplantation there are a general adaptive activation of metabolism and focal alterations in the outer cell membrane of the parenchymal cells in the transplanted liver. This alteration in the cell membrane of the liver epithelial cells causes an abnormal permeability and may lead to partial peripheral lysis and to total lytic necrosis (colliquation necrosis) of these cells. The main cause of these changes is ischaemia or hypoxia brought about by a variety of factors and the cytolytic effect of specifically sensitized lymphocytes ("killer", lymphocytes, immunocytes, effector cells) of the host organism which is the basis of the actual immunologic rejection process. The observed increase of glutamic oxalacetic transaminase (GOT) and lactate dehydrogenase (LDH) as well as potassium in the blood serum may be regarded as a sign of a progressive (developing) rejection or a chronic insufficience of blood circulation of the transplant. Long-term observations show the tendency for a slow continuous reduction in number of the erythrocytes and leucocytes in the host animals. The behaviour of the macrophages (Kupffer cells) in the liver transplant in relation to erythrocytes, thrombocytes and also lymphocytes of the host organism requires particular attention.
 ...
PMID:[Light microscopical, electron microscopical and clinical findings in orthotopic allogenic porcine liver homografts (author's transl)]. 110 5

Glycylprolyl beta-naphthylamidase activities in sera from 40 normal subjects (18-81 years) were: 22.6 +/- 0.9 (S.E.) (11.8-38.2) I.U./1 serum at 37 degrees C. The enzyme activities did not differ significantly with age between the younger group under 40-years-old and the older group over 40-years-old. Males, especially under 40-years-old, had slight but significantly higher activities than females. The levels were decreased in patients with gastric cancer. The levels were elevated in patients with hepatobiliary diseases, and had significant correlations with the results of the serum tests in hepatic diseases such as glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, alkaline phosphatase and total bilirubin, but had no correlation with serum lactate dehydrogenase. In cellulose acetate electrophoresis, normal sera had a single peak at the beta-globulin region, but the sera in hepatitis or liver cirrhosis showed not only an increase in the normal peak at the beta-globulin region but also the appearance of the other one or two new peaks in the alpha1 and alpha2-globulin regions.
 ...
PMID:Glycylprolyl beta-naphthylamidase activity in human serum. 114 81

Mucosal resistance to infection with lactate dehydrogenase-elevating virus (LDV) has been previously demonstrated, and the LDV system presents an important murine model for the study of mucosal barriers to viral infection. In the present study, duodenal molecules were isolated from normal mice which had potent virucidal activity, when tested against LDV as well as canine herpes, canine hepatitis, Semliki forest, and visna viruses. The virucidal activity was demonstrated to be non-immune in nature, and was present in apparently non-enzymatic protein molecules, having a molecular mass of between 10-100 kDa by membrane filtration and 10-17 kDa by gel filtration. The anti-LDV activity of these molecules was suppressed by anti-duodenum antibodies in vitro, and in vivo studies suggested a possible protective role for the anti-viral molecules. We conclude that the normal mouse duodenum contains potent virucidal molecules, which are of interest to the study of biological and molecular mechanisms of viral resistance.
 ...
PMID:Virucidal effect of murine duodenal extracts: studies with lactate dehydrogenase-elevating virus. 141 11

Hepatocyte growth factor, a potent mitogen for mature hepatocytes in vitro, seems to function as a hepatotrophic factor for liver regeneration. We examined the mitogenic effect of hepatocyte growth factor on mouse liver in vivo. The labeling index of hepatocytes was markedly increased when recombinant human hepatocyte growth factor was injected intravenously into mice subjected to 30% hepatectomy (control, 1.7% +/- 0.1%; 1 microgram hepatocyte growth factor, 6.4% +/- 1.3%; 5 micrograms hepatocyte growth factor, 18.3% +/- 0.2%) and into mice administered carbon tetrachloride (control, 12.7% +/- 1.0%; 1 microgram hepatocyte growth factor, 26.3% +/- 2.8%) or alpha-naphthylisothiocyanate (control, 0.4% +/- 0.1%; 1 microgram hepatocyte growth factor, 3.8% +/- 1.1%; 5 micrograms hepatocyte growth factor, 14.2% +/- 2.0%). In addition, weights of the remnant livers in mice given hepatocyte growth factor 60 hr after 30% hepatectomy were significantly greater than those of untreated control mice (control, 0.93 +/- 0.04 gm; 5 micrograms hepatocyte growth factor, 1.06 +/- 0.04 gm). Hepatocyte growth factor prevented any marked increase in the serum levels of liver enzymes and bilirubin when it was administered to mice also treated with alpha-naphthylisothiocyanate (control: ALT, 394 +/- 278 IU/L; lactate dehydrogenase, 2,644 +/- 1,109 IU/L; bilirubin, 9.6 +/- 2.6 mg/dl; and 5 micrograms hepatocyte growth factor: ALT, 135 +/- 7.9 IU/L; lactate dehydrogenase, 1,672 +/- 626 IU/L; bilirubin, 1.0 +/- 0.8 mg/dl). Our findings show that intravenously injected hepatocyte growth factor stimulates the growth of hepatocytes in mouse liver and protects the integrity of hepatocytes in vivo against hepatitis caused by hepatotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Direct evidence that hepatocyte growth factor is a hepatotrophic factor for liver regeneration and has a potent antihepatitis effect in vivo. 142 61

The 3'-terminal 1314 nucleotides of the genome of one isolate of lactate dehydrogenase-elevating virus, LDV-P, has been derived by sequence analyses of cDNAs from several genomic libraries and compared to that of another LDV isolate, LDV-C (Godeny et al. (1990) Virol. 177, 768-771). The 3'-non-coding segment of 80 nucleotides of the two LDV genomes is identical, whereas marked, but varying nucleotide and amino acid divergence is apparent in the three upstream overlapping open reading frames (ORF). The third ORF from the 3'-end exhibits only 82% nucleotide and 90% amino acid identity, whereas the 3'-terminal ORF, which encodes the nucleocapsid protein, exhibits approximately 99% amino acid identity. The second 3'-terminal ORF encodes an 18.8 kDa protein which lacks N-glycosylation sites but possesses 2 or 3 potential transmembrane helices in the N-terminal half of the molecule. A similar membrane organization is observed for the corresponding protein of equine arteritis virus and the M protein of mouse hepatitis virus. The sequence analyses combined with Northern hybridization analyses of RNA from LDV-infected macrophages and spleens of LDV-infected mice indicate that the three ORFs encoded by the 3'-terminal end of the LDV genome are expressed via the three smallest mRNAs (mRNAs 6-8) of the seven subgenomic mRNAs of LDV (mRNAs 2-8), which range in size from about 0.8 to 3.6 kb. All mRNAs have been shown to carry poly(A)-tracts and a common leader sequence. The seven mRNAs were produced in infected macrophage cultures concomitantly with genomic LDV RNA. Maximum LDV RNA synthesis was observed between 6 and 8 h post-infection. The same seven subgenomic mRNAs were detected in macrophages infected with three different isolates of LDV, but different relative amounts of some of the mRNAs were produced. The relative proportions of molecules of mRNAs 1-8 present in 6 h LDV-P-infected macrophages were about 13, 5, 5, 8, 6, 11, 11 and 27% of the total, respectively.
 ...
PMID:Lactate dehydrogenase-elevating virus (LDV): subgenomic mRNAs, mRNA leader and comparison of 3'-terminal sequences of two LDV isolates. 160 32

An acute or fulminant adenovirus hepatitis developed in 5 of 224 pediatric patients who were recipients of orthotopic liver transplants. All had received prednisolone, azathioprine, and cyclosporine as basal immunosuppression, and four received monoclonal (OKT3) or polyclonal (antithymocyte globulin) antibodies for steroid-resistant rejection episodes. These patients initially had high fever and a worsening condition for a mean of 73 days after transplantation (range 44 to 140 days). Results of biochemical tests showed very high serum levels of lactate dehydrogenase. Aspartate aminotransferase values were always markedly more elevated than those of alanine aminotransferase. Two patients had severe leukopenia. Results of histologic studies of the liver showed extensive areas of confluent necrosis and targetlike hepatocyte nuclei. Typical intranuclear viral inclusions were observed on electron microscopy. Adenovirus was cultured in all patients and in two relatives. Two patients died of liver failure; others recovered after cessation of immunosuppression. We conclude that adenovirus hepatitis can be fatal in liver transplant recipients. There is no specific treatment, and immunosuppression must be discontinued.
 ...
PMID:Acute adenovirus hepatitis in liver transplant recipients. 173 Oct 21

It is known that rodents challenged with a combination of galactosamine and endotoxin develop a fulminant hepatitis within several hours. Until now, no in-vitro correlate for this organ-specific lesion has been described. Here, in-vitro conditions have been developed which allow examination of lipopolysaccharide (endotoxin)-inducible cell injury to hepatocytes. Under these in-vitro conditions (RPMI 1640 supplemented with 10% calf serum, 40% oxygen tension) which require the presence of functionally intact Kupffer cells, a concentration-dependent lactate dehydrogenase release is inducible by different lipopolysaccharides in hepatocyte cultures from Fischer rats. It can be abrogated by polymyxin B. These co-cultures secreted tumor necrosis factor-alpha into the medium upon a lipopolysaccharide stimulus. The presence of a tumor necrosis factor-alpha antiserum reduced the major part of the endotoxin-inducible cytotoxicity. Similarities in vitro and in vivo of the cytotoxic potency of various endotoxin species and the different responsiveness of hepatocytes from two different rat strains support that this co-culture system might be useful for studying endotoxin-inducible lesions in vitro.
 ...
PMID:Endotoxin-inducible cytotoxicity in liver cell cultures--I. 187 97

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

Values for total lactate dehydrogenase (LD, EC 1.1.1.27) and LD isoenzyme-5 were determined in serum of 106 patients with benign hepatic disorders, 54 of whom had acute liver disorders, either acute hepatitis (39 patients) or acute circulatory disturbances (15 patients). Fifty-two had chronic hepatic disorders, either cirrhosis (25 patients) or chronic right heart failure (27 patients). Overall, values for LD were above normal for 86 percent of the 106 patients with benign hepatic disorders. In 83 percent of 30 patients with non-fulminant viral hepatitis, LD values were below 350 U per L, while in all nine patients with either fulminant viral or toxic hepatitis, and in all 15 patients with acute circulatory disturbances, LD values were above 500 U per L. In all 52 patients with chronic hepatic disorders, LD values were below 350 U per L. In patients with acute liver disorders, both the total LD and LD-5 proportions were sensitive for liver injury (87 percent and 91 percent, respectively). On the other hand, LD-5 proportion was much less sensitive than total LD in patients with chronic liver disorders (40 percent versus 85 percent). In conclusion, a difference was found in LD values and LD-5 ratios between patients with non-fulminant viral hepatitis and patients with other causes for acute liver injury. The LD-5 proportions are more sensitive for hepatic injury in patients with acute liver disorders than in those with chronic liver disorders.
 ...
PMID:Alterations in total lactate dehydrogenase and its isoenzyme-5 in hepatic disorders. 240 42


1 2 3 4 5 6 7 8 9 Next >>