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)

Using human peripheral blood monocytes to assay opsonic protein activity, we have examined the efficiency of various procedures for isolating fibronectin from plasma for experimental or therapeutic use. In addition, we have assessed the protein's opsonic activity after cold storage, and after heat treatment to inactivate hepatitis virus. The purification procedures recovered only 30% of available plasma fibronectin whilst cold storage and heat treatment of the purified protein removed all of its remaining opsonic activity. This was associated with no alteration in overall molecular weight or in subunit size but was accompanied by changes in ultraviolet spectrum, suggesting a conformational change in the protein structure. Initial experiments to protect the purified protein against these changes were unsuccessful and unless further attempts are more encouraging, fresh-frozen plasma may be the only current economic source of opsonically active fibronectin. Since this would waste other valuable proteins required for other purposes, the widespread use of plasma fibronectin outside of clinical trials may be unjustified at this present time.
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PMID:Conformational changes and loss of opsonic function in frozen or heat-treated plasma fibronectin. 673 Apr 22

Plasma derivatives can be separated into those with either a low or a high risk of transmitting viral hepatitis. Low-risk products, with few exceptions, will remain low-risk irrespective of the plasma from which they are manufactured because they are heated at 60 degrees C for 10 hours (Albumin, Plasma Protein Fraction) or because they contain protective antibodies (Immune Globulin). This would appear to be the case not only for hepatitis B but also for non-A, non-B hepatitis. The risk of hepatitis B associated with plasma derivatives is reduced but not eliminated by HBsAg screening of donors. Further decreasing the risk of hepatitis B associated with AHF or Factor IX lots, as well as newer products like AT-III, alpha-1 antitrypsin, Fibronectin, C-1 Inactivator, and Factor XIII, may be accomplished either by the combination of stabilization and heating or by assuring that these products contain an excess of anti-HBS. For highly-purified products with little residual immunoglobulin it may be necessary to add anti-HBs. The addition of antibodies against non-A, non-B hepatitis agents when they are identified, could prevent transmission of both forms of viral hepatitis by plasma derivatives. Methods to stabilize and heat high-risk plasma derivatives to inactivate hepatitis viruses have the potential to remove both hepatitis B and non-A, non-B hepatitis infectivity.
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PMID:Plasma derivatives and viral hepatitis. 681 45

Specific antibodies to collagen type IV, laminin, and fibronectin were used to localise these proteins by indirect immunofluorescence in frozen sections of normal and fibrotic liver. In normal livers distinct staining was found in basement membranes of blood and lymph vessels, of bile ducts and ductules and around nerve axons. Positive reactions for type IV collagen and fibronectin were also observed in the perisinusoidal space, while hepatocytes and most of the interstitial matrix of portal fields remained unstained. Liver specimens obtained from patients with alcoholic liver disease (fatty liver, hepatitis or cirrhosis) and chronic active hepatitis showed a more intense reaction with the antibodies in the perisnusoidal space including now distinct staining for laminin. These patterns were particularly prominent at borders between fibrotic septa and remnants of parenchyma or pseudolobules. Strong reactions were also found for type IV collagen and fibronectin in the periportal interstitium and in large fibrotic areas. The findings support previous electron-microscopical and chemical evidence for increased basement membrane production in human liver fibrosis and demonstrate that this may involve different proteins and occur at different anatomical sites.
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PMID:Distribution of basement membrane proteins in normal and fibrotic human liver: collagen type IV, laminin, and fibronectin. 698 3

The present study describes the plasma levels of soluble fibronectin (FN), C3d, the breakdown product of C3 complement and Ba, the breakdown product of properdin factor B, in 30 patients of uncomplicated acute viral hepatitis (AVH), 64 patients of fulminant hepatic failure (FHF) and 29 patients of subacute hepatic failure (SAHF) with different hepatitis viral infections. Aetiological analysis of these patients demonstrated hepatitis B, hepatitis C and hepatitis non-A, non-B, non-C (NANB-NC) infections in 6.7, 13.3 and 80% cases, respectively, of the AVH group; 18.8, 42.2. and 39.0% cases, respectively, of the FHF group; and 31.0, 34.5 and 34.5% cases of the SAHF group. None of them had hepatitis A infection. The analysis of data showed that the plasma FN level was significantly reduced in patients with FHF and SAHF as compared to AVH patients and healthy persons. Fibronectin levels in AVH was comparable to that in the healthy group. Further, the FN level was not dependent on the nature of aetiological virus. The level of C3d in plasma was significantly high in all patients of FHF and SAHF, irrespective of their viral aetiology, compared to the AVH group and the healthy group. Like FN, the C3d level was comparable in the AVH and healthy groups. However, the Ba level was comparable to the normal value in all types of infections including the AVH, FHF and SAHF groups. These findings were used to explain the possible roles of fibronectin and complement in the immunopathogenesis of liver injury in patients of acute liver failure of viral aetiology.
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PMID:Role of fibronectin and complement in immunopathogenesis of acute and subacute hepatic failure. 794 18

Plasma fibronectin and serum complement C3 levels were estimated in 30 patients with chronic active hepatitis (CAH) post virus "B" and another 30 patients with CAH post virus "C" as well as 20 normal healthy subjects. Fibronectin level was significantly increased in CAH when compared to normal controls. Moreover, fibronectin level was significantly increased in CAH following virus "C" when compared to CAH following virus "B" hepatitis. Concerning complement C3 there was no significant changes in the different groups studied. We may conclude that CAH following virus "C" may lead to vigorous inflammatory damage than CAH following virus "B" infection.
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PMID:Plasma fibronectin and serum complement C3 levels in chronic active hepatitis following virus "B" versus virus "C" infection. 837 76

Immunohistochemical study was carried out on D-galactosamine hydrochloride (GaIN)-induced subacute hepatitis in rats of JCL: Wistar-TGN (ARGHGEN) 1Nts strain (Mini rats), in which the expression of growth hormone gene is suppressed by the presence of an antisense transgene. Mini rats were given 1000 mg/kg of GaIN once a week for 4 consecutive weeks and killed at 1, 2, 3 and 4 weeks after the first administration. At 1 week after the first administration, proliferation of small epithelial cells positive for both alpha-fetoprotein and cytokeratin 7, i.e. so-called oval cells, was observed in the whole area of each hepatic lobule, and prominent deposition of fibronectin, laminin and type IV collagen was detected around these oval cells. Together with these extracellular matrix components, many activated Ito cells positive for both desmin and alpha-smooth muscle actin were observed. With time, most of the oval cells formed duct-like structures and lost their positive stainability for alpha-fetoprotein, and many Ito cells became inactive. Deposition of fibronectin decreased rapidly from 2 weeks after the first administration. At 4 weeks after the first administration, deposition of laminin was detected only around the duct-like structures, where that of type IV collagen was also still prominent. These results suggest that a large population of oval cells differentiated into bile duct epithelial cells and that Ito cells and extracellular matrix components might play a role in this process.
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PMID:Immunohistochemical study on galactosamine-induced subacute hepatitis in rats of JCL: Wistar-TGN (ARGHGEN) 1 Nts strain (Mini rats). 925 Apr 81

Histopathological and immunohistochemical studies were carried out on D-galactosamine (GalNAc)-induced acute hepatitis in rats of the JCI: Wistar TgN (ARGHGEN) 1 Nts strain (Mini rats), in which expression of the growth hormone gene is suppressed by an antisense transgene. Hepatitis characterized by hepatocellular acidophilic necrosis with inflammatory cell infiltration was most prominent at 2 days after GalNAc (1000 mg/kg)-injection, when proliferation of Ito cells and deposition of fibronectin and laminin were found along the sinusoidal linings. At 72 hours after GalNAc-injection, Ito cell proliferation with deposition of laminin and fibronectin became more prominent, and marked proliferation of small epithelial cells was observed in the periportal area. At 7 days after GalNAc-injection, quite a number of alpha-smooth muscle actin-positive Ito cells, surrounded by abundant fibronectin, laminin and type IV collagen, were still observed in close juxtaposition to rapidly proliferating small epithelial cells. The small epithelial cells were found to be positive for both alpha-fetoprotein and cytokeratin 7 and were therefore considered to be so-called oval cells. The results suggest that there may be some relation between oval cell proliferation, Ito cell activation and extracellular matrix accumulation in GalNAc-induced acute hepatitis in Mini rats.
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PMID:Prolonged oval cell proliferation with Ito cell activation and extracellular matrix accumulation in galactosamine-induced acute hepatitis in mini rats. 930 54

Forty-five livers from conventionally slaughtered Holstein-Friesian steers with telangiectasis were studied by histochemical methods, immunolabelling for fibronectin, laminin and type IV collagen, and transmission electron microscopy. None of the previously described changes in telangiectasis (necrosis, hepatitis, thromboembolism, dilatation of the space of Disse by glycogen extruded from hepatocytes and reduced density of the perisinusoidal reticulin framework) were evident. Pretelangiectasis (sinusoidal dilatation) and telangiectasis (blood-filled cavities) were characterized by sinusoidal barrier alterations, leading to sinusoidal capillarization; and there was progressive formation of a true basement membrane and perisinusoidal fibrosis. Comparison of bovine liver telangiectasis and human peliosis hepatis suggests that they have a similar pathogenesis. It is suggested that a primary alteration of the sinusoidal barrier is responsible for an increased deposition of basement membrane components (fibronectin, laminin, type IV collagen) in the perisinusoidal region, and fibrosis. These are likely to render the exchange of oxygen and substrates between blood and hepatocytes more difficult and to produce haemodynamic imbalances, leading to hepatocyte atrophy and eventually to sinusoidal disruption.
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PMID:Pretelangiectasis and telangiectasis of the bovine liver: a morphological, immunohistochemical and ultrastructural study. 974 55

Patients with haemophilia often exhibit a variety of disturbances in immune function. Although infections with HIV, hepatitis and other viruses no doubt contribute to these abnormalities, chronic exposure to extraneous proteins in clotting factor concentrates (CFCs) may also play a role. Numerous in vitro and ex vivo studies show that protein contaminants--such as immunoglobulins, fibrinogen and fibronectin--can depress various immune function indicators. Generally, such studies show that intermediate-purity CFCs are more inhibitory than very high-purity (e.g. monoclonal-purified) CFCs. In many, but not all, studies, the degree of immunosuppression correlates with the amount of intermediate-purity CFC administered over time. Among various indicators of immune function, CD4+ lymphocyte number is a marker for the progression of HIV infection, and maintenance of CD4+ number is associated with delayed progression. A number of studies suggest that, compared with intermediate-purity CFCs, use of very high-purity CFCs is associated with longer preservation of this class of lymphocytes. However, it remains to be seen whether this translates to improved long-term clinical outcomes. Further research is needed on the impact of CFCs on the immune system. For the time being, however, evidence to date favours the use of very high-purity products because they appear to preserve immune function and reduce the risk of infection with hepatitis and other viruses.
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PMID:Clotting factor concentrates and immune function in haemophilic patients. 987 75

Acute and fulminant liver failure induced by viral hepatitis, alcohol or other hepatotoxic drugs, are associated with tumor necrosis factor (TNF) production. In a mouse model of lethal hepatitis induced by TNF, apoptosis and necrosis of hepatocytes, but also lethality, hypothermia and influx of leukocytes into the liver, are prevented by a broad-spectrum matrix metalloproteinase (MMP) inhibitor, BB-94. Mice deficient in MMP-2, MMP-3 or MMP-9 had lower levels of apoptosis and necrosis of hepatocytes, and better survival. We found induction of MMP-9 activity and fibronectin degradation. Our findings suggest that several MMPs play a critical role in acute, fulminant hepatitis by degrading the extracellular matrix and allowing massive leukocyte influx in the liver. BB-94 also prevented lethality in TNF/interferon-gamma therapy in tumor-bearing mice. A broad-spectrum MMP inhibitor may be potentially useful for the treatment of patients with acute and perhaps chronic liver failure, and in cancer therapies using inflammatory cytokines.
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PMID:Inhibition of matrix metalloproteinases blocks lethal hepatitis and apoptosis induced by tumor necrosis factor and allows safe antitumor therapy. 1168 84


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