Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cirrhosis in male albino rats was produced after repeated subcutaneous injections of carbon tetrachloride, in dosage schedule as described. A fully developed cirrhosis was observed after 150 days. The silicosis in lungs was produced after single intratracheal injection of silica dust of particle size less than 5 microns and studied up to 180 days. The effect of damaged liver on the development of silicosis in the lungs was studied. It was found that pulmonary fibrosis caused by silica dust appeared to be a tissue reaction confined to the lung tissue alone. The dysfunction of liver did not exert any influence on fibrogenesis in the lungs.
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PMID:Effect of cirrhosis on pulmonary fibrogenesis caused by silica dust in rats. 18 70

A mortality study was carried out on 595 workers who were compensated for silicosis in the Latium region, Italy, during the period 1946-84 who died between 1 January 1969 and 31 December 1984. Respiratory disorders, tuberculosis, lung cancer, bone cancer, and cirrhosis of the liver showed significantly increased risk ratios (4.1, 3.7, 1.5, 4.1, and 1.9 respectively); excesses of brain cancer and leukaemia did not reach statistical significance. Lung cancer mortality was further analysed by age, period of compensation, final degree of disability, and occupational activity. The possible confounding role of smoking was assessed by comparing the lifetime smoking habits of a sample of silicotic subjects with those of the general male population as estimated by a national health survey; the prevalence of ever smokers among silicotic subjects (70.7%) was similar to that estimated for the general population (68.5%). The present study indicates that silicosis is associated with lung cancer even though it does not clarify the respective roles of exposure to silica and silicosis.
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PMID:Mortality pattern of silicotic subjects in the Latium region, Italy. 261 Nov 62

Pathohistological findings are playing an important role in the advice of toxic organ damages. After presentation of some details about the frequency of toxic organ damages, the pathways of toxic agents in the organism are discussed. In cells toxic damage may induce cell necrosis, functional disturbance, inhibition of cell proliferation or malignant transformation; in extracellular structures it may lead to degradation phenomena in the connective tissue matrix. As demonstrated in example of calciphylaxis, a combination of different noxes may not only add but even potentiate the effects of the single noxes. In intracellular reparation processes the lysosomal system is involved. In case of necrosis regeneration is possible in most kinds of tissues, if connective tissue rails are preserved. Otherwise an irreversible reparative fibrotic alteration of organ structure is induced which develops according to particular general and schematic rules. As mostly character and course of the tissue reaction is unspecific, pathohistological findings do not enable conclusions on the type of inducing toxic agent. The following presentation of some examples of toxic damages with pathognomonic histological appearance deals with asbestosis, silicosis, chloroquine-induced cardiomyopathy, aluminum-induced osteopathy and a recently described liver cirrhosis in early childhood induced by copper-containing drinking water. Some limits of traditional pathohistological evaluation of toxic organ damages have been overcome by application of new morphological techniques. Own investigations revealed that the immunocytochemical demonstration of the C5b-9-complement complex enables a better and earlier detection of irreversibly damaged cells. Discrimination of toxic and virus-induced tissue damage is facilitated by the technique of in-situ-hybridization. Sometimes a specific recognition and localization of toxic agents is achieved by X-ray microanalysis, electron-spectroscopic imaging (= ESI) resp. laser microprobe mass spectrometry (= LAMMA); comparing these techniques X-Ray microanalysis and ESI, both, enable specific identification of chemical elements, while LAMMA, in addition, offers some information about the involved molecules and isotopes.
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PMID:[Toxic organic damage]. 265 Apr 56

Hepatic silicosis, cirrhosis, liver cell adenoma, and carcinomas developed in nude mice (NCr-Nu) given quartz by the subcutaneous and intraperitoneal routes. Syrian golden hamsters (15:16 EHS:cr) given quartz by both routes developed extensive fibrosis and cirrhosis and had higher morbidity and mortality rates after 3 months. Crystalline silica (quartz) induces fibrosis, adenomas, and carcinomas in the lungs of Fisher 344 rats, but certain strains of mice and hamsters are resistant to quartz-induced pulmonary carcinogenesis. Pulmonary fibrosis, however, is minimal in mice and absent in hamsters who received quartz intratracheally. To determine whether species differences are due to organ-specific rather than species-specific factors, susceptibility of the liver to quartz toxicity was investigated in nude mice and hamsters. The present study shows that the differential manifestations of quartz toxicity by these rodent species are dependent on factors that are organ-specific rather than host-specific. At 3 months, hepatocytes in mice were immunostained with intracellular transforming growth factor (TGF) beta 1 (LC 1-30) but not with TGF-beta 1 latency-associated peptide (LAP) protein (266-278); at 12 months, hepatocytes were immunostained with TGF-beta 1 LAP (266-278) but not with TGF-beta 1 (LC1-30). The hepatocytes of hamsters at 3 months showed immunoreactivities to TGF-beta 1 LAP (266-278) and TGF-beta 1 (LC1-30); immunostaining to TGF-beta 1 (LC1-30) was detected in nonparenchymal cells. Extracellular TGF-beta 1 (CC1-30) was detected in the silicotic granulomas and fibrous tissue in livers of both species. Quartz-induced liver carcinoma did not express TGF-beta 1 LAP (266-278) and LC (1-30) proteins, but these were detected in the cells of the adenoma in the same liver. Control animals showed no hepatic lesions nor immunoreactivity to TGF-beta 1. The spatial and temporal patterns of expression of TGF-beta 1, TGF-beta 2, TGF-beta receptor type II messenger RNAs (mRNAs), and TGF-beta 1 proteins in the different hepatic lesions suggests that TGF-beta isoforms may play a role in the pathogenesis of quartz-induced fibrosis, cirrhosis, liver cell adenoma, and carcinoma.
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PMID:Hepatic silicosis, cirrhosis, and liver tumors in mice and hamsters: studies of transforming growth factor beta expression. 862 Nov 63

Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are major proinflammatory cytokines inducing the synthesis and release of many inflammatory mediators. They are involved in immune regulation, autoimmune diseases, and inflammation. Acanthoic acid, (-)-pimara-9(11),15-dien-19-oic acid, is a pimaradiene diterpene isolated from the Korean medicinal plant, Acanthopanax koreanum. When human monocytes/macrophages stimulated with silica were treated with 0.1-10 microg/ml acanthoic acid, the production of IL-1 and TNF-alpha was inhibited up to 90%, but the production of interleukin-6 (IL-6) was not inhibited at all. At these concentrations, it had no cytotoxic effect on human monocytes/macrophages. It also suppressed the production of TNF-alpha by alveolar macrophages and lymphocytes stimulated with silica. In addition, acanthoic acid inhibited the release of superoxide anion and hydrogen peroxide from human monocytes/macrophages and neutrophils. To know the antifibrotic effects of acanthoic acid, its effects on fibroblast proliferation and collagen synthesis were tested. The proliferation of NIH3T3 cells was inhibited almost completely by the addition of the culture supernatants of human monocytes/macrophages treated with acanthoic acid, but not by the addition of acanthoic acid only. In vitro and in vivo treatment with acanthoic acid reduced collagen production by rat lung fibroblasts and lung tissue. Furthermore, acanthoic acid suppressed granuloma formation and fibrosis in the experimental silicosis. Acanthoic acid reduced serum GOT and GPT in the rats with cirrhosis induced by CCl4, and it was effective in reducing hepatic fibrosis and nodular formation. Taken together, these data indicate that acanthoic acid has a potent anti-inflammatory and antifibrosis effect by reducing IL-1 and TNF-alpha production.
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PMID:Suppression of interleukin-1 and tumor necrosis factor-alpha production by acanthoic acid, (-)-pimara-9(11),15-dien-19-oic acid, and it antifibrotic effects in vivo. 866 Aug 20

Tetrandrine (TET), a bis-benzylisoquinoline alkaloid purified and identified an active ingredient in a Chinese medicinal herb, radix stephanae tetrandrae, has been used traditionally for the treatment of congestive circulatory disorder and inflammatory diseases. TET, together with a few of its structural analogues, has long been demonstrated to have antihypertensive action in clinical as well as animal studies. Presumably, the primary anti-hypertensive action of TET is due to its vasodilatory properties. TET prevents or inhibits vascular contraction induced by membrane depolarization with KCl or alpha-adrenoceptor activation with phenylephrine (PE). TET (30 micromol/L) also inhibits the release of endothelium-derived nitric oxide (NO) as well as NO production by inducible NO synthase. TET apparently inhibits multiple Ca2+ entry pathways as demonstrated in cell types lacking the L-type Ca2+ channels. In cardiac muscle cells, TET inhibits both L- and T-type Ca2+ channels. In addition to its actions on cardiovascular tissues, TET may also exert its anti-hypertensive action via a Ca2+-dependent manner on other tissues intimately involved in the modulation of blood pressure control, such as adrenal glands. In adrenal glomerulosa cells, KCl- or angiotensin II-induced aldosterone synthesis is highly dependent on extracellular Ca2+. Steroidogenesis and Ca2+-influx in bovine adrenal glomerulosa cells have been shown to be potently inhibited by TET. In bovine adrenal chromaffin cells, TET inhibits Ca2+ currents via L- and N-type channels as well as other unidentified channels with IC50 of 10 micromol/L. Other than the Ca2+ antagonistic effects, TET also interacts with the alpha-adrenergic receptors and muscarinic receptors based on functional as well as radioligand binding studies. Apart from its functional effects, TET and related compounds also exert effects on tissue structures, such as remodelling of hypertrophied heart and inhibition of angiogenesis, probably by causing apoptotic responses. TET is also known for its anti-inflammatory and anti-fibrogenic actions, which make TET and related compound potentially useful in the treatment of lung silicosis, liver cirrhosis, and rheumatoid arthritis.
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PMID:Tetrandrine and related bis-benzylisoquinoline alkaloids from medicinal herbs: cardiovascular effects and mechanisms of action. 1246 42

Deregulation of interleukin-6 (IL-6) expression caused the synthesis and release of many inflammatory mediators. It is involved in chronic inflammation, autoimmune diseases, and malignancy. Stephania tetrandra S. Moore is a Chinese medicinal herb which has been used traditionary as a remedy for neuralgia and arthritis in China. To investigate the anti-inflammatory effects of S. tetrandra S. Moore in vitro and in vivo, its effects on the production of IL-6 and inflammatory mediators were analysed. When human monocytes/macrophages stimulated with silica were treated with 0.1-10 mug/ml S. tetranda S. Moore, the production of IL-6 was inhibited up to 50%. At these concentrations, it had no cytotoxicity effect on these cells. It also suppressed the production of IL-6 by alveolar macrophages stimulated with silica. In addition, it inhibited the release of superoxide anion and hydrogen peroxide from human monocytes/macrophages. To assess the anti-fibrosis effects of S. tetrandra S. Moore, its effects on in vivo experimental inflammatory models were evaluated. In the experimental silicosis model, IL-6 activities in the sera and in the culture supernatants of pulmonary fibroblasts were also inhibited by it. In vitro and in vivo treatment of S. tetrandra S. Moore reduced collagen production by rat lung fibroblasts and lung tissue. Also, S. tetrandra S. Moore reduced the levels of serum GOT and GPT in the rat cirrhosis model induced by CCL(4), and it was effective in reducing hepatic fibrosis and nodular formation. Taken together, these data indicate that it has a potent anti-inflammatory and antifibrosis effect by reducing IL-6 production.
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PMID:Anti-inflammatory effects of Stephania tetrandra S. Moore on interleukin-6 production and experimental inflammatory disease models. 1847 41

Constrictive polyserositis (pleuritis, pericarditis) is a syndrome within the underlying disease (tuberculosis, periodic disease, rheumatoid arthritis, systemic lupus erythematosus, asbestos, silicosis, uremia, some genetic diseases), a complication due to chest surgery or radiation or drug therapy, is occasionally idiopathic (fibrosing mediastinitis). There are frequently great difficulties in making its nosological diagnosis. The paper describes a patient in whom the onset of disease was exudative pleurisy with the signs of constriction, arthralgias; pleural punctures provided serous exudates with 80% lymphocytes. A year later there was ascitis and shin and foot edemas, which concurrent with hepatomegaly and cholestasis was regarded as cryptogenic liver cirrhosis. The signs of constrictive pericarditis were further revealed. The disease was complicated by the development of pulmonary artery thromboembolism (PATE) (which required the use of warfarin) and hemorrhagic vasculitis. Therapy with metipred in combination with isoniazid yielded a slight effect. The diagnoses of tuberculosis, liver cirrhosis, and autoimmune hepatitis, systemic vasculitis were consecutively rejected; the diagnosis of rheumatoid polyarthritis with systemic manifestations was made, by taking into account persistent arthalgias with the minimum signs of arthritis, noticeably increased C-reactive protein, rheumatoid factor, and cyclic citrullinated peptide antibodies (CCPA); plasmapheresis, therapy with metipred and methotrexate, and subtotal pericardectomy were performed. Constrictive polyserositis concurrent with PATE, hemorrhagic vasculitis (probably, drug-induced one), and hepatic lesion has been first described in a CCPA-positive patient with rheumatoid arthritis in the presence of moderate true arthritis (during steroid therapy).
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PMID:[Severe disseminated constrictive polyserositis in a patient with rheumatoid arthritis]. 2073 Nov 14