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)

A semi-purified corn-based diet containing 50 mg/kg of pure (not less than 90%) fumonisin B1 (FB1), isolated from culture material of Fusarium moniliforme strain MRC 826, was fed to a group of 25 rats over a period of 26 months. A control group of 25 rats received the same diet without FB1. Five rats from each group were killed at 6, 12, 20 and 26 months. The liver was the main target organ in the FB1-treated rats and the hepatic pathological changes were identical to those previously reported in rats fed culture material of F.moniliforme MRC 826. All FB1-treated rats that died or were killed from 18 months onwards suffered from a micro- and macronodular cirrhosis and had large expansile nodules of cholangiofibrosis at the hilus of the liver. Ten out of 15 FB1-treated rats (66%) that were killed and/or died between 18 and 26 months developed primary hepatocellular carcinoma. Metastases to the heart, lungs or kidneys were present in four of the rats with hepatocellular carcinoma. No neoplastic changes were observed in any of the control rats. Chronic interstitial nephritis was present in the kidneys of FB1-treated rats killed after 26 months. No lesions were observed in the esophagus, heart or forestomach of FB1-treated rats and this is contrary to previous findings when culture material of the fungus was fed to rats. It is concluded that FB1 is responsible for the hepatocarcinogenic and the hepatotoxic but not all the other toxic effects of culture material of F.moniliforme MRC 826 in rats.
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PMID:Toxicity and carcinogenicity of the Fusarium moniliforme metabolite, fumonisin B1, in rats. 164 15

The fungus Fusarium moniliforme Sheldon is a common contaminant of maize (Zea mays L.) intended for human and animal consumption throughout the world. Culture material of F. moniliforme MRC 826, isolated from home-grown maize in an area in Transkei, southern Africa, with a high rate of human oesophageal cancer, was highly toxic to vervet monkeys (Cercopithecus pygerythrus). Ten monkeys were fed a standard primate diet which contained various amounts of culture material for 180 days. Two control monkeys received the standard diet without culture material. Pathological changes observed in liver biopsies taken by laparotomy were characterized by focal disturbance of the trabecular structure, degeneration and necrosis of hepatocytes, mononuclear infiltration, and in severe cases by cirrhosis. Biochemical changes, particularly increases in liver enzyme activities in serum, paralleled the liver damage seen by light microscopy. The acute, subacute and chronic toxic hepatitis induced in various degrees in all the monkeys fed fungal culture material showed close similarity with human viral hepatitis. The lesions also have some similarities to those induced in primates by aflatoxin, but differ in several respects. Ultrastructural nuclear and nucleolar changes caused by F. moniliforme, i.e. marginal clumping of chromatin and large nucleoli with segregation of fibrillar and granular components, suggested some similarity with the changes reported to be caused by aflatoxin and some other hepatocarcinogens. A long-term feeding experiment in vervet monkeys with F. moniliforme MRC 826 and attempts to isolate and chemically characterise the hepatotoxic metabolite(s) produced by this fungus are being continued.
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PMID:Hepatitis in vervet monkeys caused by Fusarium moniliforme. 288 17

Fusarium moniliforme Sheldon is one of the most prevalent fungi associated with maize throughout the world. A correlation has been found between the incidence of F. moniliforme in home-grown maize and the human oesophageal cancer rate in Transkei, southern Africa. Culture material on maize of F. moniliforme strain MRC 826, isolated from maize in a high-risk area for oesophageal cancer in Transkei, was either freeze-dried or oven-dried and fed to groups of 20 inbred male BD IX rats on a life-long basis. At a dietary level of 8%, both types of culture material were hepatotoxic and caused 100% mortality. Hepatic lesions in rats that died were characterized by cirrhosis, nodular hyperplasia and bile-duct proliferation. At a dietary level of 4% for 286 days followed by 2% for the remainder of the experiment, both types of culture material were hepatocarcinogenic and caused hepatocellular carcinoma in 80% and ductular carcinoma of the liver in 63% of the rats surviving more than 450 days. Only one of 30 such rats did not have a primary hepatic carcinoma. No hepatocellular or ductular carcinomas occurred in the controls. Hepatocellular carcinomas in the experimental rats invariably developed in severely cirrhotic livers showing nodular hyperplasia. Adenofibrosis also developed concurrently with hepatocellular carcinoma. A higher incidence of basal cell hyperplasia occurred in the oesophageal epithelia of rats fed freeze-dried than in those fed oven-dried material. The chemical nature of the hepatotoxic and hepatocarcinogenic mycotoxin(s) produced by F. moniliforme is unknown.
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PMID:Primary liver cancer and oesophageal basal cell hyperplasia in rats caused by Fusarium moniliforme. 648 Jan 56

Hyaluronan (HA), which is a major component of the extracellular matrix (ECM), is regulated during myofibroproliferative responses to numerous forms of inflammatory stimuli. It is a key factor involved in cellular migration and adherence. The development of a potent and non-toxic inhibitor of HA synthesis would open up a new avenue for the treatment of fibrocontractive diseases such as pulmonary fibrosis and liver cirrhosis. In this study, the effects of vesnarinone (OPC-8212: 3,4-dihydro-6-[4-(3, 4-dimethoxybenzoyl)-1-piperazinyl]-2(1H)-quinolinone) on the secretion of HA in human myofibroblast cell lines (MRC-5 and LI90 cells, referred to as pulmonary and hepatic myofibroblasts, respectively) were examined. Vesnarinone specifically and dose-dependently inhibited HA secretion by myofibroblasts up-regulated by fetal calf serum (FCS). The treatment of vesnarinone did not modify the phenotype of myofibroblast cells in culture. Vesnarinone also potently inhibited the HA secretion by the two myofibroblast cell lines up-regulated by transforming growth factor-beta1 (TGF-beta1) or tumor necrosis factor-alpha (TNF-alpha). The addition of vesnarinone to myofibroblasts resulted in a significant decrease of HA synthase (HAS) activity, with or without the addition of FCS or either cytokine. These findings suggest that vesnarinone inhibits the secretion of HA in myofibroblasts by specifically suppressing HAS activity, and may therefore prove useful for the treatment of chronic inflammation and tissue fibrosis.
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PMID:Inhibition of hyaluronan synthesis by vesnarinone in cultured human myofibroblasts. 1065 73

The purpose of this study was to assess the quality of biliary duct visualization using Gd-EOB-DTPA-enhanced magnetic resonance cholangiography (EOB-MRC) in patients with liver cirrhosis. Forty adult patients with liver cirrhosis (cirrhosis group) and 20 adult individuals with normal liver parenchyma (control group) underwent EOB-MRC using T1-weighted GRE imaging up to 180 min after Gd-EOB-DTPA administration. Two observers assessed the visualization of each biliary structure and the overall anatomical visualization of the biliary tree. Child-Pugh, MELD score and laboratory findings were compared. The grade of visualization for each evaluated biliary structure was statistically different in the two groups (P = 0.004 to <0.001). The overall EOB-MRC quality was rated as sufficient for anatomical visualization of the biliary tree in all individuals of the control group 20 min after Gd-EOB-DTPA application, but in only 16/40 patients (40%) of the cirrhosis group within 30 min after application. Analysis of the ROC curves revealed that the cut-off values, for non-sufficient visualization of the biliary tree 20 min after Gd-EOB-DTPA application, were MELD scores > or =11 and total serum bilirubin levels > or =30 micromol/l. Consecutively, EOB-MRC in patients with liver cirrhosis resulted in a decreased or even non-visualization of the biliary tree in a substantial percentage of patients.
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PMID:Contrast-enhanced MR cholangiography with Gd-EOB-DTPA in patients with liver cirrhosis: visualization of the biliary ducts in comparison with patients with normal liver parenchyma. 1836 32

The AKI in intensive care has been widely treated by international and national guidelines. The treatment of AKI in patients not requiring admission in Intensive Care Unit, but often hospitalized in Nephrology Unit, it is showed of less relevance. For over 5 years we have used for the treatment of AKI of patients admitted in Nephrology Unit an intermittent slow technique, implemented in approximately 600 patients with AKI for a total of about 3000 treatments. In this study we report the clinical results obtained in 100 consecutive patients referred to our Nephrology Unit from 1st January 2014. We excluded the patients with AKI and lactic acidosis by metformin, which were treated with CVVHDF. The Dialysis Protocol provides a slow low efficiency intermittent treatment called SLE-HDF (Sustained Low Efficiency Hemo-Dia-Filtration), with 10-hour duration, 1.5 L/h dialysate for a patient up to 75 kg, 2 L/h up to 85 kg, 2.5 L/h over 85 kg. Half of the dialysate was used in convention in post and half in diffusion. Endpoints were the recovery of renal function and the survival of the patient. On each patient was calculated on at least one seat, the Kt/V urea (UKt/V). Were studied 100 patients, 45 females and 55 males, with mean age 79.4 + 11 years. The weight was 74 kg + 18 kg at the start of treatment. The 65% of patients had diuresis < to 500 ml/24 hours. The causes of AKI were: 41% heart failure, 31 % AKI on MRC, 7% rhabdomyolysis, 6% Hepato-renal Syndrome, 4% sepsis, 11 % other causes. Major comorbidities were heart disease (63%), diabetes (50%), COPD (38%), age over 85 years, cancers 23, liver disease 16, hypotension requiring amine 15, sepsis 10. In total in the 100 patients, 512 treatments were performed, average 5.12 + 3.7. The mean UKt/V was 0.4 + 0.05 per session. The deaths were 43. Patients discharged were 57. Of these, 43 had a recovery of renal function. Fourteen patients have not recovered renal function and were admitted for chronic dialysis treatment. In conclusion, our protocol of SLE-HDF, which uses volumes of dialysate sharply lower than used in literature, has been shown to be effective in correcting the biochemical profile of the patient with AKI. The clinical results are considered satisfactory, having obtained the improvement in 57% of patients, considering that the 43 deaths, 10 were suffering from Hepato-cirrhosis and 13 from malignant neoplasm. Further studies are needed to confirm our findings.
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PMID:[The treatment of AKI in nephrology hospitalization: the SLE-HDF 15 litres in 10 hours]. 2870 Jan 86