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Query: UMLS:C0023890 (
cirrhosis
)
42,195
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Purified and concentrated preparations of Australia antigen had no stimulating effect on leukocytes of human subjects under study when tested either on
DNA
-polymerase activity, 3H-thymidine uptake or chromosomal alterations. Moreover, in patients with chronic hepatitis and
cirrhosis of the liver
no correlation between antigenemia and chromosome aberrations in blood leukocyte cultures could be detected. On the other hand, a serum obtained from a virus hepatitis patient with Australia antigen in the blood was found to stimulate leukocyte cultures from one patient with Down's syndrome and antigenemia, one mentally retarded patient and three normal donors. This stimulating agent is obviously not associated with Australia antigen.
...
PMID:Investigation of the nature of Australia antigen. I: The absence of biological activity of Australia antigen in human blood leukocyte culture. 12 42
A Farr technique has been used to assay antibodies to double-stranded
DNA
in the serum of patients with acute and chronic liver disease and carriers of HBsAg from the United Kingdom and Iraq. These antibodies were found in all groups from both countries. The highest levels were found in chronic active hepatitis and
cirrhosis
. In the Iraqi patients there was a strongly positive correlation between
DNA
-binding antibody levels and the presence of hepatitis B markers but not with disease activity. In the patients from the United Kingdom there was little correlation with disease activity and none with autoantibodies. Ninety-five per cent of asymptomatic carriers of HBsAG had elevated
DNA
-binding antibodies. It is suggested that hepatitis B-specific
DNA
might be one trigger to
DNA
antibody formation, though in liver disease a variety of factors are clearly operative.
...
PMID:DNA-binding antibodies and hepatitis B markers in acute and chronic liver disease. 30 8
There now appears to be a good correlation between long-term steroid treatment and the incidence of liver tumors. Certain changes in the liver cells after steroid treatment have been observed and are of the same nature as changes in livers with
cirrhosis
or viral hepatitis. These 2 diseases are known to have a high liver tumor incidence rate. Some steroids are known to be active as cocarcinogenic substances during the growth of liver tumors induced by different carcinogens. Many indices indicate that steroid hormones induce or promote tumors, but the mechanism of action remains unknown. Goldfarb (1976) proposed that these steroids may be lowgrade carcinogens or that they may be converted into carcinogenic compounds through partial degradation by intestinal bacteria or by drug metabolizing systems in hepatocytes. A different model is proposed to clarify the mechanism of steroid action and its relation to the induction of liver tumors. The physiological rate of cell renewal in the lives of adult rats is constant. At any time 1% of the liver cells are in the
DNA
synthesis phase and 0.001% are in mitosis. During pregnancy or after removal or destruction of liver cells, the rate of cell proliferation increases greatly. The intensity of cell proliferation in the liver of rats depends on the concentration of biologically active corticosterone in the blood. After total adrenalectomy of adult male rats, the corticosterone level in the serum declines in the 1st and 2nd postoperative days from 5 mcg/100 ml of serum to an undetectable amount. The inhibitory effect of the corticosteroids on
DNA
synthesis in liver cells "in vitro" is well known. It is assumed that corticosterone is an inhibitor of cell proliferation in the liver and that reduction or elimination of corticosterone results in cell proliferation in the liver. Elimination of corticosterone cannot be effected by adrenalectomy in male rats. Theoretically it is shown that the stimulation by progesterone results in inactivation of corticosterone. No significant differences are observed between the corticosterone concentrations in control and pregnant rats, but there is a significant increase of progesterone. The injection of progesterone stimulates mitoses in the liver with the number of mitoses being dependent on the amount and the number of injections of this hormone.
...
PMID:Promotion of liver tumors by steroid hormones. 46 51
Alcoholic patients frequently have evidence of nutritional deficiency the consequences of which may be seen in all systems of the body. Alcoholism is theoretically a completely preventable disorder which requires more attention by the general public, practising physicians and research workers. Rehabilitation of the established alcoholic will sometimes be limited by failure to modify behaviour or because of nutritionally induced brain damage but we are beginning to understand some of the mechanisms by which malnutrition evolves (Figure 2). Better methods must be developed to limit alcohol-induced tissue injury in patients whose drinking cannot be controlled. The final mechanisms of liver injury remain to be established.
Cirrhosis
may be induced in animals ingesting a good diet but this does not ensure adequate delivery and utilization of nutrients at the subcellular level.
Cirrhosis
takes a long time to evolve and the natural history, including longitudinal nutritional profiles in man, has not been established. Therefore, although normal liver morphology is sometimes seen in alcoholics with gross stigmata of malnutrition suggesting that factors other than malnutrition are important, it may be that critical nutrients have not been deficient for long enough in these individuals or severe depletion has been intermittent. Whether or not malnutrition is of decisive importance in the toxicity of alcoholic liver injury in man, adequate replacement is essential for protection and repair of liver cells. Established daily minimal requirements are not adequate for patients with active liver disease. Hepatocyte injury reduces the capacity of this major storage site and causes release of vitamins (co-enzymes) into the circulation in the form of holoenzymes. Liver damage reduces the conversion of nutrients into their metabolically useful forms required for catabolic processes and to meet increased needs for
DNA
/RNA synthesis necessary for repair of damaged cells and to replace necrotic cells. The choice and route of therapy must take account of the patient's metabolic needs and their absorptive defects. The effects of alcohol and maternal undernutrition on the fetus/neonate may cause intra-uterine death or varying degrees of brain damage, thus limiting the potential of the next generation.
...
PMID:Alcohol and nutrition. 68 85
A decade ago an antigen was identified by immunodiffusion and subsequently proved to be closely associated with hepatitis B virus. Further studies showed that hepatitis B virus circulates as a large particle containing a protein coat and a
DNA
core, and that excess coat particles are produced and circulate freely. Immunization with surface protein produced protective antibodies, and this led to the development of a prototype vaccine. Patients with hepatitis may develop a variety of extrahepatic manifestations, including polyarteritis, vasculitis, and glomerulonephritis. These associated symptoms may be due to immune complexes consisting of hepatitis B surface antigen and its antibody. The role of cellular immunity in hepatitis B is unknown. The relation between type B virus and the liver is both destructive (leading to severe acute hepatic disease and eventually to
cirrhosis
) and symbiotic (existing among carriers who have neither liver disease nor symptoms). If the factors that cause these divergent courses were delineated and understood, the results may lead to the prevention and cure of hepatitis B and its sequelae.
...
PMID:The liver and the antigens of hepatitis B. 78 84
The lymphocyte delayed hypersensitivity response to phytohaemagglutinin (PHA) and hepatitis B antigen (HBsAG) was evaluated by two in vitro tests-leucocyte migration inhibition and
DNA
synthesis. Patients convalescing from HBsAG-positive hepatits showed the presence of a state of cell-mediated immune responsiveness to the antigen. In Indian childhood cirrhosis, there was a failure of response to HBsAG and a slight but significant depression of reaction to PHA. It is suggested that the lack of immune reactivity to HBsAG, perhaps determined genetically, may be a significant factor in the evolution of
cirrhosis
in Indian children.
...
PMID:Lymphocyte response to hepatitis B surface antigen. Findings in hepatitis and Indian childhood cirrhosis. 81 95
The structure of the duodenum mucosa and proliferation of the epithelium were studied in 138 patients with chronic hepatitis and
cirrhosis of the liver
by count of the number of mitoses and that of cells labeled in the phase of
DNA
synthesis with 3H-thymidine. The atrophic changes revealed in the mucosa were noted together with the drop in the number of mitoses and the 3H-thymidine-labeled cells. This makes it possible to explain atrophy of the duodenum mucosa by inhibition of proliferative processes in the crypts.
...
PMID:[Proliferative properties of the epithelium of the duodenal mucosa in chronic hepatitis and liver cirrhosis]. 84 34
The effect of carbon tetrachloride on the liver of Heteropneustes fossilis has been studied. It results in centrolobular necrosis and
cirrhosis
. The hepatocyte nuclei are enlarged and balloon-shaped cells are visible at a few places. There is an increase at this stage in the
DNA
content of the hepatocyte nucleus. The cytoplasm is heavily laden with glycogen. Fatty infiltration starts and the fat content in the cytoplasm of the liver cells is increased. After 5 h of injection, the nuclei undergo lysis followed by ruptures in the cell membrane. The
DNA
content is greatly reduced. There is a marked depletion in the glycogen content. The bile canaliculi are filled with the extruded cell contents. The fatty infiltration increases at this stage.
...
PMID:Histochemical studies on the liver of Heteropneustes fossilis treated with carbon tetrachloride. 96 39
The frequency of identification of "empty" nuclei of hepatocytes was investigated in 65 patients (25 patients with hepato-cerebral dystrophy, 18 patients with
cirrhosis of the liver
, 15 patients with chronic diseases of the extrapyramidal nervous system and other diseases) with the help of fluorescent and electron microscopy, cytophotometric determination of
DNA
, and on the basks of bioptic material (in 60 patients) and autopsy findings (in 5 cases). The so-called "empty" nuclei of hepatocytes are not specific for hepato-cerebral dystrophy, although in this disease they were observed in a greater number than in other diseases. Their dependence on the degree of portal hypertension and on some endocrine factors was noted. "Empty" nuclei were identified most often in the periportal regions and were characterized by a considerable increase in the volume, invaginations of the membrane, intranuclear inclusions, polyploidy. The study of polyploidy of the ordinary nuclei of hepatocytes in hepatocytes in hepato-cerebral dystrophy, bearing in mind the reduplicated
DNA
, revealed the predominance of diploid nuclei.
...
PMID:[So-called empty liver cell nuclei in hepato-cerebral dystrophy and other diseases]. 101 96
The spontaneous restoration of
liver cirrhosis
induced by 6 and 9 month CC14 treatment has been studied. The OH-proline content of the liver stroma, the
DNA
content of the parenchyma, and the Co/
DNA
ratio were determined. Observations lasted for 4 months after completion of treatment.
Cirrhosis
developed after 6 month, CC14 administration was reversible in 3--4 months after the discontinuation of treatment; the normal stroma parenchyma ration had gradually normalized. Nine month treatment exhausted the capacity of the stroma for spontaneous recovery and the parenchyma regenerated to a lesser extent. Fibrosis remained practically irreversible 4 months after CC14 administration.
...
PMID:Spontaneous reversibility of advanced toxic liver cirrhosis. 123 28
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