Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

175 patients with histological evidence of chronic diffuse liver disease, 67 patients with heart failure, diabetes and atherosclerosis, and 118 healthy adults under 30 years of age engaged in sports were studied for the prevalence of hepatitis A virus antibody (anti-HAV) by radioimmunoassay using a HAVAB (Abbott)-kit. Infection with hepatitis-A virus is highly prevalent in Hungary, anti-HAV having been demonstrated in a very high proportion of controls as well as of patients. Over the age of 40 the incidence is 100% in controls and 98% in patients with chronic liver disease. Infection with hepatitis-A virus must have been asymptomatic in the majority, since no more than 11.4% of the subjects had a history of acute hepatitis. The prevalence of acquired anti-HAV increases with age until it attains 100% in advanced age. The present results lend no support to the possibility that hepatitis-A virus infection might be involved in the production of chronic diffuse liver disease.
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PMID:Hepatitis a virus antibody in chronic diffuse liver disease. 666 44

We investigated whether hypertension contributes to the development of atheloscrelosis in patients with chronic liver disease. There were no significant differences with respect to the ordinary biochemical data of serum concentrations of both protein and lipid metabolites between the hypertension group (n = 21) and the non-hypertension group (n = 31). In the hypertension group, serum creatinine level and serum concentration of lipoprotein (a) were significantly higher than those in non-hypertension group. However, there was no significant difference between the two groups with respect to the atherogenic index (apolipoproteins B versus A1 ratio). Serum glutamic oxaloacetic transaminase activity was positively correlated with serum apolipoprotein E concentration, and inversely correlated with serum lipoprotein (a) concentration, in 52 patients with chronic liver disease. Active hepatitis in patients with chronic liver disease might retard the development of atherosclerosis.
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PMID:[Chronic liver disease prevents the development of atherosclerosis in spite the risk factor]. 984 72

Rural health care delivery is often inferior to that of urban areas. Although health services do not have to be identical in the two settings, quality services appropriate for the needs of rural communities are imperative. Moreover, health education and promotion should be seen as an immediate and viable strategy for (a) reducing risk factors and health care needs, and (b) increasing the cost effectiveness of existing services. The appropriateness and prioritization of health care services and health education/promotion can only be realized if health professionals are aware of rural versus urban needs. To facilitate our knowledge of such differences, the mortality rates of the 10 leading causes of death were compared for each county in Ohio and differences between rural and urban mortality were analyzed. Counties were categorized according to "density" (persons per square mile) and "percent urban" (percent of county area classified as urban). The analysis demonstrated that there were no significant differences between rural and urban counties in mortality due to cancer, pulmonary disease, diabetes mellitus, atherosclerosis, and suicide. Mortality related to cardiovascular disease, cerebrovascular disease, accidents, and influenza/pneumonia was significantly higher in rural counties, while deaths due to chronic liver disease were significantly greater in urban counties.
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PMID:Difference in rural and urban mortality: implications for health education and promotion. 1029 26

Today's patient population is increasingly older. Patients with chronic renal failure therefore start extracorporeal substitutive treatment having congestive heart failure, chronic liver disease, diabetes and so forth. In these patients, however, long-term haemodialytic treatment may add further aggravation on their pre-existing pathological conditions. Oxidative stress and alterations in lipid metabolism are caused by haemodialysis mainly due to (1) bioincompatibility type of reactions such as production of reactive oxygen species by inflammatory cells due to complement-mediated or -independent pathways, and (2) the imbalance between oxidants and antioxidants due to the diffusive loss of hydrophilic vitamins such as ascorbic acid. The events related to the oxidant stress may sustain a state of chronic inflammation. Recent advances suggest that atherosclerosis and proliferation of the smooth muscle are initiated and sustained by inflammatory mechanisms. Therefore, attempts to counterbalance the prooxidant effect of haemodialysis and to reduce the chronic inflammatory state will be presented.
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PMID:An overview of haemodialysis and oxidant stress. 1044 69

The aim of this study was to assess the effect of ZR on the growth of cultured human hepatic myofibroblast cells (hMF). The zedoary (Zedoariae Rhizoma) made from the dried rhizome of Curcuma zedoaria Roscoe is an herbal drug used as an aromatic stomachic. The plant is a perennial herb which is natively distributed throughout Korea and is a traditional Korean herbal medicine. Zedoariae rhizoma is a bioactive traditional medicine with anti-tumor, anti-atherosclerosis, anti-inflammation, and growth-regulating properties. During the course of liver fibrogenesis, hMF, mostly derived from hepatic stellate cells, proliferate and synthesize excessive amounts of extracellular matrix components. To evaluate the antiproliferative effect of a traditional herbal medicine, Zedoariae rhizoma water extracts (ZR) was examined on the growth inhibition of hMF since proliferation of hMF is known to be central for the development of fibrosis during liver injury, and factors that may limit their growth are potential antifibrotic agents. The aim of this study was to test the effects of ZR on the proliferation in cultured hMF. hMF were obtained by outgrowth from human liver explants. ZR markedly reduced serum driven cell proliferation, as assessed by nuclear autoradiography experiments and measurement of actual cell growth. Growth inhibition was totally reversed after removal of the ZR. ZR potently inhibited hMF growth (IC50 = 8.5 microg/ml), in a pertussis toxin-insensitive manner. Analysis of the mechanisms involved in growth inhibition revealed that ZR rapidly increased prostaglandin E2 production and in turn cAMP, which inhibited hMF proliferation, did not affect cAMP levels. Production of cAMP by ZR was abolished by NS-398, a selective inhibitor of cycloxygenase (COX)-2. Also, ZR potently induced COX-2 protein expression. Blocking COX-2 by NS-398 blunted the antiproliferative effect of ZR. We conclude that ZR inhibits proliferation of hMF, probably via an intracellular mechanism, through early COX-2-dependent release of prostaglandin E2 and cAMP, and delayed COX-2 induction. Our results indicated a novel role for ZR as a growth inhibitory mediator and pointed out its potential involvement in the negative regulation of liver fibrogenesis. The results that ZR exhibits potent antiproliferative and antifibrogenic effects toward hMF, indicated that ZR might have therapeutic implications in chronic liver disease.
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PMID:The inhibitory effect of a Korean herbal medicine, Zedoariae rhizoma, on growth of cultured human hepatic myofibroblast cells. 1596 8

Non-alcoholic fatty liver disease is present in 15-25% of the general population. The fundamental derangement in non-alcoholic fatty liver disease is insulin resistance, a key component of the metabolic syndrome, which includes type 2 diabetes mellitus, dyslipidemia, hypertension, and obesity. The natural history of non-alcoholic fatty liver disease is not always benign, and causality for chronic liver disease and cirrhosis is well known in clinical practice and sometimes it is accompanied by hepatocellular carcinoma. Non-alcoholic fatty liver disease is likely to be associated with increased cardiovascular disease risk, and it raises the possibility that non-alcoholic fatty liver disease may be not only a marker but also an early mediator of atherosclerosis. Therapy is currently directed at treating components of the metabolic syndrome which may be beneficial also for the liver.
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PMID:[Non-alcoholic fatty liver disease and cardiovascular risk]. 1861 57

The liver is the main metabolic organ of the body and is strongly associated with lifestyle-related diseases in which abnormal metabolism of glucose and lipid are the main manifestations. Recently, the prevalence of nonalcoholic fatty liver disease(NAFLD), including nonalcoholic steatohepatitis (NASH), has been increasing due to a higher rates of obesity. It has been reported that the presence of NAFLD/NASH and associated liver dysfunction are predictors for cardiovascular disease. In addition, attention has been paid to the link between chronic hepatitis C and lifestyle-related diseases such as obesity and insulin resistance. Atherosclerosis is an important risk factor for cardiovascular disease and is associated with lifestyle-related diseases. Thus, chronic liver disease seems to be strongly associated with atherosclerosis. Cardiovascular disease induced by atherosclerosis should be attended to along with liver cirrhosis and hepatocellular carcinoma, and medications for lifestyle-related diseases are needed in patients with chronic liver disease.
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PMID:[Chronic liver disease and arteriosclerosis]. 2122 76

Nonalcoholic fatty liver disease (NAFLD), which spans a spectrum of conditions ranging from simple steatosis to progressive nonalcoholic steatohepatitis (NASH), is the most common chronic liver disease and a relevant public health issue. The prevalence of NAFLD depends on adiposity, age, gender and ethnicity. The natural history of liver disease in those with NAFLD critically depends on liver histological changes. However, cardiovascular mortality is increased in NAFLD, particularly in middle-aged adults. Against such a background, this review consists of three sections. First, data on NAFLD as a novel mechanism of increased cardiovascular risk via hyperinsulinism, pro-thrombotic potential, and subclinical inflammation are summarized. Next, the role of atherogenic liver in the development of manifestations of oxidative stress and atherosclerosis is emphasized. Finally, whether and how treating NAFLD will mechanistically result in reduced cardiovascular risk through ameliorated metabolic syndrome is discussed.
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PMID:Treatment of atherogenic liver based on the pathogenesis of nonalcoholic fatty liver disease: a novel approach to reduce cardiovascular risk? 2184 65

Nonalcoholic fatty liver disease (NAFLD) encompasses a range of liver histology severity and outcomes in the absence of chronic alcohol use. The mildest form is simple steatosis in which triglycerides accumulate within hepatocytes. A more advanced form of NAFLD, non-alcoholic steatohepatitis, includes inflammation and liver cell injury, progressive to cryptogenic cirrhosis. NAFLD has become the most common cause of chronic liver disease in children and adolescents. The recent rise in the prevalence rates of overweight and obesity likely explains the NAFLD epidemic worldwide. NAFLD is strongly associated with abdominal obesity, type 2 diabetes, and dyslipidemia, and most patients have evidence of insulin resistance. Thus, NAFLD shares many features of the metabolic syndrome (MetS), a highly atherogenic condition, and this has stimulated interest in the possible role of NAFLD in the development of atherosclerosis. Accumulating evidence suggests that NAFLD is associated with a significantly greater overall mortality than in the general population, as well as with increased prevalence of cardiovascular disease (CVD), independently of classical atherosclerotic risk factors. Yet, several studies including the pediatric population have reported independent associations between NAFLD and impaired flow-mediated vasodilatation and increased carotid artery intimal medial thickness-two reliable markers of subclinical atherosclerosis-after adjusting for cardiovascular risk factors and MetS. Therefore, the rising prevalence of obesity-related MetS and NAFLD in childhood may lead to a parallel increase in adverse cardiovascular outcomes. In children, the cardiovascular system remains plastic and damage-reversible if early and appropriate interventions are established effectively. Therapeutic goals for NAFLD should address nutrition, physical activity, and avoidance of smoking to prevent not only end-stage liver disease but also CVD.
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PMID:Pediatric nonalcoholic fatty liver disease, metabolic syndrome and cardiovascular risk. 2191 50

Non-alcoholic fatty liver disease is recognized as the most common and emerging chronic liver disease in western countries. The disease has been traditionally interpreted as a possibly progressing condition to liver fibrosis and cirrhosis. However, recently, a large number of publications have demonstrated that people with non-alcoholic fatty liver have an increased chance of developing cardiovascular diseases, which represent the major causes of death in this setting. This association is mainly explained by the atherogenic profile of the metabolic syndrome a condition frequently associated with fatty liver, which may represent its hepatic component. Some studies have also shown an association independent of traditional risk factors or of the clinical features of the metabolic syndrome. In this setting, cardiovascular disease seems to be the consequence of low-grade chronic inflammation and increased oxidative stress. Most studies did not differentiate cardiovascular risk between simple steatosis and non-alcoholic steatohepatitis, although the latter seems to be at higher cardiovascular risk. Few studies have investigated the direct correlation between hepatic inflammation and atherosclerosis. Genetic studies will probably improve the interpretation of the increased cardiovascular risk in patients with fatty liver and no metabolic syndrome.
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PMID:Non-alcoholic fatty liver disease and cardiovascular disease: epidemiological, clinical and pathophysiological evidences. 2307 70


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