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)

This study evaluates the correlation between long-term weight history and health risks. One thousand three hundred and sixteen male subjects of normal weight (-5%(-)+5% by Broca's obesity index) at age twenty, were studied. The average age of the subjects was 43.7 +/- 6.5 (M. +/- S.D.) years old. According to their long-term weight history, the subjects were classified into four groups: weight lost (N = 35), weight stable (N = 502), mild weight gain (N = 187), severe weight gain (N = 592). Odds ratios for systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, uric acid, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, hyperperspiration, angina pectoris, and hypertension were significantly higher in the severe weight gain group than in the stable weight group. Stepwise logistic regression analysis was performed by choosing weight history, obesity index, age, and smoking and drinking habits as the independent variables. Weight history was shown to be a significant variable in systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, chronic hepatitis and liver cirrhosis. Odds ratios for factors suspected of promoting atherosclerosis were significantly higher in the severe weight gain group. Results of this study indicate that a weight gain of over 7 kilograms appears to be the critical level that is associated with health risks.
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PMID:[Health risk assessment of long-term weight history]. 213 52

In 130 type I and II diabetics with normal serum lipids and in 98 diabetics with type IIa-V hyperlipoproteinemia (HLP), liver biopsies were performed if clinically indicated. During histological examinations of one half of the biopsy specimen lipid droplet size was classified into 4 categories, which were proved by morphometric studies, independent of the amount of fat. From the remaining part the fatty acid composition of triglycerides was analyzed by gas liquid chromatography. Moreover, the fatty acid pattern of serum triglycerides and subcutaneous adipose tissue from the abdominal wall was estimated. The percentage of eicosapentaenoic acid (EPA) in triglycerides of normal diabetic liver (no visible fat) was remarkably high (greater than 30 per cent). In adipose tissue it was low (less than 1 per cent). In serum triglycerides it remained between liver and depot fat (about 3 per cent). EPA decreased with rising lipid droplet size in hepatocytes. Liver diseases, like chronic hepatitis, had no influence on the results. One year after clofibrate treatment, the percentage of EPA in liver appeared increased. In adipose tissue, however, it remained constant. In general, EPA in liver and serum triglycerides was higher in diabetics with normal serum lipids as compared to diabetics with HLP. The decreased availability of EPA in liver and serum triglycerides of diabetics with HLP suggests a significant correlation between this fatty acid and hepatic lipid accumulation which itself is associated with diseases known as risk factors of atherosclerosis.
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PMID:Negative correlation of eicosapentaenoic acid and lipid accumulation in hepatocytes of diabetics. 609 38

This article summarizes the results of a recent study of atomic bomb radiation and non-cancer diseases in the AHS (Adult Health Study) population by the RERF (Radiation Effects Research Foundation) along with a general discussion of previous studies. The association of atomic bomb radiation and CVD was examined by incidence studies and prevalence studies of various endpoints of atherosclerosis, such as MI, stroke, aortic arch calcification, isolated systolic hypertension, and pulse wave velocity, and, although the excess was small, all endpoints indicated an increase of CVD in the heavily exposed group. Because of the consistency of the results, it is almost certain that CVD is higher among atomic bomb survivors. However, all CVD risk factors associated with lifestyle had not necessarily been adjusted for in studies to date, and it is difficult at present to conclude that the increase in CVD among survivors was a direct effect of radiation. Recent studies have demonstrated almost certainly that uterine myoma is more frequent among atomic bomb survivors. It cannot, at present, be concluded that uterine myoma is caused by radiation, because there are no reported studies of other exposed populations. Further analyses including the role of confounding factors as well as molecular approaches are needed to verify this radiation effect. The relationship between atomic bomb radiation exposure and hyperparathyroidism can now be said to have been established in view of the strong dose response, the agreement with results of studies of other populations, the high risk in the younger survivors, and the biological plausibility. Future studies by molecular approaches, etc., are needed to determine the pathogenic mechanism. Among other benign tumours, a dose response has been demonstrated for tumours of the thyroid, stomach and ovary. Although fewer studies have been conducted than for cancer, a clear association between radiation and various benign tumours is emerging. Concerning the association between atomic bomb radiation exposure and chronic liver diseases, the recent incidence study of members of the AHS population demonstrated a significant dose response. Both chronic hepatitis and cirrhosis were suggested as being associated with exposure. The possibility that the increased occurrence of chronic liver diseases among the survivors may be due to hepatitis virus infection cannot be excluded, and the results of the ongoing hepatitis C virus antibody titre studies are awaited.
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PMID:Profiles of non-cancer diseases in atomic bomb survivors. 889 51

Monocyte chemoattractant protein-1 (MCP-1), which binds to C-C chemokine receptor 2, has been implicated as the primary source of monocyte chemoattractant function in the early stages of atherosclerosis. Recently, propagermanium, a drug used clinically for the treatment of chronic hepatitis in Japan, has been shown to inhibit C-C chemokine receptor 2 function and suppress monocyte/macrophage infiltration in vitro and in vivo. Given the importance of monocyte infiltration in atherogenesis, the inhibition of it by propagermanium might prevent atherosclerosis. Apolipoprotein E knockout (apoE-KO) mice were fed an atherogenic high cholesterol diet with or without 0.005% propagermanium for 8 or 12 weeks. Although the plasma lipid levels were unchanged by the drug treatment, atherosclerotic lesion area in the aortic root was reduced by 50% in the drug-treated apoE-KO mice compared with the nontreated apoE-KO mice after 8 weeks of cholesterol feeding (0.62+/-0.12 versus 1.27+/-0.07 mm2, respectively; P<0.01). Moreover, the accumulation of macrophages in the lesions was markedly reduced in the drug-treated group (macrophage positive area, 0.23+/-0.06 mm2 [drug-treated group] versus 0.67+/-0.07 mm2 [control group]; P<0.01). After 12 weeks of cholesterol feeding, atherosclerotic lesion formation in the aortic root and in the descending thoracic aorta was significantly reduced in the drug-treated group. Inhibition of macrophage infiltration by propagermanium prevented the formation of atherosclerotic lesions in apoE-KO mice. This drug may serve as a therapeutic tool for the treatment of atherosclerosis.
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PMID:Propagermanium reduces atherosclerosis in apolipoprotein E knockout mice via inhibition of macrophage infiltration. 1206 6

Inflammation is overall a protective response, whose main goal is to liberate the human being of cellular lesions caused by micro-organisms, toxins, allergens, etc., as well as its consequences, and of death cells and necrotic tissues. Chronic inflammation, which is detrimental to tissues, is the basic pathogenic mechanism of hypersensitivity reactions against xenobiotics. Other frequent pathologies, for instance atherosclerosis, chronic hepatitis, inflammatory bowel disease (IBD), liver cirrhosis, lung fibrosis, psoriasis, and rheumatoid arthritis are also chronic inflammatory diseases. Chemical mediators of inflammation are derived from blood plasma or different cell-type activity. Biogenic amines, eicosanoids and cytokines are within the most important mediators of inflammatory processes. The different activities of eicosanoids derived from arachidonic acid (20:4 n-6) versus those derived from eicosapentaenoic acid (20:5 n-3) are one of the most important mechanisms to explain why n-3, or omega-3, polyunsaturated fatty acids (PUFA) exhibit anti-inflammatory properties in many inflammatory diseases. Dietary supplements ranging 1-8 g per day of n-3 PUFA have been reportedly beneficial in the treatment of IBD, eczema, psoriasis and rheumatoid arthritis. In addition, recent experimental studies in rats with experimental ulcerative colitis, induced by intrarectal injection of trinitrobenzene sulphonic acid, have documented that treatment with n-3 long-chain PUFA reduces mucosal damage as assessed by biochemical and histological markers of inflammation. Moreover, the defence antioxidant system in this model is enhanced in treated animals, provided that the n-3 PUFA supply is adequately preserved from oxidation.
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PMID:Polyunsaturated fatty acids and inflammatory diseases. 1244 11

Shosaikoto, a Kampo medicine used clinically to treat patients with chronic hepatitis or cirrhosis in Japan, displays immunoregulatory effects, especially on macrophage functions. Oral administration of shosaikoto influences the synthesis of humoral factors such as the interleukins, nitric oxide and prostaglandins in macrophages. In addition, phagocytic activity is enhanced by treatment with shosaikoto, resulting in an antigen that is effectively presented to T lymphocytes to produce more antibodies. The role of macrophages in the pathogenesis of atherosclerosis is well recognized, although a therapeutic agent targeted at macrophages has not yet been developed. When shosaikoto was administered to atherosclerotic rabbits, it did not exhibit antihyperlipidemic effects but did reduce the formation of atherosclerotic lesions. In addition, treatment with shosaikoto suppressed intimal hyperplasia in apoE-deficient mice fed a cholesterol-enriched diet for nine weeks. Biochemical studies demonstrated that the mechanism of the antiatherosclerotic effect was partly due to the increase of oxidized low-density lipoprotein (oxLDL) elimination by macrophages, resulting from stimulation of oxLDL uptake through scavenger receptors, activation of acyl-CoA:cholesterol acyltransferase and neutral cholesteryl ester hydrolase, and increase of cholesterol elimination by high-density lipoprotein. Furthermore, shosaikoto is able to reverse the depression of macrophage functions caused by hyperlipidemia. These results indicate the potential of this medicine as a new type of preventive or therapeutic agent for atherosclerosis.
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PMID:Shosaikoto as a potential antiatherosclerotic agent. 1293 13

Sixty patients with chronic hepatitis of various etiology at the stage of hepatic cirrhosis with hepatic encephalopathy syndrome (HES), thirty patients with cerebral atherosclerosis with dyscirculatory encephalopathy (DE) and 60 healthy controls have been examined in the study of basic diagnostic criteria of encephalopathies by short-chain fatty acids (SCFA) serum levels. Sensitivity and specificity of this test was also evaluated. Gas-liquid chromatography determined SCFA in the feces and peripheral blood serum from the above examinees. It was found that relative consent of SCFA and for the most part profiles of propionic and fat acids, acids with long chains, SCFA isomers in patients with encephalopathy of different genesis correlate with the results of clinical, laboratory and psychometric methods of examination and should be used together. Basic criteria are devised.
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PMID:[Short-chain fatty acids and implications of their measurement in the diagnosis of encephalopathies]. 1497 Nov 59

Tibetan herbal remedy PADMA 28 revealed promising results to support treatment of intermittent claudication, atherosclerosis and chronic hepatitis. The remedy was confirmed to be closely linked with anti- and pro-oxidative properties in vitro. In this study, effect of PADMA 28 was investigated in stimulated and unstimulated human peripheral blood mononuclear cells (PBMC) in vitro. Neopterin production and tryptophan degradation were measured in supernatants of PBMC in the presence or absence of mitogens phytohaemagglutinin (PHA) and concanavalin A (Con A). Stimulation of PBMC induced neopterin formation and tryptophan degradation (p<0.001 compared to unstimulated PBMC), and PADMA 28 inhibited both immunobiochemical effects (p<0.001) in a concentration-dependent manner. Higher concentrations of PADMA 28 were more effective and were able to completely block the pathways induced upon mitogenic stimulation. Data allow to conclude that PADMA 28 is able to inhibit immunobiological effects in stimulated PBMC in vitro. The suppression of neopterin production and tryptophan degradation suggests a specific influence on biochemical pathways induced by Th1-type cytokine interferon-gamma.
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PMID:PADMA 28 modulates interferon-gamma-induced tryptophan degradation and neopterin production in human PBMC in vitro. 1513 23

The present paper proposes a new therapy using Trypanosoma cruzi trans-sialidase to treat diseases with unclear pathogenesis that present in common chronic inflammation and fibrosis. This hypothesis is based on recent findings that co-infection with mycoplasma and chlamydia is present in many of these diseases and that this enzyme was capable to eliminate or decrease the co-infection from the host. We identified that mycoplasmas and chlamydias are present in atherosclerosis, aortic valve stenosis, dilated cardiomyopathy, chronic chagasic myocarditis and cancer. We hypothetized that mycoplasmal infection may induce immunodepression in the host, favoring proliferation of pre-existent chlamydial infection and that elimination of mycoplasma would lead to improvement of the immune system resistance and the control of chlamydial proliferation. Mycoplasma has a particular parasitic relationship with host cells, involving strong adherence of their membranes, making it extremely difficult to eradicate mycoplasmal infection from the host. A new therapeutic approach is suggested using one or more agents that prevent or inhibit the adherence of mycoplasma to host cell membranes by removing sialic acid residues and preventing oxidation of the cells. The use of a neuraminidase enzyme, particularly the T. cruzi trans-sialidase enzyme, associated with treatment using anti-oxidating agents is proposed. Preliminary experimental animal and laboratory tests showed good results. The proposal that trans-sialidase from T. cruzi is efficient in combating co-infection of mycoplasma and chlamydia is based, at least in part, on the observation that chagasic patients suffering from T. cruzi infection present less mycoplasma and chlamydia infection in their tissues. Also, a lower incidence of the diseases above described to be related to mycoplasma infection is observed in chagasic patients. It is also hypothesized that co-infection with mycoplasma and chlamydia may induce oxidation of the host cells. Anti-oxidants such as those present in plant extracts may also be used in the treatment. Other diseases such as chronic hepatitis, glomerulonephritis, Multiple Sclerosis, Alzheimer's Syndrome and idiopathic encephalitis are other examples of chronic diseases where mycoplasma and chlamydia might be present, as they have the characteristics of unknown etiology, persistent chronic inflammation and fibrosis.
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PMID:Trypanosoma cruzi trans-sialidase as a new therapeutic tool in the treatment of chronic inflammatory diseases: possible action against mycoplasma and chlamydia. 1532 5

Hepatic steatosis is the hallmark of nonalcoholic fatty liver disease (NAFLD), which is the consequence of multiple metabolic derangements among which insulin resistance plays a pivotal role. Steatosis is, also, a feature of hepatitis C virus (HCV) infection. However, in chronic hepatitis C, the prevalence of steatosis is 2.5-fold more elevated than that expected by a chance concurrence with NAFLD, suggesting that HCV may be implied in the development of steatosis. As observed in NAFLD, in patients infected with HCV genotype 1 steatosis is associated with an increased body mass index. On the other hand, in patients infected with genotype 3 the extent of steatosis strictly correlates with the viral load indicating that steatosis is mainly "virus-related". Regardless of the "metabolic" or "viral" etiology, hepatic steatosis in HCV contributes to the progression of liver fibrosis, to the development of hepatocellular carcinoma and to an impaired response to interferon treatment. Features such as obesity, insulin resistance and type 2 diabetes mellitus are shared by NAFLD and HCV-associated steatosis. In addition, HCV infection, directly or through steatosis, favors the development of type 2 diabetes mellitus. Hyperlipidemia is an independent predictor of the development of NAFLD, but not of HCV-associated steatosis. Arterial hypertension is common in nonalcoholic steatohepatitis patients, and HCV infection has recently been acknowledged as an independent risk factor for atherosclerosis. The role of iron in the progression of both NAFLD and HCV-associated steatosis remains controversial while lipoperoxidation and oxidative stress are pathogenic mechanisms shared by both. Some metabolic risk factors may be shared by both HCV-associated steatosis and NAFLD although the disease progression and pathophysiological background may be different. Preliminary data suggest that the therapeutic options for NAFLD may also be useful to improve HCV-associated steatosis.
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PMID:[Hepatitis C virus-associated and metabolic steatosis. Different or overlapping diseases?]. 1585 90


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