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)

The results of a social-nutritional investigation in a maternal school are reported. Aim of the present study was to evaluate the dietary habits and life style in a group of 3-6 years old children and their compliance in following a diet in accordance with the LARN86 recommendations. The enquiry was carried out by a questionnaire, by an analysis of the ingesta and by a paediatric and auxological examination. Blood and instrumental tests (Lipids panel, Blood glucose, Insulin, Fructosamine, IgE, ECG) were performed in children with high familial risk of atherosclerosis. The main findings were the following: i. 17 children (21%) were classified as having high atherosclerosis familial risk; ii. the atherosclerosis high risk group showed also increased incidence (p less than 0.01) of familial allergy; iii. children had higher approval for food with high carbohydrate and animal protein content; iv. fat intake was proportional to the number of different types of fat bought by the families; v. excessive dietary lipids and low carbohydrate intake were found in most families. The revaluation at the end of the study showed a good compliance for the proposed diet scheme by children, but a poor compliance by their families.
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PMID:[Nutrition in school-age children: a survey at a nursery school]. 263 80

Mast cells and their chemical mediators play a role in cardiac and systemic anaphilaxis. Perivascular and cardiac mast cells have been implicated in the pathogenesis of coronary artery spasm, atherosclerosis, myocardial ischemia, and cardiomyopathy. Despite this, nothing is known about the immunological and biochemical characteristics of the human heart mast cell (HHMC). We have isolated and partially purified HHMC and compared them with mast cells isolated from lung (HLMC) and skin (HSMC) tissues. Cross-linking of the high-affinity receptor for IgE (Fc epsilon RI) by a polyclonal anti-Fc epsilon antibody caused the release of preformed (histamine and tryptase) and de novo synthesized mediators [peptide leukotriene C4 (LTC4) and prostaglandin D2 (PGD2)]. The tryptase content of HHMC (19.4 +/- 1.5 micrograms/10(6) cells) was lower than HSMC (33.4 +/- 2.5 micrograms/10(6) cells) and higher than HLMC (10.6 +/- 1.9 micrograms/10(6) cells). Maximal stimulation of HHMC with anti-IgE led to the release of LTC4 (17.5 +/- 5.1 ng/10(6) mast cells) and PGD2 (17.8 +/- 5.0 ng/10(6) mast cells, whereas HSMC synthesized more PGD2 (65.0 +/- 6.8 ng/10(6) mast cells) and much less LTC4 (< 5 ng/10(6) cells). Recombinant human C5a anaphylatoxin and protamine induced histamine release from HHMC and HSMC, but not from HLMC. Substance P and morphine selectively induced the release of histamine from HSMC, but not from HHMC and HLMC. Compound 48/80 caused histamine release from HSMC and HHMC, but not from HLMC. The pattern of mediators synthesized and the responsiveness of HHMC to different secretagogues appear unique providing strong evidence of human mast cell heterogeneity.
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PMID:Human heart mast cells: a definitive case of mast cell heterogeneity. 753 2

Out of 60 males aged 41 +/- 1 suffering from mild arterial hypertension (158 +/- 4/100 +/- 2 mm Hg) a hereditary load by hypertension was found in 63.3%, serum cholesterol levels reached 200 mg/dl in 85% of the patients. The patients with the load and enhanced Na-Li countertransport (403 +/- 49 mumol Li/1/cell/hr against 185 +/- 28 mumol Li/1/cell/hr in those without hereditary predisposition, p < 0.05) showed a significantly higher serum level of IgA and IgE (3.68 +/- 0.33 g/l and 127 +/- 14 U/ml vs 2.61 +/- 0.33 g/l and 79 +/- 15 U/ml, respectively, in those without the load, p < 0.01, p < 0.05). An IgE level significantly correlated with the amplitude of norepinephrine vascular reactivity (r = 0.35, p < 0.05). The discussion is concerned with IgE hyperproduction significance. Correlating with the amplitude of vascular reactivity on sympathetic stimuli and being independent of hypertension magnitude, this hyperproduction may underlie a high risk of atherosclerosis and vascular complications as a result of IgE-mediated vascular reactions in young subjects with mild hypertension in hereditary loading, erythrocytic accelerated Na-Li countertransport and lipid metabolism derangement.
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PMID:[The humoral immunity indices and vascular reactivity of patients with hypertension and an elevated blood lipid level]. 805 4

The examination of 50 patients with nonspecific aortic arteritis (NAA) discovered that 14% of the patients had aneurysms. The latter occurred more frequently in the ascending aorta and manifest clinically as aortic regurgitation and angina pectoris. Immunological disorders were compared in NAA patients with stenotic and aneurysmic lesions (groups 1 and 2, respectively). In group 1 high IgE and CIC concentrations occurred more frequently suggesting the involvement of immunological abnormalities in genesis of aneurysms in NAA. Most of group I patients had disturbances of lipid metabolism indicated by elevated cholesterol level. The latter promoted development of atherosclerosis.
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PMID:[Clinicoimmunological characteristics of aneurysmic lesion in nonspecific aortic arteritis]. 903 4

In the last decade, new information was achieved on mast cells (MC). Their origin is assumed to be different from that of the basophils. There are two types of MC with differences in structure, distribution and function: conjunctival and mucosal. MCs are among the most important cells in the development of allergic inflammation through the cytokines and mediators released on the activation of the surface receptors (high-affinity receptors for IgE: Fc epsilon R1). The cytokines released by MCs, e.g., interleukin 5 (IL5), IL8, are chemoattractants for eosinophils and neutrophils, respectively. The two types of mediators released by MC-those preformed, such as histamine, tryptase, serotonin, and the newly-synthetized ones, such as prostaglandin D2 (PGD2), leukotrienes C4 (LTD4), D4 (LTD4), E4 (LTE4), induce vasodilatation, bronchoconstriction, cellular chemotaxis, increase vascular permeability. The involvement of MC in many human diseases was shown within in vivo and in vitro studies (in allergy, lung fibrosis, atherosclerosis, carcinogenesis, etc.).
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PMID:Mast cells as potent inflammatory cells. 916 16

Mast cells are characterized by numerous granules released extracellularly in response to stimuli, e.g. IgE and complement. These cells are believed to be crucial in the development of certain inflammatory or immune-mediated diseases, such as allergy and dermatitis, and it has recently been demonstrated that a large number of mast cells are present in atherosclerotic lesions. Atherosclerosis bears several similarities to chronic inflammation, characterized by T cell and monocyte infiltration, immunoglobulin-complement deposition, and lipid accumulation. The presence of mast cells in atherosclerotic lesions could be significant because they can release large amounts of chemotactic agents, inflammation activators, and granule remnants, and they may be responsible for mononuclear cell recruitment and smooth muscle cell proliferation. Furthermore, granule remnants nonspecifically bind to low-density lipoproteins, which can be phagocytosed by macrophages to form foam cells, a major cellular component of the early stage of atherosclerotic lesions. Thus, further elucidation of the role of mast cells in quantitative studies could enhance our understanding of the mechanism of atherogenesis, and may lead to new therapeutic strategies for atherosclerosis.
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PMID:The role of mast cells in atherosclerosis. 930 25

Mast cells are multifunctional, tissue-dwelling cells capable of secreting a wide variety of mediators. They develop from bone marrow-derived progenitor cells, primed with stem cell factor (SCF), which mediates its actions by interacting with the SCF receptor or c-kit on the cell surface. Mast cells continue their maturation and differentiation in peripheral tissue, developing into two well described subsets of cells, MCT and MCTC cells, varying in content of tryptase and chymase as well as in immunobiology. Mast cells are activated by numerous stimuli, including antigen (acting via the high affinity IgE receptor, Fc?RI), superoxides, complement proteins, neuropeptides and lipoproteins resulting in activation and degranulation. Following activation, these cells express mediators such as histamine, leukotrienes and prostanoids, as well as proteases, and many cytokines and chemokines, pivotal to the genesis of an inflammatory response. Recent data suggests that mast cells may play an active role in such diverse diseases as atherosclerosis, malignancy, asthma, pulmonary fibrosis and arthritis. Mast cells directly interact with bacteria and appear to play a vital role in host defense against pathogens. Drugs, such as glucocorticoids, cyclosporine and cromolyn have been demonstrated to have inhibitory effects on mast cell degranulation or mediator release.
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PMID:The human mast cell: functions in physiology and disease. 1153 8

Chlamydia pneumoniae is the most commonly occurring intracellular bacterial pathogen. It is frequently involved in respiratory tract infections and to a lesser degree in extrapulmonary diseases. According to seroepidemiologic surveys, C. pneumoniae infection seems to be both endemic and epidemic. Such studies indicate that C. pneumoniae infection is widespread, with frequent reinfection during a lifetime. In Western countries the highest rate of new infections occurs between the ages of 5 and 15. The antibody prevalence worldwide is higher in adult males than in females. Currently available data suggest that C. pneumoniae is primarily transmitted from human to human without any animal reservoir. Transmission seems to be inefficient, although household outbreaks with high transmission rates are reported. Most reports rank C. pneumoniae among the three most common etiologic agents of community-acquired pneumonia, with an incidence ranging from 6% to 25%, and generally presenting a mild and, in some cases, self-limiting clinical course. Recent reports also indicate a possible role for C. pneumoniae in severe forms of community-acquired pneumonia and in respiratory infections in immunocompromised patients. C. pneumoniae infection has also been implicated in the pathogenesis of asthma in both adults and children. The hypothesis that C. pneumoniae infection could lead to asthma is based on clinical studies and on the evidence of specific IgE production, direct epithelial damage, induction of T-cell immunopathologic diseases, and vascular smooth cell infection. Chronic C. pneumoniae infection seems to be common in patients with chronic bronchitis whether exacerbated or not, and is characterized by a strong humoral immune response to this intracellular microorganism, which is present in the majority of patients with severe chronic bronchitis. More than 60% of subjects with chronic bronchitis have specific C. pneumoniae antibody titers, and the microorganism may be identified by culture or PCR in almost 40% of these patients. This pathogen has also been recently associated with atherosclerosis and coronary heart disease (CHD). Seroepidemiological evidence indicates that the majority of patients with CHD present an anti-C. pneumoniae antibody pattern consistent with chronic infection. Furthermore, C. pneumoniae has been detected in atherosclerotic coronary plaques by several methods, including immunocytochemistry, transmission electron microscopy and molecular biology techniques. Recently, we detected C. pneumoniae DNA in a high percentage (51%) of aortic aneurysm plaques. Moreover, our serologic data support the hypothesis that a chronic C. pneumoniae antibody pattern may be a possible risk marker for atherosclerosis. Recently, C. pneumoniae has been isolated by culture from the coronary artery of a patient with coronary atherosclerosis, providing direct evidence of the presence of viable organisms in atheromatous lesions. Moreover, we recently demonstrated an association between C. pneumoniae reinfection and acute myocardial infarction.
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PMID:Epidemiology of Chlamydia pneumoniae. 1186 64

IgE plus antigen-stimulated mast cells degranulate, synthesize leukotrienes and secrete cytokines. According to the coalescence model this process is initiated in specific membrane compartments termed rafts. There, enhanced levels of glycosphingolipids and cholesterol stabilize the interaction of FcepsilonRI and Lyn, and thus facilitate the first steps of signal transduction. Enforced changes in raft architecture by cholesterol deprivation and exogenous application of glycosphingolipids influence these early events by loss of tyrosine kinase activity or receptor-independent signal initiation respectively. Here we show that exogenously added cholesterol accumulates in rafts and activates mast cells. An investigation of the signaling events reveals that in contrast to IgE plus antigen-mediated stimulation, cholesterol triggers p38 mitogen-activated protein kinase and preferentially induces expression of FosB. Consequently, a comparative large-scale microarray analysis demonstrates that a number of IgE plus antigen-induced immediate early genes (peak expression at 30 min after induction) are repressed by cholesterol. These changes further translate into altered expression levels and time kinetics of a number of early genes (peak expression at 2 h after stimulation). As the most prominent example for cholesterol-dependent genes, we identified PAI1 (plasminogen activator inhibitor 1), a protein regarded as a risk factor for atherosclerosis.
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PMID:Activation of mast cells by incorporation of cholesterol into rafts. 1367 90

IL-18 is a pleiotropic cytokine and is produced by various types of cells including activated macrophages, particularly Kupffer cells. IL-18 has potential to activate inflammatory responses through induction of IFN-gamma production in collaboration with IL-12. Somewhat paradoxically, IL-18 also has the capacity to induce allergic responses via induction of IL-4 production by T helper cells and to activate mast cells and basophils to release atopic effector molecules such as histamine. Indeed, IL-18 is involved in inflammatory tissue injuries, such as Crohn's disease and atherosclerosis, and also in hyper IgE and atopic dermatitis. IL-18 is particularly important for induction of experimental liver diseases. Endotoxin-induced liver injury or Fas ligand-induced hepatitis is caused by endogenous IL-18 in mice. Moreover, patients with liver diseases such as fulminant hepatitis, liver cirrhosis due to hepatitis virus infection and primary biliary cirrhosis show elevation of serum levels of IL-18, that correlates with the corresponding disease severity. Therefore, endogenous IL-18 plays a major role in induction of some types of liver injuries in mice and human. NKT cells that express both T cell receptor and NK cell marker are abundant in the liver of mice and human. Recent studies have revealed that NKT cells participate in some types of liver injuries, such as concanavalin A-induced T cell-mediated hepatitis and malaria hepatitis. In this review article, we focus on IL-18-involving liver damages and NKT-cell-mediated liver injuries.
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PMID:Cytokine-induced inflammatory liver injuries. 1452 86


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