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)

Reticuloendothelial (RE) phagocytes (macrophages and histiocytes) can be distinguished from locally-derived lipid-containing cells (e.g., arterial smooth muscle) or locally derived phagocytes (e.g., Schwann cells and microglia) by the demonstration of a diffuse catalase reaction in a proportion of these RE cells with a short incubation modification of the Novikoff-Golfischer diaminobenzidine histochemical methods. Even though only a proportion of an RE population is catalase-positive, the results accord with the majority of current opinion that most of the cells in atherosclerotic lesions are derived locally, whereas the phagocytes in lipid implants and xanthomas are of RE origin. The phagocytes in the peripheral nerve undergoing Wallerian degeneration appear to be of mixed RE and endogenous origin, whereas microglia around multiple sclerosis plaques seem to be derived locally. Lipid in lesions with RE phagocytes (subcutaneous lipid implants and xanthomas) is relatively rapidly resorbed, whereas lipid in lesions with few RE phagocytes (atherosclerosis) or phagocytes of endogenous origin (CNS degeneration) is more slowly resorbed or partly retained within the tissue. Wallerian degeneration in the peripheral nerve, with its mixed population of RE and endogenous phagocytes, occupies an intermediate position in the speed of lipid removal.
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PMID:Phagocytes, lipid-removal and regression of atheroma. 81 81

Energy-calorie malnutrition (ECM) is the commonest nutritional problem in developing countries in Africa: 0.5-5% of the population under 6 years of age suffer from the severe forms and 4-40% from the moderate forms. It is possible that as many as two-thirds of the preschool children in developing countries in Africa suffer from some EPM (protein-calorie malnutrition). The recent Sahelian drought and civil wars in some countries in Africa have increased the size of the problem and the severity and prevalence of EPM in several parts of Africa. The aetiological factors of EPM in Africa include shortage of calories and protein, as well as increasing and recent tendency to abandon too early breast feeding, sensory deprivation, psychological and emotional trauma, ignorance, superstition and cultural taboos. The evidence available at the moment does not clearly indicate that effects of EPM on learning and behaviour are permanent, although the functions of the brain in the acutely malnourished child are defective. Malnutrition impairs immunological capability and surveillance, and hence augments the mortality and morbidity of infections such as measles especially by impairing cell-mediated immunity and, to a lesser extent, synthesis of immunoglobulins. Endemic goitre (prevalence varies from 2 to 90% in various age groups) in several parts of Africa is due to either iodine deficiency (Ethiopia) or to the goitrogenic effect of cassava diet (Zaire and Nigeria). Deficiencies of vitamins A, B complex and D have been reported in several parts of Africa, albeit sporadically. Dietary intoxications include: a) aflatoxins which may be important in the pathogenesis of hepatic carcinoma, one of the commonest neoplasms in developing countries in Africa; b) chronic cyanide intoxication from cassava (manihot) food derivatives, which on circumstancial evidence seems to be an important aetiological factor of a crippling neurological disease, the tropical ataxic neuropathy in Nigeria and Tanzania; c) organophosphate insecticides. The rarity of certain diseases in the Africans may be related specifically to the African diet, especially the high fibre and low animal fat content of many of the African diets. Examples of such diseases are atherosclerosis in the non-hypertensive non-diabetic population, cancer of the large bowel, varicose veins and perhaps multiple sclerosis.
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PMID:Nutritional problems in the African region. 82 71

Epidemiological investigations were carried out in an industrial plant in a population of about 16 000 people. The overall morbidity was 1 241.8 cases of nervous system diseases per 100 000 of population and the annual prevalence of neurological diseases was 473.7 per 100 000. The most frequent disease was sciatic pain, followed in order of frequency by epilepsy, vasomotor headaches, subjective symptoms after craniocerebral trauma, Parkinson's disease, clinically evident cerebral atherosclerosis and disseminated sclerosis. No significant effect of the type of occupation on the development of nervous system diseases was observed.
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PMID:[Nervous system diseases in workers of a large metallurgic plant]. 98 Feb

The importance of vitamin B6 in human nutrition is discussed with special reference to the possibility of undetected long-term subclinical deficiencies in the population at large. It is well known that this vitamin plays a vital role in many physiological processes, such as amino acid metabolism, lipid metabolism and the immune process. In view of the well-documented photo- and thermolability of the different B6 vitamers it stands to reason that serious dangers to health may be associated with undetected, lingering subclinical deficiencies, e.g. induction of and predisposition to various diseases (such as atherosclerosis, multiple sclerosis, degeneration of the myelin sheath of the central nervous system). With the advent of modern analytical techniques it is now imperative that a survey of the vitamin B6 status of a representative sample of the population at large be performed, and that fortification of key food items and/or other means of B6 supplementation be considered pending the outcome of such a survey.
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PMID:Vitamin B6 revisited. Evidence of subclinical deficiencies in various segments of the population and possible consequences thereof. 638 7

There are two families of essential fatty acids, the linoleic and linolenic. Linoleic acid (C18:2n-6), found mainly in vegetable seed oils, is desaturated and elongated in the body, forming arachidonic acid (C20:4n-6). Linolenic acid (C18:3n-3), the main dietary source of which is leaves, is desaturated and elongated, forming two fatty acids that are prevalent in fish oils: timnodonic (C20:5n-3) and clupanodonic (C22:6n-3). EFA are very easily peroxidized in air, but vitamin E protects against this. There are three functions of EFA. The most important is as part of phospholipids in all animal cellular membranes: in deficiency of EFA faulty membranes are formed. A second is in the transport and oxidation of cholesterol: EFA tend to lower plasma cholesterol. A third function is as precursors of prostanoids which are only formed from EFA. Deficiency of EFA in experimental animals causes lesions mainly attributable to faulty cellular membranes: sudden failure of growth, lesions of skin and kidney and connective tissue, erythrocyte fragility, impaired fertility, uncoupling of oxidation and phosphorylation. In man pure deficiency of EFA has been studied particularly in persons fed intravenously. A relative deficiency (that is, a low ratio in the body of EFA to long-chain saturated fatty acids and isomers of EFA) is common on Western diets and plays an important part in the causation of atherosclerosis, coronary thrombosis, multiple sclerosis, the triopathy of diabetes mellitus, hypertension and certain forms of malignant disease. Various factors affect the dietary requirement of EFA.
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PMID:Essential fatty acids in perspective. 646 3

There are three types of interferons (IFN), alpha, beta and gamma. IFN-alpha is produced in the leukocytes infected with virus, while IFN-beta is from fibroblasts infected with virus. IFN-gamma is induced by the stimulation of sensitized lymphocytes with antigen or non-sensitized lymphocytes with mitogens. It is believed that IFN-alpha and beta originated from the same ancestral gene, whereas IFN-gamma did not. IFN has not only an antiviral activity, but also various kinds of biological activities including cell growth inhibition, immunosuppressive effects, enhancement of macrophage, natural killer (NK) cell, killer (K) cell and neutrophil functions, and cell differentiation-inducing activity. IFN also shows the antitumor activity resulting from the integration of the above-mentioned biological activities. IFN is also deeply involved in the pathogenesis of various diseases, e.g., collagen diseases such as SLE and rheumatoid arthritis, insulin-dependent diabetes mellitus, fulminant hepatitis, severe pancreatitis, nephritis, multiple sclerosis, allergic diseases, and atherosclerosis. At present, IFN is clinically used in therapy against virus infections such as hepatitis B and C, and for malignancies such as renal cell carcinoma, multiple myeloma, malignant melanoma, glioblastoma, skin cancers, malignant lymphoma and chronic myelogenous leukemia.
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PMID:[Interferon-alpha, beta, gamma]. 799 28

The appearance of specific types of leukocytes in inflammatory infiltrates may be governed by cell-specific chemoattractants called chemokines. In particular, monocyte chemoattractant protein 1 (MCP-1) has been implicated in diseases characterized by monocyte-rich infiltrates, including atherosclerosis, rheumatoid arthritis and multiple sclerosis. While we are beginning to understand the structural determinants that govern the activities of MCP-1 in vitro, we know much less about its physiological functions in vivo and its pathogenetic role in disease. However, recent data from genetically modified mice have begun to place MCP-1 in a central position in monocyte trafficking and activation.
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PMID:Monocyte chemoattractant protein 1: a potential regulator of monocyte recruitment in inflammatory disease. 879 88

Monocyte chemoattractant protein-1 (MCP-1) attracts monocytes, memory T lymphocytes, and natural killer (NK) cells in vitro. Its expression has been documented in disorders characterized by mononuclear cell infiltrates, suggesting that it may contribute to the inflammatory component of such diseases as atherosclerosis, multiple sclerosis, or rheumatoid arthritis. To prove a causal association, the in vivo properties of MCP-1 must be understood. Several lines of transgenic mice have been constructed to address this question. A transgenic line in which MCP-1 expression is controlled by the MMTV-LTR expressed high levels of MCP-1 in multiple organs but showed no evidence for monocyte infiltration. Instead, these mice were more susceptible to infection by the intracellular pathogens, Listeria monocytogenes and Mycobacterium tuberculosis. These mice had high serum levels of MCP-1, suggesting that their circulating monocytes may have been desensitized or that MCP-1 stimulated a Th2-dominant response. In contrast, another model in which MCP-1 expression was controlled by the insulin promoter demonstrated a monocytic infiltrate in pancreatic islets. These results indicate that MCP-1 expression at low levels in an anatomically confined area results in monocyte infiltration, suggesting that when properly expressed, MCP-1's in vitro properties are reproduced in vivo. This justifies the examination of MCP-1-deficient mice in disease models in order to explore MCP-1's role in pathogenesis.
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PMID:In vivo properties of monocyte chemoattractant protein-1. 936 11

beta-chemokines play an important role in the development of immunologic reactions. Macrophages are major beta-chemokine-producing cells during T-cell directed, delayed-type hypersensitivity reactions in tissues, and have been reported to be important producers of beta-chemokines in the lymph nodes of HIV-1-infected individuals. However, the physiological signals responsible for inducing macrophages to produce beta-chemokines have not been established. Two soluble T cell products, interferon-gamma and granulocyte-macrophage colony stimulating factor, were added to cultured macrophages, but failed to stimulate the production of macrophage inflammatory protein-1alpha and -1beta; regulated upon activation, normal T cell expressed and secreted (RANTES); or monocyte chemoattractant protein-1. Instead, direct cell-cell contact between macrophages and cells engineered to express CD40L (also known as CD154) resulted in the production of large amounts of macrophage inflammatory protein-1alpha and -1beta, and RANTES (all ligands for CCR5), and monocyte chemoattractant protein-1 (a ligand for CCR2). Supernatants from CD40L-stimulated macrophages protected CD4(+) T cells from infection by a nonsyncytium-inducing strain of HIV-1 (which uses CCR5 as a coreceptor). These results have implications for granulomatous diseases, and conditions such as atherosclerosis and multiple sclerosis, where CD40L-bearing cells have been found in the macrophage-rich lesions where beta-chemokines are being produced. Overall, these findings define a pathway linking the specific recognition of antigen by T cells to the production of beta-chemokines by macrophages. This pathway may play a role in anti-HIV-1 immunity and the development of immunologic reactions or lesions.
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PMID:CD40 ligand (CD154) stimulation of macrophages to produce HIV-1-suppressive beta-chemokines. 956 Feb 54

Increasing amounts of evidence support the involvement of inflammation and immunity in atherogenesis, but mediators of communication between the major cell types in atherosclerotic plaques are poorly defined. Cells in human atherosclerotic lesions express the immune mediator CD40 and its ligand CD40L (also known as CD154 or gp39). The interaction of CD40 with CD40L figures prominently in both humoral and cell-mediated immune responses. CD40L-positive T cells accumulate in atheroma, and, by virtue of their early appearance, persistence and localization at sites of lesion growth and complication, activated T cells may coordinate important aspects of atherogenesis. Interruption of CD40L-CD40 signalling by administration of an anti-CD40L antibody limits experimental autoimmune diseases such as collagen-induced arthritis, lupus nephritis, acute or chronic graft-versus-host disease, multiple sclerosis and thyroiditis. Ligation of CD40 on atheroma-associated cells in vitro activates functions related to atherogenesis, including induction of proinflammatory cytokines, matrix metalloproteinases, adhesion molecules and tissue factor. However, the role of CD40 signalling in atherogenesis in vivo remains unknown. Here we determine whether interruption of CD40 signalling influences atherogenesis in vivo in hyperlipidaemic mice. Treatment with antibody against mouse CD40L limited atherosclerosis in mice lacking the receptor for low-density lipoprotein that had been fed a high-cholesterol diet for 12 weeks. This antibody reduces the size of aortic atherosclerotic lesions by 59% and their lipid content by 79%. Furthermore, atheroma of mice treated with anti-CD40L antibody contained significantly fewer macrophages (64%) and T lymphocytes (70%), and exhibited decreased expression of vascular cell adhesion molecule-1. These data support the involvement of inflammatory pathways in atherosclerosis and indicate a role for CD40 signalling during atherogenesis in hyperlipidaemic mice.
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PMID:Reduction of atherosclerosis in mice by inhibition of CD40 signalling. 967 6


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