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)

Thioglycollate-elicited mouse peritoneal macrophages were cultured in contact with the mixture of extracellular matrix proteins produced by rat smooth muscle cells in culture. Both live macrophages and their conditioned media hydrolyzed glycoproteins, elastin, and collagen. Live macrophages also degraded extracellular connective tissue proteins secreted by endothelial cells and fibroblasts. The glycoproteins in the matrix markedly inhibited the rate of digestion of the other macromolecules, particularly elastin. When plasminogen was added to the matrix, activation of plasminogen to plasmin resulted in the hydrolysis of the glycoprotein components, which then allowed the macrophage elastase easier access to its substrate, elastin. Thus, although plasmin has no direct elastinolytic activity, its presence accelerated the rate of hydrolysis of elastin and therefore the rate of matrix degradation. These findings may be important in an understanding of disease states, such as emphysema and atherosclerosis, that are characterized by the destruction of connective tissue.
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PMID:Degradation of connective tissue matrices by macrophages. II. Influence of matrix composition on proteolysis of glycoproteins, elastin, and collagen by macrophages in culture. 645 Feb 58

On the basis of a morphological examination of the heart and lungs at 337 autopsies of patients who had died of acute primary myocardial infarction, 108 cases were specified where myocardial infarction was related to a 3-10 year old history of chronic bronchitis. With regard to the bronchopulmonary system, autopsy findings in this series revealed manifestations of bronchitis, pneumosclerosis and emphysema. The myocardial infarction was underlied by stenosing coronary atherosclerosis (89%) in conjunction with thrombosis (76%). A conclusion is drawn as to a more severe course of myocardial infarction in chronic bronchitis patients.
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PMID:[Features of myocardial infarction in chronic bronchitis patients]. 670 Jan 31

A common feature of cigarette-smoke (CS)-associated diseases such as atherosclerosis and pulmonary emphysema is the activation, aggregation, and adhesion of leukocytes to micro- and macrovascular endothelium. A previous study, using a skinfold chamber model for intravital fluorescence microscopy in awake hamsters, has shown that exposure of hamsters to the smoke generated by one research cigarette elicits the adhesion of fluorescently labeled leukocytes to the endothelium of arterioles and small venules. By the combined use of intravital microscopy and scanning electron microscopy, we now demonstrate in the same animal model that (i) CS-induced leukocyte adhesion is not confined to the microcirculation, but that leukocytes also adhere singly and in clusters to the aortic endothelium; (ii) CS induces the formation in the bloodstream of aggregates between leukocytes and platelets; and (iii) CS-induced leukocyte adhesion to micro- and macrovascular endothelium and leukocyte-platelet aggregate formation are almost entirely prevented by dietary or intravenous pretreatment with the water-soluble antioxidant vitamin C (venules, 21.4 +/- 11.0 vs. 149.6 +/- 38.7 leukocytes per mm2, P < 0.01; arterioles, 8.5 +/- 4.2 vs. 54.3 +/- 21.6 leukocytes per mm2, P < 0.01; aortas, 0.8 +/- 0.4 vs. 12.4 +/- 5.6 leukocytes per mm2, P < 0.01; means +/- SD of n = 7 animals, 15 min after CS exposure). No inhibitory effect was observed by pretreatment of the animals with the lipid-soluble antioxidants vitamin E or probucol. The protective effects of vitamin C on CS-induced leukocyte adhesion and aggregation were seen at vitamin C plasma levels (55.6 +/- 22.2 microM, n = 7) that can easily be reached in humans by dietary means or supplementation, suggesting that vitamin C effectively contributes to protection from CS-associated cardiovascular and pulmonary diseases in humans.
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PMID:Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo. 751 84

Human leucocyte elastase is a serine proteinase involved in phagocytosis, defence against invading micro-organisms, degradation of elastin, collagen, proteoglycans, fibrinogen and fibrin, being also responsible for the digestion of damaged tissues and of the bacterial degradation products. Lack of the enzyme regulation is at the basis of pathological states, such as pulmonary emphysema, cystic fibrosis, rheumatoid arthritis, atherosclerosis and glomerulonephritis. A detailed characterisation of the enzyme:inhibitor recognition process, based on extensive thermodynamic, kinetic and structural information, as well as on the comparative analysis with the homologous proteinase from porcine pancreas, is reported in the present review.
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PMID:Molecular bases for human leucocyte elastase inhibition. 804 99

A review of the perioperative morbidity and mortality and long-term survival in elderly and high-risk patients with colorectal neoplasia was undertaken. Elderly high-risk patients with localized disease were compared with those with advanced disease. Over a five-year period, 82 high-risk (at least one major organ system disease), or elderly (age > or = 70 years) patients underwent an operation for colorectal neoplasia. Overall, 43 of 82 (52 percent) had advanced disease (obstruction, perforation, hemorrhage, or metastatic disease), while 39 of 82 (48 percent) had localized disease. The mean age of all patients was 78.2 years. Preoperative comorbid diseases included: coronary atherosclerosis, 59 (72 percent); previous myocardial infarction, 17 (21 percent); previous arrhythmia, 10 (12 percent); emphysema, 32 (39 percent); renal failure, 6 (7 percent); and cirrhosis, 3 (4 percent). At the time of surgery, 26 patients (32 percent) had metastatic disease. Six patients (7 percent) died in the perioperative period. The presence of advanced neoplasia did not significantly affect 30-day mortality. There was no difference in major morbidity between patients operated on for localized and for advanced disease. The mean actuarial 18-month survival was less for patients with advanced disease (P < 0.05). Sixty-eight patients (83 percent) are alive at a follow-up of 17.7 +/- 29 months postoperatively. The morbidity and mortality associated with resection of colorectal neoplasia in high-risk elderly patients are acceptable even in the presence of advanced disease. In select patients, resection offers the best palliation and may improve the quality of remaining life.
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PMID:Advanced colorectal neoplasia in the high-risk elderly patient: is surgical resection justified? 842 20

Several samples of oversulfated chondroitin and dermatan were obtained by chemical sulfation and by SAX-HPLC enrichment. The starting products and oversulfated products were tested as potential inhibitors of human leukocyte elastase, an enzyme hypothesized to be involved in the etiology of diseases such as emphysema, atherosclerosis, and rheumatoid arthritis. Chemical oversulfation (SO3H/COOH 1.6-3.2), preferentially occurring at C-6 of galactosamine residues, was found generally to increase the inhibitory power on elastase. Chemically oversulfated galactosaminoglycans thus have potential as therapeutic agents, considering that they produce non-significant effects on the hemocoagulative system. Two naturally oversulfated dermatans sulfate (SO3H/COOH ca. 1.2), mainly oversulfated at C-2 of iduronic acid residues, showed comparatively higher anticoagulant activity (in the HC-II mediated thrombin inhibition test).
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PMID:Inhibition of human leukocyte elastase by chemically and naturally oversulfated galactosaminoglycans. 854 7

The mechanisms by which exposure to cigarette smoke dramatically increase the incidence and severity of atherosclerosis and the incidence of lung cancer, chronic obstructive airways disease, and emphysema are incompletely understood. Epidemiologic evidence has suggested a modifying role for antioxidant micronutrients, including tocopherols and carotenoids, in these disease processes. It has been suggested that oxidants in cigarette smoke could be involved. We exposed freshly obtained human plasma to the gas phase of cigarette smoke to assess its effects on tocopherols, carotenoids, and retinol. Exposure to cigarette smoke led to the depletion of most of the lipophilic antioxidants in 20 mL human plasma. The order of disappearance was lycopene > alpha-tocopherol > trans-beta-carotene++ > (lutein + zeaxanthin) = cryptoxanthin > gamma-tocopherol = retinol. However, despite a substantial loss of alpha-tocopherol, there was very little peroxidative damage to lipids, and no detectable change in the content of polyunsaturated fatty acid-rich cholesterol esters. We conclude that a wide spectrum of lipophilic micronutrients undergo degradation when exposed to gas-phase cigarette smoke. The relevance of these in vitro findings to possible cigarette smoke-induced depletions of respiratory tract lipophilic antioxidants remains to be clarified.
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PMID:Destruction of tocopherols, carotenoids, and retinol in human plasma by cigarette smoke. 859 20

Cysteine proteases have traditionally been viewed as lysosomal mediators of terminal protein degradation. However, recent findings refute this limited view and suggest a more expanded role for cysteine proteases in human biology. Several newly discovered members of this enzyme class are regulated proteases with limited tissue expression, which implies specific roles in cellular physiology. These roles appear to include apoptosis, MHC class II immune responses, prohormone processing, and extracellular matrix remodeling important to bone development. The ability of macrophages and other cells to mobilize elastolytic cysteine proteases to their surfaces under specialized conditions may also lead to accelerated collagen and elastin degradation at sites of inflammation in diseases such as atherosclerosis and emphysema. The development of inhibitors of specific cysteine proteases promises to provide new drugs for modifying immunity, osteoporosis, and chronic inflammation.
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PMID:Emerging roles for cysteine proteases in human biology. 907 57

Infections are an increasing problem in the elderly population, because of the often atypical presentation and the more frequent occurrence of complications, which lead to increased morbidity and mortality. The increased prevalence of infections in the elderly is due to a number of factors: increased exposure to micro-organisms (especially in nursing homes); degeneration of various organs (atherosclerosis, pulmonary emphysema, diverticulosis, prolapse); decreased immune response; concomitant diseases (e.g. diabetes mellitus) and (or) use of medication. There is often a delay in the diagnosis because the presentation of infection in the elderly is frequently atypical and symptoms are attributed to old age, rather than to infection. Treatment may be hampered by increased resistance of micro-organisms, interaction with other drugs and toxicity problems.
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PMID:[Infections in elderly patients]. 955 Jul 96

A significant effect of the population structure on the incidence of multifactorial diseases affecting the viability of the adult population was found in rural districts of Kursk oblast. The diseases studied were chronic bronchitis, pulmonary emphysema, pneumosclerosis, and atherosclerosis. The incidence of multifactorial pathology increased with an increase in the homozygosity level of district populations. On average, the population structure affected the incidence of multifactorial diseases by 30-50%.
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PMID:[The population-demographic structure and the prevalence of multifactorial diseases affecting the viability of the population of Kursk region]. 977 64


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