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)

Extrinsic allergic alveolitis (EAA) (synonym: hypersensitivity pneumonitis) is a hypersensitivity lung disease characterized by lymphocytic infiltrates in the pulmonary interstitial tissues. We have previously reported that the numbers of lymphocytes in bronchoalveolar lavage (BAL) samples in this disease correlate with levels of cholesterol and neutral lipid-laden 'foamy' macrophages. We have also reported that the macrophages express an increased density of MHC class II antigens (in particular HLA-DQ) which are known to be essential for antigen recognition by T lymphocytes. The aim of the present study was to explore whether cholesterol is capable of enhancing the antigen-presenting function of mononuclear phagocytes by modulating the expression of HLA-D region products. Incubation of purified monocytes from healthy volunteers with cholesterol in serum-free medium induced a significant increase in both the percentages of monocytes expressing HLA-DQ (P less than 0.02) and in the intensity of expression of the three HLA-D sub-region products, HLA-DQ, -DP and -DR (P less than 0.02, less than 0.01, less than 0.05, respectively). The cholesterol pre-incubated monocytes also exhibited enhanced antigen-presenting function (P less than 0.05), compared with controls pre-incubated without cholesterol. These findings indicate that increases in cholesterol in the extracellular milieu may augment antigen presentation by modulating the expression of HLA-D region products on antigen-presenting cells. Apart from EAA, this observation may also have relevance to inflammatory mechanisms in atherosclerosis, where 'foamy' macrophages also occur in association with hypercholesterolaemia.
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PMID:Enhancement of the antigen-presenting function of monocytes by cholesterol: possible relevance to inflammatory mechanisms in extrinsic allergic alveolitis and atherosclerosis. 137 Sep 28

The fields of heart and combined heart-lung transplantation are in a constant state of evolution. As greater experience is gained in posttransplant management, more patients with end-stage heart and lung disease can be treated. Because the postoperative course and rehabilitation phase may be extremely difficult, only candidates who meet specific medical and psychosocial criteria are selected. During the waiting period, critical care nurses along with the transplant team are instrumental in stabilizing the emotional and physical condition of the transplant candidate. Postoperative complications requiring intensive therapy include decreased cardiac output, respiratory dysfunction, rejection, and infection. Graft atherosclerosis, obliterative bronchiolitis, and malignancy are long-term complications that may limit survival. Life-long immunosuppression and careful long-term medical surveillance are crucial to the health of the recipient. Although there are numerous emotional and physical challenges related to potentially life-threatening complications and other disturbances in daily living, the quality of life for most recipients has greatly improved.
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PMID:Heart and heart-lung transplantation. 156 9

Fibrinolytic system, immune reactivity and isoelectric focusing of serum albumin were examined in 94 patients exhibiting combination of obstructive lung disease (chronic obstructive bronchitis and bronchial asthma) with atherosclerosis. Plasminogen activator showed discrete activity, the discreteness being less in respiratory distress of the I degree but higher in the distress of the II and III degree. Relative number of E-RFC and monocytes expressing receptors to IgM and IgG Fc-fragment decreased. Percentage of EAC-RFC rose. Serum albumin fractions changed pH range due to modification of albumin molecules resultant from forming complexes with fibrinogen degradation products. Concentration of the latter under conditions of respiratory distress induced by obstructive lung diseases associated with atherosclerosis substantially exceeded the standard levels.
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PMID:[Fibrinolysis, immune reactivity and the structure of the blood serum albumin in obstructive lung diseases combined with atherosclerosis]. 207 78

The review examines the effects of smoking on blood parameters, concentrating on those seen as responses or reactions to the insult of smoking, and finds evidence that smoking causes chronic leucocytosis, macrocytosis and raised haematocrit, raised plasma fibrinogen concentration, reduction of the serum ratio of high to low density lipoprotein (HDL/LDL ratio), and platelet changes. Each of the changes resolved on "quitting", though for fibrinogen the evidence was indirect. Reports that elevations of the white cell count (WCC), and plasma fibrinogen and reduction of the HDL/LDL ratio each predict myocardial infarction, and that higher haematocrit increases the risk of cerebro-vascular incidents are reviewed, with reports of associations with other forms of arterial disease and COPD, and of their significance for the prognosis of established disease. After noting pathological mechanisms which implicate each of these factors, and platelets, in reactions likely to contribute to the development of atherosclerosis, infarction, arterial spasm, and/or lung damage, the author concludes that the evidence in man, backed up by experimental data, provides very strong support for the view that elevations of WCC, haematocrit, plasma fibrinogen and reduction of the HDL/LDL ratio represent (or are closely associated with) intermediate causal mechanisms through which smoking induces arterial disease and probably lung disease, and that experimental evidence indicates that platelet changes and macrocytosis also contribute. Differences in the extent of these responses to smoking could be valuable in differentiating the relative harmfulness of different types of cigarette (or of other inhaled pollutants) in terms of these diseases, and in predicting the susceptibility of individuals to these smoking-related diseases.
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PMID:Reactive changes in the blood of smokers and the development of arterial diseases and COPD, a review: evidence of associations between changes and subsequent disease with implications for the evaluation of harmful effects of cigarettes, and for susceptibility to the chronic effects of inhaled pollutants. 248 24

The fields of heart and combined heart-lung transplantation continue to evolve, allowing treatment of more individuals with end-stage heart and lung disease. The postoperative course and rehabilitation phase may be arduous, emphasizing the importance of selecting candidates who meet specific medical and psychosocial criteria. Life-long immunosuppression and meticulous long-term medical surveillance are mandatory practices to promote the health of the recipient. The major complications that contribute to morbidity and mortality, especially during the first post-transplant year, are infection and rejection. Graft atherosclerosis, obliterative bronchiolitis, and malignancy are long-term complications that may limit survival. In spite of the emotional and physical challenges related to potentially life-threatening complications and other disturbances in daily living, the quality of life for most recipients has markedly improved.
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PMID:Heart and heart-lung transplantation. 268 76

A recent report based on data from the first National Health and Nutrition Examination Survey suggested that low intake of vitamin A may be associated with a greater risk of airway obstruction. We attempted to replicate these findings in a population-based sample of middle-aged adults (n = 15,743) who participated in the baseline examination of the Atherosclerosis Risk in Communities (ARIC) Study. Vitamin A intake was estimated from a 66-item food frequency questionnaire, and the presence of airway obstruction was determined by spirometry. Although airway obstruction was associated in ARIC with well-established risk factors such as age, sex, and smoking, there was little evidence for a role of vitamin A. With only one exception, vitamin A intake was unrelated to airway obstruction in all smoking categories using either categorical or continuous measures of lung function (FEV1, FVC, FEV1/FVC). Only among current smokers in the upper tertile of lifetime cigarette smoking (> 41 pack-years) was the odds ratio of having airway obstruction for the lowest quartile of vitamin A intake compared with the highest quartile elevated (1.7 [95% confidence interval 1.1 to 2.7]). Despite some biological plausibility that vitamin A intake may prevent obstructive lung disease, the inability to demonstrate association in a larger population study, with better estimation of usual dietary intake, casts doubt on the existence of causal relationship.
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PMID:Does dietary vitamin A protect against airway obstruction? The Atherosclerosis Risk in Communities (ARIC) Study Investigators. 792 73

Psychological status, including depressive symptoms, anxiety, and mastery, was measured in a community-based sample of 3,076 persons aged 55 to 85 with various chronic diseases. Strong, linear associations were found between the number of chronic diseases and depressive symptoms and anxiety, indicating that psychological distress among elderly people is more apparent in the presence of (more) diseases. Furthermore, in contrast to general assumptions that mastery is a relatively stable state, our results indicate that mastery is affected by having chronic diseases. The 8 groups of chronically ill patients (with cardiac disease, peripheral atherosclerosis, stroke, diabetes, lung disease, osteoarthritis, rheumatoid arthritis, or cancer) did differ in their associations with psychological distress. Psychological distress is most frequently experienced by patients with osteoarthritis, rheumatoid arthritis, and stroke, whereas diabetic and cardiac patients appear to be the least psychologically distressed. Differences in disease characteristics, such as functional incapacitation and illness controllability, may partly explain these observed psychological differences across diseases.
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PMID:Psychological status among elderly people with chronic diseases: does type of disease play a part? 880 61

Long-term outcome was studied in 233 patients who had undergone renal artery revascularization (51 with balloon angioplasty, 182 with surgery) between 1976 and 1992. Patients (excluding renal transplants) were treated for renal vascular hypertension without or with renal insufficiency (serum creatinine > 1.6 mg/dl. All patients still alive (n = 188) were contacted to determine current blood pressure, medications, serum creatinine, and subsequent significant medical events. In patients who had died the cause of death was determined and renal function status at the time of death noted from medical records. Some follow-up information was obtained on all 233 patients; follow-up serum creatinine data were obtained in 193 (82.8%) patients. Some 24 patients (10.3%) became dialysis-dependent. Using a multiple logistic regression analysis only, preoperative creatinine maintained significance (P < 0.001) for increased dialysis risk. There was no statistically significant association of dialysis for type of revascularization (percutaneous transluminal angioplasty, autogenous artery, saphenous vein, endarterectomy or synthetic material), simultaneous or previous aortic or other vascular surgery (carotid endarterectomy, femoropopliteal bypass, etc.), pathology (atherosclerosis or fibromuscular dysplasia), number of renal arteries stenosed or treated, length of follow-up, age, coronary artery disease, congestive heart failure, stroke, chronic lung disease or type II diabetes. It is concluded that, in patients with renal artery stenosis, the timing of renal artery revascularization relative to the level of renal function is the most important determinant for long-term renal salvage.
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PMID:Late renal function in patients undergoing renal revascularization for control of hypertension and/or renal preservation. 890 17

Nitrotyrosine in human and animal tissues has been associated with pathologic conditions such as atherosclerosis, renal failure, and acute lung disease. In this study, free and protein-associated nitrotyrosine were determined in plasma and tissue samples using a dual-channel electrochemical detection method. Free nitrotyrosine was quantified in acetonitrile-extracted samples while protein-associated nitrotyrosine was determined in proteinase K-digested samples. In human plasma, total nitrotyrosine increased from 2.3 to 4.3 and 13.2 mumol/mol Tyr following addition of 0, 0.5, and 1 mM ONOO-. To determine if nitrotyrosine was produced during ex vivo hypothermic preservation, rat livers were stored in University of Wisconsin solution (UW) for 0, 6, or 8 h and reperfused for 3 h. Total nitro-tyrosine increased 359 and 908% after 6 and 8 h preservation compared to 0 h. To determine if nitrotyrosine was produced in vivo following hepatic ischemia, a rat preservation-transplantation model was utilized in which livers were flushed with cold UW (0-h group) or transplanted following 6 h hypothermic preservation in UW. Free nitrotyrosine increased from 15.7 +/- 0.3 in the 0-h group to 23.6 +/- 2.5 mumol/mol Tyr, 24 h posttransplant of 6-h preserved livers. Protein-associated nitrotyrosine increased from 9.5 +/- 1.1 in the 0-h group to 27.5 +/- 0.7 mumol/mol Tyr in the 6-h preservation-transplantation group. Protein-associated nitrotyrosine provides an integrative determination of nitration. Detection of free and protein-associated nitrotyrosine in biologic samples may allow insight into the role of .NO-derived oxidants in tissue injury associated with various pathologic conditions.
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PMID:Free and protein-associated nitrotyrosine formation following rat liver preservation and transplantation. 918 89

Monocyte chemoattractant protein-1 (MCP-1) is a potent agonist for mononuclear leukocytes and has been implicated in the pathogenesis of atherosclerosis and granulomatous lung disease. To determine the role of MCP-1 and related family members in vivo, we used homologous recombination in embryonic stem cells to generate mice with a targeted disruption of C-C chemokine receptor 2 (CCR2), the receptor for MCP-1. CCR2-/- mice were born at the expected Mendelian ratios and developed normally. In response to thioglycollate, the recruitment of peritoneal macrophages decreased selectively. In in vitro chemotaxis assays, CCR2-/- leukocytes failed to migrate in response to MCP-1. Granulomatous lung disease was induced in presensitized mice by embolization with beads coupled to purified protein derivative (PPD) of Mycobacterium bovis. As compared with wild-type littermates, CCR2-/- mice had a decrease in granuloma size accompanied by a dramatic decrease in the level of interferon gamma in the draining lymph nodes. Production of interferon gamma was also decreased in PPD-sensitized splenocytes from CCR2-/- mice and in naive splenocytes activated by concanavalin A. We conclude that CCR2-/- mice have significant defects in both delayed-type hypersensitivity responses and production of Th1-type cytokines. These data suggest an important and unexpected role for CCR2 activation in modulating the immune response, as well as in recruiting monocytes/macrophages to sites of inflammation.
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PMID:Impaired monocyte migration and reduced type 1 (Th1) cytokine responses in C-C chemokine receptor 2 knockout mice. 936 70


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