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Query: UMLS:C0004153 (
atherosclerosis
)
77,401
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Atherosclerosis
1978
Dec
PMID:Effects of some benzodiazepine derivatives on fibrinolysis and serum lipids in normolipidaemic rats and in humans. 3 94
Arteriosclerosis is caused by many factors. These pathogenic factors especially over-nutrition, nicotinabusus, deficiency of muscular exercise, muscular overstrain, emotional stress and concomitant basic diseases, especially arterial hypertension, diabetes mellitus and dyslipidemia are the most important points for preventive and therapeutical action. When possible the risk factors has to be eliminated, arterial hypertension, diabetes mellitus and dyslipidemia have to be treated orderly. In the pathogenesis of arteriosclerosis and
atherosclerosis
are known disturbances of the lipid metabolism, the blood coagulation and the metabolism of the arterial wall cells most important. Application of anticoagulants and lipid lowering medicaments did not come up to our expectations. Experiences with animal models and a double blind study (secondary prevention of myocardial infarction) have given good reason for recommending antirheumatic or as we like to say, mesenchyme suppressive drugs.
Aktuelle Gerontol 1978
Dec
PMID:[Prevention and therapy of arteriosclerosis (author's transl)]. 3 60
53 patients coming to amputation of one or more toes for the late results of degenerative vascular disease were studied prospectively. By a median time of thirteen months, 26 of the 53 had undergone a major amputation of the affected side. Diabetes was associated with the same prognosis as
atherosclerosis
obliterans uncomplicated by diabetes. A palpable pedal pulse or a functioning arterial reconstruction carried a virtual guarantee of success for the toe amputation. The presence of a popliteal pulse, however, was not associated with any better prognosis than the presence of a femoral pulse alone. Smoking seemed to exert little influence. With the passage of time, the major-amputation rate rose steadily, and by 3 1/2 years almost three-quarters of the patients had come to major amputation.
Lancet 1976
Dec
18
PMID:Amputation of the toes for vascular disease: fate of the affected leg. 6
A number of soluble proteins contained in human aortic intimal tissue was extracted into buffered saline (pH 7.4) and identified and quantitated by immunoelectrophoresis and immunodiffusion. The proteins included IgA, IgG, IgM, B1C (C3), alpha 1-antitrypsin, alpha 2-macroglobulin, fibrinogen, albumin, LDL, HDL, alpha 1-acid glycoprotein, beta 2-glycoprotein, transferrin and ceruloplasmin. The concentration of soluble proteins was significantly higher in the atherosclerotic intima than in the normal intima. The diseased intima also contained a small amount of tissue-bound IgG, IgA and B1C which was extractable with citrate buffer at pH 3.2. The vascular band IgG, and B1C were shown by enzymatic and immunohistochemical studies to be closely associated with the collagenous tissue of the plaque. The Ig contained in the atherosclerotic plaque may be derived in part from the biosynthesis of Ig by the artery, since the incorporation of 14C-labeled leucine into IgG by the atheromatous plaque was demonstrable by radioimmunoelectrophoresis. In contrast to the diseased artery, the normal artery did not synthesize IgG and did not contain vascular bound IgG or complement. However, the normal artery was capable of fixing IgG and B1C eluted from the diseased artery. The present studies suggested that the IgG contained and synthesized by the plaque might represent an immune response to an endogenous or exogenous antigen closely associated with plaque collagen. IgG and B1C either alone or in the form of an immune complex also may play an important role in phagocytosis in the plaque and thereby influence the course of
atherosclerosis
. The proteolytic inhibitors, alpha 1-antitrypsin and alpha 2-macroglobulin, found in relatively high concentrations in the plaque, could enhance fibrosis of the lesion because of thier known inhibitory effects on collagenase and elastase.
Atherosclerosis
1979
Dec
PMID:Soluble proteins in the human atherosclerotic plaque. With spectral reference to immunoglobulins, C3-complement component, alpha 1-antitrypsin and alpha 2-macroglobulin. 9 93
The aortic localization of diet-induced fatty streaks in relation to focal increases in intimal permeability was evaluated in cynomoglus monkeys. Animals fed a hypercholesterolemic diet and studied at 10, 15, and 100 days had increasing intensity of Evans blue dye uptake. The overlap of fatty streaks with areas of dye intake increased as the areas of dye uptake enlarged, but all hypercholesterolemic groups showed some fatty streaks not topographically related to areas of dye uptake or flow instability. Because the upper thoracic aorta tended to show more advanced fatty streak formation dissociated from evident permeability change or hydraulic instability, it is suggested that mechanical factors associated with the geometric configuration of the descending thoracic aorta may have a significant role in the localization of some hypercholesterolemic fatty streaks.
Atherosclerosis
1978
Dec
PMID:The relation of hypercholesterolemic fatty streaks to intimal permeability changes shown by Evans blue. 10 62
Longevity and morbidity and death from myocardial infarction were examined in eight kindreds with familial hypobeta lipoproteinemia and in 18 kindreds with familial hyperalpha lipoproteinemia. Expectation of life for males and females from kindreds with hypobeta lipoproteinemia was 9 and 12 years longer (p less than or equal to 0.002) than that indicated by population statistics for U.S. white populations, whereas expectation of life for males and females from kindreds with hyperalpha lipoproteinemia was 5 and 7 years longer (p less than 0.02). Morbidity from myocardial infarction in 115 living first-degree adult relatives of probands with hypobeta and hyperalpha lipoproteinemia and in 364 living first-degree adult relatives of normolipemic spouse controls were compared. Nonfatal myocardial infarction (MI) was reported for 18 of 364 (5 per cent) relatives of normal spouse controls and in 0 of 115 relatives of hypobeta and hyperalpha subjects (p less than 0.05). The ratios (mean+/-S.E.) of C-LDL to C-HDL in familial hypobeta and hyperalpha lipoproteinemia were 0.79+/-0.06 and 1.21+/-0.06, as compared to 2.41+/-0.12 in a control population (p less than 0.001). If high-density lipoproteins confer protection against development of
atherosclerosis
, whereas low-density lipoproteins have opposite effects, then we speculate that the low ratio of C-LDL:C-HDL may be related to prolonged longevity and decreased morbidity from myocardial infarction in familial hypobeta and hyperalpha lipoproteinemia.
J Lab Clin Med 1976
Dec
PMID:Longevity syndromes: familial hypobeta and familial hyperalpha lipoproteinemia. 18 45
Atherosclerosis
1977
Dec
PMID:Chemical and morphological changes of rat plasma lipoproteins after a prolonged administration of diets containing olive oil and cholesterol. 20 91
We determined serum high-density lipoprotein cholesterol content and analyzed the approtein structure of the various lipoprotein fractions in 21 patients on chronic hemodialysis. High-density lipoprotein cholesterol was significantly reduced in all patients as compared with 11 normal persons (mean +/-1 standard deviation: 26 +/- 13 vs. 52 +/- 9 mg per 100 ml; P less than 0.001) whether or not triglyceride levels were raised. In seven of those with Type IV hyperlipoproteinemia, protein content of high-density lipoprotein and its subfractions 1, 2 and 3 were also reduced (P less than 0.001) in parallel with reductions in cholesterol in these fractions. Apoprotein electrophoresis showed an increase in "arginine-rich" peptide in very-low-density lipoprotein and high-density lipoprotein fraction 1, and a reduction in apoprotein Cll in very-low-density and high-density lipoprotein. In addition to their reduced high-density lipoprotein cholesterol levels, a major factor in the
atherosclerosis
of these patients may be their abnormal high-density lipoprotein composition. Their raised triglyceride levels could be due to defective lipoprotein lipase activation by the reduced very-low-density lipoprotein apoprotein.
N Engl J Med 1978
Dec
14
PMID:Defective high-density lipoprotein composition in patients on chronic hemodialysis. A possible mechanism for accelerated atherosclerosis. 21 15
The hypolipidemic and antiatherogenic effects of different nicotinic acid derivatives were studied. Five rabbit groups maintained on an atherogenic diet were given simultaneously various nicotinic acid derivatives (50 mg/kg body weight/day): nicotinic acid, Xantinol-nicotinate, beta-pyridylcarbinol or Pirozadil (bis-3,4,5-trimethoxybenzoate, 2,6-pyridindiyldimethylene). All 4 compounds showed a clear hypocholesterolemic and antiatherogenic effect, as measured by serum cholesterol, and by planimetric evaluation of the aortic lesions in terms of percent surface area affected in the aortas and coronary lumen. The simultaneously observed elevation of the HDL/LDL cholesterol ratio of the aortic tissue possibly indicates an antiatherogenic effect of these changes.
Atherosclerosis
1978
Dec
PMID:Efficacy of hypolipidemic treatment in inhibition of experimental atherosclerosis: the effect of nicotinic acid and related compounds. 21 72
Gradient density ultracentrifugation was used to assess the lipid binding of 125I-labelled structural glycoproteins and standard proteins. The results show that solubilized structural glycoproteins from cartilage or aorta will associate spontaneously with lipids or lipoproteins. In addition, structural glycoprotein preparations from tissues which have not been delipidated contain a fraction which is already associated with lipid. Standard proteins do not behave in the same way. It is proposed that structural glycoprotein-lipid binding may be one of the mechanisms involved in the intercellular deposition of plasma lipoproteins in atherosclerotic arteries.
Atherosclerosis
1978
Dec
PMID:Association of structural glycoproteins with lipids or lipoproteins. 21 73
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