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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apolipoproteins from human plasma high density (HDL), low density (LDL) and very low density lipoproteins (VLDL) were visualized in human arteries employing immunofluorescence techniques. Comparison between the localization patterns in extracranial and intracranial arteries and those in coronary arteries and the aorta was made. ApoA-I from HDL, apoB from LDL, and apoC-III from VLDL, as well as neutral lipid, were all localized to connective tissue and extracellular lipid pools in atherosclerotic lesions, and only to areas of intimal thickening in grossly "uninvolved" arteries. The degree of superposition of localizations was similiar in each vascular bed, and within the error resulting from the structural changes due to the focal nature of the atherosclerotic process. These results suggest a broad specificity in localization of apolipoproteins in most arterial lesions, and suggest that no differences in apolipoprotein accumulation exist between extracranial and intracranial arteries, coronary arteries, or the aorta. Variations in prevalence for atherosclerosis in each arterial bed must be accounted for on other bases.
Stroke
PMID:Apolipoprotein localization in human cranial arteries, coronary arteries, and the aorta. 78 16

A plasma protein is required as a cofactor for the binding of antiphospholipid antibodies to phospholipids. This protein has been identified as beta 2-glycoprotein I, an apolipoprotein that binds to negatively charged phospholipids and is a natural inhibitor of the coagulation cascade. It is not certain whether antiphospholipid antibodies bind to beta 2-glycoprotein I alone, to beta 2-glycoprotein I-phospholipid complex, or to a phospholipid epitope modified by beta 2-glycoprotein I. We used isolated beta 2-glycoprotein I and purified IgG and IgM antiphospholipid antibodies from serum or plasma of patients with the antiphospholipid syndrome to study the relation between antiphospholipid antibodies and beta 2-glycoprotein I in enzyme-linked immunosorbent assays. IgG antiphospholipid antibodies did not bind to beta 2-glycoprotein I when it was used as an antigen on the assay plate. The binding of IgG and IgM antiphospholipid antibodies to phospholipid was enhanced when beta 2-glycoprotein I was added to the phospholipid antigens either before or together with the antiphospholipid antibodies. The degree of enhancement varied across patients. IgM antiphospholipid antibodies required less cofactor for binding to phospholipid antigens. These results confirm the requirement of beta 2-glycoprotein I as a cofactor for the binding of autoimmune antiphospholipid antibodies to phospholipids.
Stroke 1992 Feb
PMID:Antiphospholipid cofactor. 144 Jul 26

Increased general and abdominal obesity has been independently associated with diabetes, increased risk of stroke, and coronary artery disease (CAD). It is more prevalent in developed countries and in urban areas of nonindustrialized nations than in less developed and rural areas. To evaluate the associations between general and abdominal obesity (as determined by total body fat, waist to hip ratio, umbilical to triceps ratio, and umbilical to subscapular ratio) with glucose, plasma lipoproteins, apolipoprotein (apo) A-I and B concentrations, and low density lipoprotein (LDL) particle size (LDL 1-7), we randomly selected 222 men and 243 women from rural and urban areas of Puriscal, Costa Rica. Abdominal obesity, as assessed by the waist to hip ratio, was independently and significantly associated with higher triglyceride levels (p less than 0.01) and with lower high density lipoprotein cholesterol levels (p less than 0.05) in men and women and with higher glucose levels (p less than 0.05) and smaller LDL particle size (p less than 0.01) in women. Abdominal obesity, as assessed by the umbilical to subscapular ratio, was independently and significantly associated with higher total cholesterol (p less than 0.005) and apo B (p less than 0.01) levels. Umbilical to triceps ratio was positively associated with blood pressure in men. Urban men had increased general and abdominal obesity (p less than 0.0001), number of cigarettes smoked per day (p less than 0.0001), and diastolic blood pressure (p less than 0.05) and had a decreased fitness level (p less than 0.0001) as well as higher (p less than 0.05) plasma glucose, triglyceride, and total cholesterol concentrations and lower (p less than 0.05) apo A-I and HDL cholesterol levels compared with rural men. The differences between rural and urban women were not as striking. Urban women had increased general and abdominal obesity, glucose, and apo B levels (p less than 0.05) and a decreased fitness level (p less than 0.0001). Our data indicate that general and abdominal obesity, increased cigarette smoking, diastolic blood pressure, and decreased fitness level are more prevalent in an urban than in a rural area in Costa Rica, particularly in men. The higher prevalence of such risk factors in the urban area is associated with a more atherogenic plasma lipoprotein profile.
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PMID:Relations of body habitus, fitness level, and cardiovascular risk factors including lipoproteins and apolipoproteins in a rural and urban Costa Rican population. 206 29

Recently, food intake in Japan has been characterized by an increase in fat intake, especially animal-fat intake and the maintenance of excess salt (sodium chloride) intake. It is generally accepted that the increase in fat intake is closely related to atherosclerosis, and excess salt intake is a high risk factor for the development of hypertension and cerebrovascular lesions. So far, in almost all reports, the increase in fat intake and excess salt intake have been studied independently, and there have been few reports on the combined effects of these two factors. Taking the above things into consideration, it would seem to be very interesting to investigate the effect of excess salt intake on lipid metabolism. In this paper, we studied the effects of excess salt intake on lipoprotein and apolipoprotein metabolisms, using stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Kyo: Wistar rats (WKY) as model animals. The results obtained were as follows: A significant increase in the concentration of serum total cholesterol (TC) was observed in SHRSP and WKY, when the rats were given a regular diet (CE-2, Clea Japan Inc.) and 1% sodium chloride solution (1% NaCl) as drinking water for 4 weeks. This was accompanied by a tendency toward increases in the concentrations of serum apolipoproteins in both strains. These results suggest that excess salt intake could accelerate the production of serum total lipoproteins in SHRSP and WKY, when the rats are fed a regular diet. Next, 1% NaCl and a high-fat and high-cholesterol diet (HFC diet) were simultaneously given to SHRSP and WKY for 6 weeks. The effects of simultaneous administration on lipoprotein and apolipoprotein metabolisms were compared with those of HFC feeding. One percent NaCl did not markedly affect hypercholesterolemia in WKY, while it induced more marked hypercholesterolemia in SHRSP that was associated with extreme elevations of serum TC and the atherogenic index (A.I.). This deleterious effect of 1% NaCl in SHRSP was due to drastic elevations of cholesterol contents in the very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) fractions. This was also associated with marked increases in apo B contents in the VLDL, IDL and LDL fractions and significant increases in apo E contents in the VLDL and IDL fractions. These results indicate that 1% NaCl induced much larger increases in serum atherogenic beta-lipoproteins in SHRSP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on stroke-prone spontaneously hypertensive rats (SHRSP) fed a high-fat and high-cholesterol diet--effects of salt intake on serum lipoprotein and apolipoprotein metabolism]. 263 85

Common and internal carotids have been studied by noninvasive method (echo-Doppler) in 30 normotensive patients with familial hypercholesterolemia (FH). Vascular lesions were detected in 14 patients (46%), who presented one or more lesions of different degree (between 1-15% and 16-49%). In one case, only one carotid had stenosis greater than 50%. Severity and number of stenosis were related to age and levels of hypercholesterolemia. FH patients with carotid lesions showed a significantly higher LDL-cholesterol (p less than 0.01) and plasma apolipoprotein B (p less than 0.001) concentrations and a significantly lower HDL-cholesterol (p less than 0.05) and plasma apolipoprotein A (p less than 0.001) levels as compared to those with normal echo-Doppler findings. These data indicate that investigation of arterial districts other than coronaries are useful in quantitative evaluation of atherosclerotic involvement.
Stroke
PMID:Carotid atherosclerosis in familial hypercholesterolemia. 389 94

Advances in the study of cerebrovascular disease suggest that many risk factors for stroke are under genetic influence. Epidemiologic studies show that parental and sibling histories of cerebral ischemic events are associated with an increased risk of stroke. Explanations for familial stroke aggregation include differential phenotypic expression of apolipoprotein (a) and apolipoprotein E, racial variations in the distribution of vascular disease, identification of the autosomal-dominant disorder cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy, specific point mutations in the mitochondrial-related disorders, and identification of the clinical significance of hereditable coagulopathies. Greater understanding of these factors may lead to early recognition of and intervention in stroke.
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PMID:Genetics of ischemic stroke. 774 12

We studied apolipoprotein (a) (apo(a)) phenotypes of 69 myocardial infarction survivors and 56 stroke patients, and compared them with those of 190 healthy Chinese. The distribution of apo(a) phenotype frequency in cardio-cerebrovascular disease patients was different from those of controls. The frequency of the phenotypes B, S1 and S2 in patients was remarkably higher than that in controls within the same single-band apo(a) phenotype. Moreover, the Lp(a) serum concentrations in CCVD patients were significantly higher than those in controls within the same single-band apo(a) phenotype.
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PMID:[Apolipoprotein (a) phenotypes of patients with myocardial infarction]. 778 Aug 20

Decreased levels of plasma high density lipoprotein (HDL) cholesterol have been associated with premature cardiovascular disease (CVD). Tangier disease is an autosomal co-dominant disorder in which homozygotes have a marked deficiency of HDL cholesterol and apolipoprotein (apo) A-I levels (both < 10 mg/dl), decreased low density lipoprotein (LDL) cholesterol levels (about 40% of normal), and mild hypertriglyceridemia. Homozygotes develop cholesterol ester deposition in tonsils (orange tonsils), liver, spleen, gastrointestinal tract, lymph nodes, bone marrow, and Schwann cells. Our purpose was to assess the prevalence of CVD in Tangier disease. We reviewed published clinical information on 51 cases of homozygous Tangier disease, report 3 new cases and provide autopsy information on 3 cases. Mean (+/- S.D.) lipid values of all cases were as follows: total cholesterol 68 +/- 30 mg/dl (32% of normal), triglycerides 201 +/- 118 mg/dl (162% of normal), HDL cholesterol 3 +/- 3 mg/dl (6% of normal) and LDL cholesterol 50 +/- 38 mg/dl (37% of normal). The most common clinical finding in these subjects (n = 54) was peripheral neuropathy which was observed in 54% of cases versus < 1% of control subjects (n = 3130). CVD was observed in 20% of Tangier patients versus 5% of controls (P < 0.05), and in those that were between 35 and 65 years of age, 44% (11 of 25) had evidence of CVD (either angina, myocardial infarction or stroke) versus 6.5% in 1533 male controls and 3.2% in 1597 female controls in this age group (P < 0.01). In 9 patients who died, 2 died prior to age 20 of probable infectious diseases, 3 of documented coronary heart disease at ages 48, 64, and 72, 2 of stroke at ages 56 and 69, one of valvular heart disease, and 1 of cancer. In three autopsy cases, significant diffuse atherosclerosis was observed in one at age 64, moderate atherosclerosis and cerebral infarction in another at age 56, but no atherosclerosis was noted in the third case who died of lymphoma at age 62. In one patient with established coronary heart disease, none of the lipid lowering agents used (niacin, gemfibrozil, estrogen or lovastatin) raised HDL cholesterol levels above 5 mg/dl. However, these agents did have significant effects on lowering triglyceride and LDL cholesterol levels. Our data indicate that there may be heterogeneity in these patients with regard to CVD risk, that peripheral neuropathy is a major problem in many patients, and that CVD is a significant clinical problem in middle aged and elderly Tangier homozygotes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Homozygous Tangier disease and cardiovascular disease. 794 62

Lipoprotein (a) is a major inherited risk factor for vascular diseases, including coronary atherosclerosis, restenosis, and stroke. The pathologic mechanisms are uncertain, but are likely to involve the unique plasminogen-like component of this lipoprotein, apolipoprotein (a). Studies suggest that apolipoprotein (a) can enhance lipid deposition in vessel walls, interfere with fibrinolysis, modulate smooth muscle cell activity, and induce endothelial dysfunction. This review discusses the key concepts relating to these mechanisms, with emphasis on recent studies.
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PMID:Vascular interactions of lipoprotein (a). 798 58

Apolipophorin III (apoLp-III) from the migratory locust, Locusta migratoria, represents the only full-length apolipoprotein whose three-dimensional structure has been solved. In the present study, spectroscopic methods have been employed to investigate the effects of deglycosylation (via endoglycosidase F treatment) and complexation with lipid on the stability and conformation of this protein. Addition of isolated lipid-free apoLp-III to sonicated vesicles of dimyristoylphosphatidylcholine (DMPC) resulted in the formation of relatively uniform disklike complexes with an average Strokes diameter of 13.5 nm. Flotation equilibrium experiments conducted in the analytical ultracentrifuge revealed a particle molecular mass of 588 500 Da. Chemical cross-linking and compositional analysis of apoLp-III.DMPC complexes indicated five apoLp-III molecules per disk and an overall DMPC:apoLp-III molar ratio of 122:1. Circular dichroism (CD) spectra of apoLp-III samples suggested a loss of alpha-helical structure upon deglycosylation, while complexation with DMPC did not significantly alter the helix content (estimated to be > 75%). Fluorescence spectroscopy revealed that the apoLp-III tryptophan fluorescence emission maximum was blue-shifted from 347 to 332 and 321 nm upon deglycosylation and complexation with DMPC, respectively. In quenching experiments with native apoLp-III, tryptophan residues were shielded from the positively charged quencher, CsCl. Increased exposure to KI, CsCl, and acrylamide was observed upon deglycosylation, whereas complexation with DMPC yielded lower Ksv values for KI and acrylamide and an increased value for CsCl versus native lipid-free apoLp-III. In guanidine hydrochloride denaturation studies monitored by CD or fluorescence, native, lipid-free apoLp-III displayed a denaturation midpoint of 0.60 M, and delta GDH2O = 5.37 kcal/mol was calculated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting the stability and conformation of Locusta migratoria apolipophorin III. 814 60


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