Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

The apolipoprotein genetic polymorphism (APO E) is part of a broader paradigm, highlighting the role of gene-environment interactions as risk factors for human diseases such as cardiovascular disease, Alzheimer's disease, dementia, atherosclerosis, multiple sclerosis, peripheral artery disease, diabetes, stroke, and most recently, cancer. APO E, a normal constituent of very-low-density lipoproteins and high-density lipoproteins, is involved in many functions, including lipid metabolism, cholesterol transport, tissue repair, immune response and regulation, as well as cell growth and differentiation. The location, frequency and functional effects of this gene have been reviewed elsewhere in terms of cardiovascular disease, Alzheimer's disease, neuromuscular disease, multiple sclerosis, stroke and diabetes. However, while the majority of studies have examined the significance of APO E as a molecular marker for a variety of diseases in multiethnic populations, few evaluate its role as a putative marker of cancer susceptibility. Fewer explore the importance of APO E on the risk of breast cancer, although some report an association. None have been designed to study its relevance as a marker of breast cancer risk in multiethnic populations. The purpose of this review was to evaluate the association between APO E and the risk for breast cancer in non-Hispanic white and African-American women.
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PMID:Apolipoprotein E and the risk of breast cancer in African-American and non-Hispanic white women. A review. 1513 59

Early diagnosis and immediate therapeutic interventions are crucial factors to reduce the damage extent and the risk of death. Currently, the diagnosis of stroke relies on neurological assessment of the patient and neuro-imaging techniques including computed tomography and/or magnetic resonance imaging scan. An early diagnostic marker of stroke, ideally capable to discriminate ischemic from hemorrhagic stroke would considerably improve patient acute management. Using surface-enhanced laser desorption/ionization (SELDI) technology, we aimed at finding new early diagnostic plasmatic markers of stroke. Strong anionic exchange (SAX) SELDI profiles of plasma samples from 21 stroke patients were compared to 21 samples from healthy controls. Seven peaks appeared to be differentially expressed with significant p values (p < 0.05). Proteins were stripped from the SAX chips, separated on a one-dimensional electrophoresis (1-DE) gel and stained using mass spectrometry (MS)-compatible silver staining. Following in-gel tryptic digestion, the peptides were analyzed by MS. Four candidate proteins were identified as apolipoprotein CI (ApoC-I), apolipoprotein CIII (ApoC-III), serum amyloid A (SAA), and antithrombin-III fragment (AT-III fragment). Assessment of ApoC-I and ApoC-III levels in plasma samples using a sandwich enzyme-linked immunosorbent assay (ELISA) allowed to distinguish between hemorrhagic (n = 15) and ischemic (n = 16) stroke (p < 0.001). To the best of our knowledge, ApoC-I and ApoC-III are the first reported plasmatic biomarkers capable to accurately distinguish between ischemic and hemorrhagic stroke in a small number of patients. It requires further investigation in a large cohort of patients.
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PMID:ApoC-I and ApoC-III as potential plasmatic markers to distinguish between ischemic and hemorrhagic stroke. 1527 18

The aim of the work was to recognize whether often observed high levels of apolipoprotein (a) [Lp(a)] in patients shortly after an ischemic stroke are a result of the acute phase reaction. In 13 patients Lp(a) was determined within the first 24 hours after the stroke onset, after the next 7 days and after three months i.e. when it could be considered that Lp(a) level was the same as before onset of the disease. In 17 patients only two determinations were performed. Another acute phase indicator: C-reactive protein (CRP), as well as serum lipids were also determined. CRP level was increased in the first determination and increased further after 7 days. After three months it returned to low values. High density lipoprotein (HDL) cholesterol which demonstrates a negative acute phase response changed in the opposite way. No similar fluctuations of Lp(a) level were observed. It can be concluded that during the investigated period Lp(a) had no properties of the acute phase reactant.
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PMID:[Changes in lipoprotein (a) [Lp(a)] level after an ischemic stroke]. 1535 32

Whole-blood viscosity appears to be an independent predictor of stroke, carotid intima-media thickening, and carotid atherosclerosis. The purpose of this study was to examine for relationships between whole-blood viscosity and blood lipids in young healthy subjects over a range of shear rates. Twenty-seven healthy men and women aged 10 to 25 years having a range of low-density lipoprotein (LDL) cholesterol values 88 to 258 mg/dL and body mass index z scores -1.18 to 2.64 SDs were studied. Whole-blood viscosity at shear rates from 1 to 1000 per second was measured using an automated capillary viscometer. Blood lipids were measured using standard techniques. Triglyceride-rich lipoproteins were isolated by ultracentrifugation at density of <1.020 g/mL, and a high ratio of cholesterol to triglyceride was used as an indicator of lipoprotein remnants. Whole-blood viscosity at shear rates of 100 to 1000 per second showed significant negative correlations with apolipoprotein A-1, but not with high-density lipoprotein cholesterol. Whole-blood viscosity at a shear rate of 1000 per second correlated with LDL cholesterol and inversely with LDL size. On stepwise multivariate analysis, apolipoprotein A-1 accounted for 14.7% of the variation in whole-blood viscosity at a shear rate of 150 per second. This study points to the importance of high-density lipoprotein particle number on whole-blood viscosity at physiological shear rates. The physiological significance of the relationships between whole-blood viscosity and LDL cholesterol and LDL particle size at a very high shear rate remains to be determined.
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PMID:The influence of lipoproteins on whole-blood viscosity at multiple shear rates. 1593 11

In a population-based case-control study, we investigated the association of acute ischaemic stroke with lipoprotein(a) (Lp(a)) levels and apolipoprotein (Apo) (a) isoform size in subjects aged older than 70 years. A total of 163 patients with a first-ever-in-a-lifetime acute ischaemic/nonembolic stroke and 166 controls were included. Compared to controls, stroke patients exhibited higher Lp(a) concentrations (median value, 12.2 mg/dl versus 6.4 mg/dl, p < 0.001) and a higher frequency of small Apo(a) isoforms (44.2% versus 29.5%, p < 0.01). Multivariate logistic regression analysis showed a significant association of acute ischaemic stroke with Lp(a) levels [adjusted odds ratio (OR), 1.37, 95% CI (1.12-1.67); p = 0.002], and small Apo(a) isoform size [OR, 1.74 (1.10-3.03); p = 0.04]. Compared to subjects with Lp(a) levels in the lowest quintile, those within the highest quintile had a 3.2-times adjusted risk to suffer an acute ischaemic/nonembolic stroke (1.60-6.62, 95% CI; p < 0.001). Furthermore, analysis of interaction between lipid variables revealed that in the presence of elevated Lp(a) levels the inverse relationship between HDL-cholesterol levels and ischaemic stroke was negated [OR, 1.01 (1.00-1.03); p = 0.015]. Our study suggests that determination of Lp(a) levels and Apo(a) isoform size may be important in identifying elderly individuals at risk of ischaemic stroke independently of other risk factors and concurrent metabolic derangements.
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PMID:Serum lipoprotein(a) levels and apolipoprotein(a) isoform size and risk for first-ever acute ischaemic nonembolic stroke in elderly individuals. 1619 51

Early diagnosing and modification or elimination of atherosclerosis risk factors with the descendants of the ill with past ischemic stroke (IS) might reduce risk of subsequent stroke incidence in the family, or myocardial infarction or other disease being atherosclerosis - derivative. This subject seems to be essential because it concerns young people. The purpose of the present study is identification and assessment of metabolic atherosclerosis risk factors with adult progeny of the ill with past IS at young age. There were examined 43 adult children of the parents who fell ill at young age (between 39 and 55 years in case of men and 60 years in case of women) with IS. The test group included 21 men and 22 women aged from 19 to 39 years (average age - 26.3 years). The reference group consisted of 40 persons, including 18 men and 22 women aged from 22 to 39 years (average age - 26.8 years). The persons from reference group were corresponding (in respect of structural aspects, such as age and sex) to the test group, their parents had negative history towards atherosclerosis - derivative illnesses. None of the patients under examination was a cigarette smoker. Examination of both groups consisted in conducting anamnesis, measurement of body weighing and height, blood pressure as well as evaluation of biochemical atherosclerosis risk factors. Blood testing (blood serum or plasma) consisted of blood cell count and ESR as well as blood glucose level, creatinine, urea, transaminase and bilirubin levels as well as total cholesterol, LDL cholesterol and HDL cholesterol fractions, apolipoprotein B, apolipoprotein AI, lipoprotein (a), triglycerides, homocysteine, folate, fibrinogen, von Willebrand factor and C-reactive protein level. Among persons whose parents were affected, at young age, with IS higher average level of BMI (24.2 +/- 3.8 kg/m2) was detected as compared with that in the reference group (22.4 +/- 2.5 kg/m2), LDL cholesterol fraction (2.7 +/- 0.8 mmol/l vs 2.4 +/- 0.6 mmol/l) and triglycerides (1.1 +/- 0.4 mmol/l vs 0.8 +/- 0.4 mmol/l) as well as lower level of apolipoprotein Al (1.5 +/- 0.2 g/l vs 1.6 +/- 0.2 g/l). Average values of other factors in the blood serum were not significantly different in both with compared groups. In case of women, whose parents were affected with IS, higher levels of the following indicators were detected: BMI (24.3 +/- 3.9 kg/mz vs 21.5 +/- 2.3 kg/m2), total cholesterol (5.1 +/- 0.7 mmol/l vs 4.4 +/- 0.5 mmol/l, LDL cholesterol (2.7 +/- 0.6 mmol/l vs 2.1 +/- 0.4 mmol/l), apolipoprotein B (1.0 +/- 0.1 g/l vs 0.8 +/- 0.1 g/l), lipoprotein (a) (0.3 +/- 0.2 g/l vs 0.2 +/- 0.1 g/l) and triglycerides (1.0 +/- 0.4 mmol/l vs 0.7 +/- 0.2 mmol/l). In group of men whose parents were affected with IS lower levels of apolipoprotein Al (1.3 +/- 0.2 g/l vs 1.5 +/- 0.2 g/l) and of von Willebrand factor (71.4 +/- 23.9% vs 87.1% +/- 16,8%) were detected. Descendents of the ill with past IS should be treated as higher risk group especially when supranormative values of metabolic atherosclerosis risk factors are detected with them. In case of persons with positive family history of IS, having higher values of metabolic atherosclerosis risk factors, it is necessary to apply intensive actions towards change of their life styles, and if necessary - also to include pharmacological treatment.
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PMID:[Assessment of metabolic atherosclerosis risk factors in progeny of patients with past ischemic stroke]. 1620 32

Recently, we found that 4-hydroxyderricin, one of the major chalcones in Angelica keiskei extract (an ethyl acetate extract from the yellow liquid of stems), suppressed increases in systolic blood pressure and reduced both serum very low-density lipoprotein levels and liver triglyceride content in stroke-prone spontaneously hypertensive rats (SHRSP). In the present study, we have isolated laserpitin, a characteristic coumarin, from the A. keiskei extract and examined the effect of dietary laserpitin on blood pressure and lipid metabolism in SHRSP. Six-week-old male SHRSP were fed diets containing 0.1% laserpitin for 7 weeks with free access to the diet and water. Bodyweight gain was reduced by dietary laserpitin after 4 weeks through to 7 weeks without any significant change in daily food intake. Serum total cholesterol, phospholipid and apolipoprotein (apo) E levels were significantly increased, which was due to significant increases in cholesterol, phospholipid and apoE contents in the low- and high-density lipoprotein (LDL and HDL, respectively) fractions. These results suggest that dietary laserpitin increases serum apoE-HDL levels. In the liver, significant decreases in relative liver weight and triglyceride content were found after treatment with laserpitin for 7 weeks. An investigation of hepatic mRNA expression of proteins involved in lipid metabolism indicated that a significant decrease in hepatic triglyceride lipase may be responsible for the increase in serum HDL levels and also indicated that a marked decrease in adipocyte determination and differentiation factor 1 may be responsible, at least in part, for the decrease in hepatic triglyceride content. In conclusion, dietary laserpitin produces increases in serum HDL levels, especially apoE-HDL, and decreases in the hepatic triglyceride content in SHRSP.
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PMID:Beneficial effect of laserpitin, a coumarin compound from Angelica keiskei, on lipid metabolism in stroke-prone spontaneously hypertensive rats. 1644 77

Statins inhibit cholesterol synthesis and are effective in lowering total cholesterol levels in plasma or serum due to reductions in low-density lipoprotein and very low-density lipoproteins, as well as reducing progression of coronary atherosclerosis, coronary heart disease, and stroke morbidity and mortality. These agents also modestly raise levels of high-density lipoprotein (HDL) cholesterol and its major protein, apolipoprotein (apo) A-I. The more effective statins can also raise the levels of large alpha-1 HDL particles as assessed by two-dimensional gel electrophoresis. High levels of these particles promote reverse cholesterol transport and protect against coronary heart disease and progression of coronary atherosclerosis. The mechanism whereby statins alter HDL and its subspecies appears to be due to reduction of triglyceride-rich lipoproteins, with a secondary decrease in cholesteryl ester transfer protein activity, and less transfer of HDL cholesterol to triglyceride-rich lipoprotein acceptor particles. Increasingly, statins will be combined with other agents such as ezetimibe, fibrates, niacin, and cholesteryl ester transfer protein inhibitors to optimize the entire lipoprotein profile to alter not only low-density lipoprotein, but also HDL, triglycerides, lipoprotein(a), and C-reactive protein, and also to reduce cardiovascular morbidity and mortality.
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PMID:The effects of statins on high-density lipoproteins. 1645 13

The possible pathogenic role of triglycerides (TG) in the development of ischemic stroke is still under extensive investigation. Recently, apolipoprotein (apo)A5 gene promoter region T-1131C polymorphism has been shown to associate with elevated serum TG levels. In the current work, a total of 302 subjects were classified as being large vessel-associated, small vessel-associated, or belonging to a mixed group of ischemic stroke-affected patients. The level of TG was increased in all groups (p < 0.01). The apoA5-1131C allele frequency was approximately twofold in all groups of stroke patients compared with the controls (5 vs 10-12%; p < 0.05); and the apoA5-1131C allele itself was also found to associate with increased TG levels in all groups. In a multivariate logistic regression analysis model adjusted for differences in age, gender, serum cholesterol, hypertension, presence of diabetes mellitus, smoking and drinking habits, and ischemic heart disease, a significantly increased risk of developing stroke disease was found in patients carrying the apoA5-1131C allele (p < 0.05; odds ratio OR = 2.1 [1.3-4.7]); this association was also proven for all subtypes of the stroke. The results presented here suggest that the apoA5-1131C allele is an independent risk factor for the development of stroke. Being that apoA5 gene is under the control of the peroxisome proliferator-activated receptor alpha, theoretically, the current observations also can have long-term therapeutic consequences.
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PMID:Apolipoprotein A5 gene promoter region T-1131C polymorphism associates with elevated circulating triglyceride levels and confers susceptibility for development of ischemic stroke. 1695 7

This study investigates the ability of a single, low dose of apolipoprotein (apo) A-I, the main lipoprotein of high density lipoproteins (HDL), to inhibit acute vascular inflammation in normocholesterolemic New Zealand White rabbits. Acute vascular inflammation was induced in the animals by placing a non-occlusive, silastic collar around the left common carotid artery. The animals (n=5/group) received a single, low dose infusion of saline or lipid-free apoA-I at the time of, or 3 or 9h after collar insertion. The animals were sacrificed 24h post-collar insertion. Inflammatory markers in the artery wall were quantitated immunohistochemically. The saline-treated animals exhibited substantial pan-arterial inflammation, which was inhibited by a single apoA-I infusion (2 or 8 mg/kg) at the time of collar insertion. A single 8 mg/kg infusion of lipid-free apoA-I administered 3h post-collar insertion reduced neutrophil recruitment into the vessel wall, and MPO expression, as well as endothelial expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) by >85% (p<0.01 for all). A single 8 mg/kg infusion of lipid-free apoA-I administered 9h after collar insertion decreased VCAM-1 expression, neutrophil infiltration and MPO expression by 88% (p<0.001), 47% (p<0.01), and 90% (p<0.01), respectively. This indicates that a single low dose infusion of apoA-I administered after the onset of acute inflammation in carotid arteries decreases neutrophil infiltration and inhibits neutrophil and endothelial cell activation. These findings have potential implications for treating acute vascular inflammation in conditions such as acute coronary and stroke syndromes.
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PMID:Low dose apolipoprotein A-I rescues carotid arteries from inflammation in vivo. 1758 10


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