INT9650
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Bezafibrate produced significant reductions in LDL-C (-17%), total cholesterol (-13%), LDL-C/HDL-C (-24%), triglycerides (-28%), apo B (-15%), and LpA-I (-10%) and significantly increased HDL-C (+12%), apo A-I (+9%), apo A-II (+30%), apo E (+14%), and Lp(a) (+3%). | |||||||||||||||
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The levels of serum Lp(a), total cholesterol, high density lipoprotein-cholesterol, triglyceride, and remnant lipoprotein cholesterol were determined on admission. | |||||||||||||||
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Based on their serum Lp(a) levels, patients were classified into tertiles as follows: Tertile 1 (n=276), Lp(a)<13.8 mg/dL; Tertile 2 (n=279), Lp(a)=13.8-30.6 mg/dL; and Tertile 3 (n=277), Lp(a)? | |||||||||||||||
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Total cholesterol, low density lipoprotein-cholesterol, and apolipoprotein B levels were adjusted for Lp(a) contribution,10) according to compositional data in which cholesterol accounts for ? | |||||||||||||||
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To test for differences between Lp(a) tertiles, categorical variables were compared using the ? | |||||||||||||||
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Several changes were observed at this time point including: ipsilateral dorsal root ganglion (DRG) neurons were labeled by injured neurons marker ATF3; LPA(1) receptor expression in DRG neurons was increased; sural C-fibers were more sensitive to LPA stimuli, and this response could be blocked by LPA receptor and substance P receptor antagonists. | |||||||||||||||
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The 113 men with intermittent claudication, in contrast to men without this symptomatology, were older at entry (49 +/- 7 vs 45 +/- 7 years), and had higher systolic pressure (144 +/- 20 vs 136 +/- 16 mmHg) and Lp(a) levels (46 +/- 45 vs 33 +/- 35 mg/dl) (all p < 0.05). | |||||||||||||||
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The 113 men with intermittent claudication, in contrast to men without this symptomatology, were older at entry (49 +/- 7 vs 45 +/- 7 years), and had higher systolic pressure (144 +/- 20 vs 136 +/- 16 mmHg) and Lp(a) levels (46 +/- 45 vs 33 +/- 35 mg/dl) (all p < 0.05). | |||||||||||||||
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Plasma concentrations of fasting blood glucose, hemoglobin A1c, insulin, triglyceride, apoB/apoA-1 ratio, TNF-? | |||||||||||||||
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Plasma concentrations of insulin, total cholesterol, LDL-cholesterol, HDL-cholesterol, leptin and adiponectin were significantly higher in females than in males (p<0.05), however, no differences were found in insulin resistance (KITT), fasting blood glucose, hemoglobin A1c, triglyceride, apoB/apoA-1 ratio, CRP, TNF-? | |||||||||||||||
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Autotaxin is the enzyme responsible for the production of lysophosphatidic acid (LPA) from lysophosphatidyl choline (LPC), and it is up-regulated in many inflammatory conditions, including but not limited to cancer, arthritis, and multiple sclerosis. | |||||||||||||||
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Autotaxin's role in producing LPA in plasma and at the site of inflammation was tested in a rat air pouch model. | |||||||||||||||
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Collectively, the association of parental history of premature heart attack appears associated with levels of Lp(a) > 30 mg/dl, may lend support to the theory of genetic underpinning for the higher levels of Lp(a) observed in black children. | |||||||||||||||
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Predictors or independent variables were: gender, age, BMI, smoking, diabetes, hypertension, hypercholesterolemia, Lp(a) levels and apo(a) phenotypes. | |||||||||||||||
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In our study we found that Lp(a) plasma levels do not seem to show significant differences between the whole group of overweight and normal weight controls. | |||||||||||||||
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Therefore, it seems to be worthy of investigation whether Lp(a) levels and apo(a) isoforms are independent risk factors for CHD in overweight subjects. | |||||||||||||||
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CONCLUSIONS: With the cautions due to the cross-sectional design of the study and the limited statistical power, these results suggest a possible synergistic effect between elevated Lp(a) levels and other pro-atherogenic factors such as smoking on the risk of vascular diseases in older individuals.
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Lp(a) levels determined by an ELISA method. | |||||||||||||||
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RESULTS: No association was observed between elevated Lp(a) levels alone and any of the examined vascular diseases (stroke, myocardial infarction, angina, and intermittent claudication). | |||||||||||||||
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Hence, anti-thrombotic therapy targeting LPA production or receptor-mediated signaling may be a novel strategy to prevent thrombus formation. | |||||||||||||||
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