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Muriel J. Caslake

Researcher at University of Glasgow

Publications -  165
Citations -  14834

Muriel J. Caslake is an academic researcher from University of Glasgow. The author has contributed to research in topics: Lipoprotein & Very low-density lipoprotein. The author has an hindex of 63, co-authored 165 publications receiving 13806 citations. Previous affiliations of Muriel J. Caslake include Glasgow Royal Infirmary & University Hospitals of Morecambe Bay NHS Foundation Trust.

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C-Reactive Protein, Fibrinogen, and Cardiovascular Disease Prediction

Stephen Kaptoge, +82 more
TL;DR: It is estimated that under current treatment guidelines, assessment of the CRP or fibrinogen level in people at intermediate risk for a cardiovascular event could help prevent one additional event over a period of 10 years for every 400 to 500 people screened.
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Lipoprotein-Associated Phospholipase A2 as an Independent Predictor of Coronary Heart Disease

TL;DR: Elevated levels of lipoprotein-associated phospholipase A2 appear to be a strong risk factor for coronary heart disease, a finding that has implications for atherogenesis and the assessment of risk.
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Genetic associations with valvular calcification and aortic stenosis.

TL;DR: Genetic variation in the LPA locus, mediated by Lp(a) levels, is associated with aortic-valve calcification across multiple ethnic groups and with incident clinical aorti stenosis.
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C-Reactive Protein Is an Independent Predictor of Risk for the Development of Diabetes in the West of Scotland Coronary Prevention Study

TL;DR: Observations about C-reactive protein add to the notion that low-grade inflammation is important in the pathogenesis of type 2 diabetes, and have clinical potential in helping to better predict individuals destined to develop type 1 diabetes.
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Overproduction of large VLDL particles is driven by increased liver fat content in man.

TL;DR: It is proposed that the metabolic effect of insulin resistance, partly mediated by depressed plasma adiponectin levels, increases fatty acid flux from adipose tissue to the liver and induces the accumulation of fat in the liver, resulting in overproduction of VLDL1 particles and leading to the characteristic dyslipidaemia associated with type 2 diabetes.