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209 results on '"Caslake, Muriel J"'

7. CD36 and SR-BI Are Involved in Cellular Uptake of Provitamin A Carotenoids by Caco-2 and HEK Cells, and Some of Their Genetic Variants Are Associated with Plasma Concentrations of These Micronutrients in Humans1-3

Author

Borel, Patrick, Lietz, Georg, Goncalves, Aurélie, de Edelenyi, Fabien Szabo, Lecompte, Sophie, Curtis, Peter, Goumidi, Louisa, Caslake, Muriel J., Miles, Elizabeth A., Packard, Christopher, Calder, Philip C., Mathers, John C., Minihane, Anne M., Tourniaire, Franck, Kesse-Guyot, Emmanuelle, Galan, Pilar, Hercberg, Serge, Breidenassel, Christina, Gross, Marcela González, Moussa, Myriam, Meirhaeghe, Aline, and Reboul, Emmanuelle

Published
2013
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11. Lipoprotein-associated phospholipase A(sub 2) as an independent predictor of coronary heart disease

Author

Packard, Chris J., O'Reilly, Denis S.J., Caslake, Muriel J., McMahon, Alex D., Ford, Ian, Cooney, Josephine, Macphee, Colin H., Suckling, Keith E., Krishna, Mala, Wilkinson, Francis E., Rumley, Ann, and Lowe, Gordon D.O.

Subjects
Phospholipases -- Health aspects, Coronary heart disease -- Patient outcomes, Heart attack -- Risk factors
Abstract

Elevated blood levels of lipoprotein-associated phospholipase A(sub 2) may predict which men will have a heart attack or die from coronary artery disease. This enzyme may modify low-density lipoproteins inside coronary arteries.

Published
2000

14. Association Between Apolipoprotein E4 and Cognitive Decline in Elderly Adults

Author

Packard, Chris J., Westendorp, Rudi G.J., Stott, David J., Caslake, Muriel J., Murray, Heather M., Shepherd, James, Blauw, Gerard J., Murphy, Michael B., Bollen, Edward L.E.M., Buckley, Brendan M., Cobbe, Stuart M., Ford, Ian, Gaw, Allan, Hyland, Michael, Jukema, J. Wouter, Kamper, Adriaan M., Macfarlane, Peter W., Jolles, Jellemer, Perry, Ivan J., Sweeney, Brian J., and Twomey, Cillian

Published
2007

21. Effects of dietary monounsaturated fatty acids on lipoprotein concentrations, compositions, and subfraction distributions and on VLDL apolipoprotein B kinetics: dose-dependent effects on LDL

Author

Gill, Jason MR, Brown, Jacqueline C, Caslake, Muriel J, Wright, Dawn M, Cooney, Josephine, Bedford, Dorothy, Hughes, David A, Stanley, John C, and Packard, Chris J

Subjects
Saturated fatty acids -- Health aspects, Monounsaturated fatty acids -- Physiological aspects, Cholesterol, LDL -- Physiological aspects, Food/cooking/nutrition, Health
Abstract

Background: Replacing dietary saturated fatty acids (SFAs) with monounsaturated fatty acids (MUFAs) lowers LDL cholesterol, but the underlying mechanisms remain unclear. Objective: We assessed the effects of replacing dietary SFAs with MUFAs on concentrations and subclass distributions of VLDL, intermediate-density lipoprotein, LDL, and HDL and on VLDL apolipoprotein B kinetics. Design: Thirty-five moderately hypercholesterolemic, middle-aged volunteers consumed for 6 wk, in random order, diets containing low (L-MUFA; 7.8% of energy from MUFAs), moderate (M-MUFA; 10.3% from MUFAs), or high (H-MUFA; 13.7% from MUFAs) amounts of MUFAs. Fasting blood samples were taken from all subjects after each intervention. VLDL apolipoprotein B kinetic studies were performed in a subgroup after the L-MUFA and H-MUFA diets. Results: Plasma cholesterol concentrations decreased in a dose-dependent manner with increasing intakes of dietary MUFAs. This change was entirely accounted for by reduced LDL cholesterol (-0.20 and -0.49 mmol/L after the M-MUFA and H-MUFA diets, respectively, compared with the concentration after the L-MUFA diet; P for trend < 0.01). Plasma triacylglycerol and HDL cholesterol were not significantly affected by the dietary intervention, nor were the concentrations of [VLDL.sub.1] ([S.sub.f] 60-400), [VLDL.sub.2] ([S.sub.f] 20-60), or intermediate-density lipoprotein ([S.sub.f] 12-20). Production and catabolic rates for [VLDL.sub.1] and [VLDL.sub.2] were also unaffected. HDL and LDL subclass distributions were not significantly altered, but as a consequence of the overall LDL lowering, concentrations of atherogenic LDL-III were 25% lower after the H-MUFA diet than after the L-MUFA diet (P = 0.02). Conclusion: The effects of replacing dietary SFAs with MUFAs on lipoprotein metabolism appear to be almost exclusively limited to the LDL density class. KEY WORDS Monounsaturated fatty acids, saturated fatty acids, LDL, VLDL, lipoprotein subfractions, cholesterol

Published
2003

26. Familial combined hyperlipidaemia linked to the apolipoprotein AI-CIII-AIV gene cluster on chromosome 11q23-q24

Author

Wojciechowski, Andrew P, Farrall, Martin, Cullen, Paul, Wilson, Teresa M E, Bayliss, Jayne D, Farren, Bernadette, Griffin, Bruce A, Caslake, Muriel J, Packard, Christopher J, Shepherd, James, Thakker, Rajesh, and Scott, James

Subjects
Familial diseases -- Genetic aspects, Hyperlipidemia -- Genetic aspects, Hyperlipidemia -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Familial combined hyperlipidemia (FCHL) is an inherited disorder of fat metabolism that causes as many as 10 percent of the cases of premature disease of the coronary arteries, which supply the heart with blood. One fifth of the patients with FCHL develop premature coronary heart disease. FCHL sufferers have elevated blood cholesterol and/or triglyceride levels, as well as abnormal low-density lipoproteins (forms in which fats are carried in the blood). To better characterize the gene defect associated with FCHL, members of eight FCHL families were studied. Techniques of DNA analysis and linkage analysis were used to identify the gene cluster associated with FCHL in the families evaluated. It was found to be the AI-CIII-AIV gene cluster, which contained the X2 allele in half the affected families. This region appears to carry a genetic defect that causes a metabolic disorder that in turn predisposes the individual to develop premature coronary heart disease. Further research is needed to identify the mutation present in people at risk. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

33. Does high-density lipoprotein protect vascular function in healthy pregnancy?

Author

Sulaiman, Wan N Wan, Caslake, Muriel J, Delles, Christian, Karlsson, Helen, Mulder, Monique T, Graham, Delyth, Freeman, Dilys J, Sulaiman, Wan N Wan, Caslake, Muriel J, Delles, Christian, Karlsson, Helen, Mulder, Monique T, Graham, Delyth, and Freeman, Dilys J

Abstract

The maternal adaptation to pregnancy includes hyperlipidaemia, oxidative stress and chronic inflammation. In non-pregnant individuals, these processes are usually associated with poor vascular function. However, maternal vascular function is enhanced in pregnancy. It is not understood how this is achieved in the face of the adverse metabolic and inflammatory environment. Research into cardiovascular disease demonstrates that plasma HDL (high-density lipoprotein), by merit of its functionality rather than its plasma concentration, exerts protective effects on the vascular endothelium. HDL has vasodilatory, antioxidant, anti-thrombotic and anti-inflammatory effects, and can protect against endothelial cell damage. In pregnancy, the plasma HDL concentration starts to rise at 10 weeks of gestation, peaking at 20 weeks. The initial rise in plasma HDL occurs around the time of the establishment of the feto-placental circulation, a time when the trophoblast plugs in the maternal spiral arteries are released, generating oxidative stress. Thus there is the intriguing possibility that new HDL of improved function is synthesized around the time of the establishment of the feto-placental circulation. In obese pregnancy and, to a greater extent, in pre-eclampsia, plasma HDL levels are significantly decreased and maternal vascular function is reduced. Wire myography studies have shown an association between the plasma content of apolipoprotein AI, the major protein constituent of HDL, and blood vessel relaxation. These observations lead us to hypothesize that HDL concentration, and function, increases in pregnancy in order to protect the maternal vascular endothelium and that in pre-eclampsia this fails to occur., Funding agencies: Malaysian Ministry of Higher Education; grant EU-MASCARA from the European Commission [278249]; grant sysVASC from the European Commission [603288]

Published
2016
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35. Consumption of Fish Oil Providing Amounts of Eicosapentaenoic Acid and Docosahexaenoic Acid That Can Be Obtained from the Diet Reduces Blood Pressure in Adults with Systolic Hypertension: A Retrospective Analysis

Author

Minihane, Anne M, primary, Armah, Christopher K, additional, Miles, Elizabeth A, additional, Madden, Jacqueline M, additional, Clark, Allan B, additional, Caslake, Muriel J, additional, Packard, Chris J, additional, Kofler, Bettina M, additional, Lietz, Georg, additional, Curtis, Peter J, additional, Mathers, John C, additional, Williams, Christine M, additional, and Calder, Philip C, additional

Published
2016
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37. Maternal obesity is associated with the formation of small dense LDL and hypoadiponectinemia in the third trimester

Author

Meyer, Barbara J, Stewart, Frances M, Brown, Elizabeth A, Cooney, Josephine, Nilsson, Solveig, Olivecrona, Gunilla, Ramsay, Jane E, Griffin, Bruce A, Caslake, Muriel J, Freeman, Dilys J, Meyer, Barbara J, Stewart, Frances M, Brown, Elizabeth A, Cooney, Josephine, Nilsson, Solveig, Olivecrona, Gunilla, Ramsay, Jane E, Griffin, Bruce A, Caslake, Muriel J, and Freeman, Dilys J

Abstract

CONTEXT: Maternal obesity is associated with high plasma triglyceride, poor vascular function, and an increased risk for pregnancy complications. In normal-weight pregnant women, higher triglyceride is associated with increased small, dense low-density lipoprotein (LDL). HYPOTHESIS: In obese pregnancy, increased plasma triglyceride concentrations result in triglyceride enrichment of very low-density lipoprotein-1 particles and formation of small dense LDL via lipoprotein lipase. DESIGN: Women (n = 55) of body mass index of 18-46 kg/m(2) were sampled longitudinally at 12, 26, and 35 weeks' gestation and 4 months postnatally. SETTING: Women were recruited at hospital antenatal appointments, and study visits were in a clinical research suite. OUTCOME MEASURES: Plasma concentrations of lipids, triglyceride-rich lipoproteins, lipoprotein lipase mass, estradiol, steroid hormone binding globulin, insulin, glucose, leptin, and adiponectin were determined. RESULTS: Obese women commenced pregnancy with higher plasma triglyceride, reached the same maximum, and then returned to higher postnatal levels than normal-weight women. Estradiol response to pregnancy (trimester 1-3 incremental area under the curve) was positively associated with plasma triglyceride response (r(2) adjusted 25%, P <.001). In the third trimester, the proportion of small, dense LDL was 2-fold higher in obese women than normal-weight women [mean (SD) 40.7 (18.8) vs 21.9 (10.9)%, P =.014], and 35% of obese, 14% of overweight, and none of the normal-weight women displayed an atherogenic LDL subfraction phenotype. The small, dense LDL mass response to pregnancy was inversely associated with adiponectin response (17%, P =.013). CONCLUSIONS: Maternal obesity is associated with an atherogenic LDL subfraction phenotype and may provide a mechanistic link to poor vascular function and adverse pregnancy outcome.

Published
2013

39. Apolipoprotein E genotype and the cardiovascular disease risk phenotype: Impact of sex and adiposity (the FINGEN study)

Author

Kofler, Bettina M., primary, Miles, Elizabeth A., additional, Curtis, Peter, additional, Armah, Christopher K., additional, Tricon, Sabine, additional, Grew, Jilly, additional, Napper, Frances L., additional, Farrell, Leslie, additional, Lietz, Georg, additional, Packard, Christopher J., additional, Caslake, Muriel J., additional, Mathers, John C., additional, Williams, Christine M., additional, Calder, Philip C., additional, and Minihane, Anne Marie, additional

Published
2012
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43. Lipoprotein-associated phospholipase A2, inflammatory biomarkers, and risk of cardiovascular disease in the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER)

Author

Caslake, Muriel J., primary, Packard, Chris J., additional, Robertson, Michele, additional, Cooney, Josephine, additional, Nelson, Jeanenne J., additional, Ford, Ian, additional, Gaw, Allan, additional, Jukema, J. Wouter, additional, Macfarlane, Peter W., additional, Stott, David J., additional, and Shepherd, James, additional

Published
2010
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