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149 results on '"Caslake, Muriel"'

1. Exome Chip Meta-analysis Fine Maps Causal Variants and Elucidates the Genetic Architecture of Rare Coding Variants in Smoking and Alcohol Use

Author

Surendran, Praveen, Young, Robin, Barnes, Daniel R., Nielsen, Sune Fallgaard, Rasheed, Asif, Samuel, Maria, Zhao, Wei, Kontto, Jukka, Perola, Markus, Caslake, Muriel, de Craen, Anton J.M., Trompet, Stella, Uria-Nickelsen, Maria, Malarstig, Anders, Reily, Dermot F., Hoek, Maarten, Vogt, Thomas, Jukema, J. Wouter, Sattar, Naveed, Ford, Ian, Packard, Chris J., Alam, Dewan S., Majumder, Abdulla al Shafi, Di Angelantonio, Emanuele, Chowdhury, Rajiv, Amouyel, Philippe, Arveiler, Dominique, Blankenberg, Stefan, Ferrières, Jean, Kee, Frank, Kuulasmaa, Kari, Müller-Nurasyid, Martina, Veronesi, Giovanni, Virtamo, Jarmo, EPIC-CVD Consortium, Frossard, Philippe, Nordestgaard, Børge Grønne, Saleheen, Danish, Danesh, John, Butterworth, Adam S., Howson, Joanna M.M., Erzurumluoglu, A. Mesut, Jackson, Victoria E., Melbourne, Carl A., Varga, Tibor V., Warren, Helen R., Tragante, Vinicius, Tachmazidou, Ioanna, Harris, Sarah E., Evangelou, Evangelos, Marten, Jonathan, Zhang, Weihua, Altmaier, Elisabeth, Luan, Jian’an, Langenberg, Claudia, Scott, Robert A., Yaghootkar, Hanieh, Stirrups, Kathleen, Kanoni, Stavroula, Marouli, Eirini, Karpe, Fredrik, Dominiczak, Anna F., Sever, Peter, Poulter, Neil, Rolandsson, Olov, Baumbach, Clemens, Afaq, Saima, Chambers, John C., Kooner, Jaspal S., Wareham, Nicholas J., Renström, Frida, Hallmans, Göran, Marioni, Riccardo E., Corley, Janie, Starr, John M., Verweij, Niek, de Boer, Rudolf A., van der Meer, Peter, Yavas, Ersin, Vaartjes, Ilonca, Bots, Michiel L., Asselbergs, Folkert W., Grabe, Hans J., Völzke, Henry, Nauck, Matthias, Weiss, Stefan, Pharoah, Paul D.P., Dunning, Alison M., Dennis, Joe G., Thompson, Deborah J., Michailidou, Kyriaki, Easton, Douglas F., Antoniou, Antonis C., Tyrrell, Jessica, Mihailov, Evelin, Samani, Nilesh J., Zhou, Kaixin, Neville, Matthew J., Metspalu, Andres, Palmer, Colin N.A., Hall, Ian P., Strachan, David P., Deary, Ian J., Frayling, Tim M., Hayward, Caroline, van der Harst, Pim, Zeggini, Eleftheria, Understanding Society Scientific Group, Munroe, Patricia B., Jansson, Jan-Håkan, Franks, Paul W., Deloukas, Panos, Caulfield, Mark J., Wain, Louise V., Tobin, Martin D., Brazel, David M., Jiang, Yu, Hughey, Jordan M., Turcot, Valérie, Zhan, Xiaowei, Gong, Jian, Batini, Chiara, Weissenkampen, J. Dylan, Liu, MengZhen, Bertelsen, Sarah, Chou, Yi-Ling, Faul, Jessica D., Haessler, Jeff, Hammerschlag, Anke R., Hsu, Chris, Kapoor, Manav, Lai, Dongbing, Le, Nhung, de Leeuw, Christiaan A., Loukola, Anu, Mangino, Massimo, Pistis, Giorgio, Qaiser, Beenish, Rohde, Rebecca, Shao, Yaming, Stringham, Heather, Wetherill, Leah, Agrawal, Arpana, Bierut, Laura, Chen, Chu, Eaton, Charles B., Goate, Alison, Haiman, Christopher, Heath, Andrew, Iacono, William G., Martin, Nicholas G., Polderman, Tinca J., Reiner, Alex, Rice, John, Schlessinger, David, Scholte, H. Steven, Smith, Jennifer A., Tardif, Jean-Claude, Tindle, Hilary A., van der Leij, Andries R., Boehnke, Michael, Chang-Claude, Jenny, Cucca, Francesco, David, Sean P., Foroud, Tatiana, Kardia, Sharon L.R., Kooperberg, Charles, Laakso, Markku, Lettre, Guillaume, Madden, Pamela, McGue, Matt, North, Kari, Posthuma, Danielle, Spector, Timothy, Stram, Daniel, Weir, David R., Kaprio, Jaakko, Abecasis, Gonçalo R., Liu, Dajiang J., and Vrieze, Scott

Published
2019
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11. Microsomal triglyceride transfer protein -493T variant reduces IDL plus LDL apoB production and the plasma concentration of large LDL particles

Author

Lundahl, Bjorn, Skoglund-Andersson, Camilla, Caslake, Muriel, Bedford, Dorothy, Stewart, Philip, Hamsten, Anders, Packard, Christopher J., and Karpe, Fredrik

Subjects
Lipoproteins -- Research, Lipoproteins -- Analysis, Proteolipids -- Research, Proteolipids -- Analysis, Lipids -- Research, Biological sciences
Abstract

The microsomal triglyceride transfer protein (MTP) is essential for the synthesis and secretion of apolipoprotein B (apoB)-containing lipoproteins. We investigated the role the MTP -493G/T gene polymorphism in determining the apoB-100 secretion pattern and LDL heterogeneity in healthy human subjects. Groups of carriers of the T and the G variants (n = 6 each) were recruited from a cohort of healthy 50-yr-old men. Kinetic studies were performed by endogenous [[sup.2][H.sub.3]]leucine labeling of apoB and subsequent quantification of the stable isotope incorporation, apoB production rates, metabolic conversions, and eliminations were calculated by multicompartmental modeling (SAAM-II). LDL subfraction distribution was analyzed in the entire cohort (n = 377). Carriers of the MTP -493T allele had lower plasma LDL apoB and lower concentration of large LDL particles [LDL-I: 136 [+ or -] 57 (TT) vs. 175 [+ or -] 55 (GG) mg/l, P < 0.01]. Kinetic modeling suggested that MTP -493T homozygotes had a 60% lower direct production rate of intermediate-density lipoprotein (IDL) plus LDL compared with homozygotes for the G allele (P < 0.05). No differences were seen in production rates of large and small VLDL, nor were there any differences in metabolic conversion or elimination rates of apoB between the genotype groups. This study shows that a polymorphism in the MTP gene affects the spectrum of endogenous apoB-containing lipoprotein particles produced in humans. Reduced direct production of LDL plus IDL appears to be related to lower plasma concentrations of large LDL particles. intermediate-density lipoprotein; low-density lipoprotein; apolipoprotein B; very-low-density lipoprotein secretion; lipidation; microsomal triglyceride transfer protein

Published
2006

12. 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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13. Genetic Associations with Valvular Calcification and Aortic Stenosis

Author

Thanassoulis, George, Campbell, Catherine Y., Owens, David S., Smith, J. Gustav, Smith, Albert V., Peloso, Gina M., Kerr, Kathleen F., Pechlivanis, Sonali, Budoff, Matthew J., Harris, Tamara B., Malhotra, Rajeev, OʼBrien, Kevin D., Kamstrup, Pia R., Nordestgaard, Børge G., Tybjaerg-Hansen, Anne, Allison, Matthew A., Aspelund, Thor, Criqui, Michael H., Heckbert, Susan R., Hwang, Shih-Jen, Liu, Yongmei, Sjogren, Marketa, van der Pals, Jesper, Kälsch, Hagen, Mühleisen, Thomas W., Nöthen, Markus M., Cupples, L. Adrienne, Caslake, Muriel, Di Angelantonio, Emanuele, Danesh, John, Rotter, Jerome I., Sigurdsson, Sigurdur, Wong, Quenna, Erbel, Raimund, Kathiresan, Sekar, Melander, Olle, Gudnason, Vilmundur, OʼDonnell, Christopher J., and Post, Wendy S.

Published
2013
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17. 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

23. 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

35. 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

36. Replication of LDL GWAs hits in PROSPER/PHASE as validation for future (pharmaco)genetic analyses

Author

Stott David J, Caslake Muriel, Sattar Naveed, Ford Ian, Postmus Iris, de Craen Anton JM, Trompet Stella, Buckley Brendan M, Sacks Frank, Devlin James J, Slagboom P, Westendorp Rudi GJ, and Jukema J

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background The PHArmacogenetic study of Statins in the Elderly at risk (PHASE) is a genome wide association study in the PROspective Study of Pravastatin in the Elderly at risk for vascular disease (PROSPER) that investigates the genetic variation responsible for the individual variation in drug response to pravastatin. Statins lower LDL-cholesterol in general by 30%, however not in all subjects. Moreover, clinical response is highly variable and adverse effects occur in a minority of patients. In this report we first describe the rationale of the PROSPER/PHASE project and second show that the PROSPER/PHASE study can be used to study pharmacogenetics in the elderly. Methods The genome wide association study (GWAS) was conducted using the Illumina 660K-Quad beadchips following manufacturer's instructions. After a stringent quality control 557,192 SNPs in 5,244 subjects were available for analysis. To maximize the availability of genetic data and coverage of the genome, imputation up to 2.5 million autosomal CEPH HapMap SNPs was performed with MACH imputation software. The GWAS for LDL-cholesterol is assessed with an additive linear regression model in PROBABEL software, adjusted for age, sex, and country of origin to account for population stratification. Results Forty-two SNPs reached the GWAS significant threshold of p = 5.0e-08 in 5 genomic loci (APOE/APOC1; LDLR; FADS2/FEN1; HMGCR; PSRC1/CELSR5). The top SNP (rs445925, chromosome 19) with a p-value of p = 2.8e-30 is located within the APOC1 gene and near the APOE gene. The second top SNP (rs6511720, chromosome 19) with a p-value of p = 5.22e-15 is located within the LDLR gene. All 5 genomic loci were previously associated with LDL-cholesterol levels, no novel loci were identified. Replication in WOSCOPS and CARE confirmed our results. Conclusion With the GWAS in the PROSPER/PHASE study we confirm the previously found genetic associations with LDL-cholesterol levels. With this proof-of-principle study we show that the PROSPER/PHASE study can be used to investigate genetic associations in a similar way to population based studies. The next step of the PROSPER/PHASE study is to identify the genetic variation responsible for the variation in LDL-cholesterol lowering in response to statin treatment in collaboration with other large trials.

Published
2011
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47. Interleukin-6 blockade raises LDL via reduced catabolism rather than via increased synthesis: a cytokine-specific mechanism for cholesterol changes in rheumatoid arthritis.

Author

Robertson, Jamie, Porter, Duncan, Sattar, Naveed, Packard, Chris J., Caslake, Muriel, McInnes, Iain, and McCarey, David

Subjects
ANTIRHEUMATIC agents, C-reactive protein, CHOLESTEROL, COMPARATIVE studies, DYNAMICS, HIGH density lipoproteins, INTERLEUKINS, LOW density lipoproteins, RESEARCH methodology, MEDICAL cooperation, MONOCLONAL antibodies, RESEARCH, RHEUMATOID arthritis, EVALUATION research, TREATMENT effectiveness, SEVERITY of illness index, CHEMICAL inhibitors
Abstract

Objectives: Patients with rheumatoid arthritis (RA) have reduced serum low-density lipoprotein cholesterol (LDL-c), which increases following therapeutic IL-6 blockade. We aimed to define the metabolic pathways underlying these lipid changes.Methods: In the KALIBRA study, lipoprotein kinetic studies were performed on 11 patients with severe active RA at baseline and following three intravenous infusions of the IL-6R blocker tocilizumab. The primary outcome measure was the fractional catabolic rate (FCR) of LDL.Results: Serum total cholesterol (4.8 vs 5.7 mmol/L, p=0.003), LDL-c (2.9 vs 3.4 mmol/L, p=0.014) and high-density lipoprotein cholesterol (1.23 vs 1.52 mmol/L, p=0.006) increased following tocilizumab therapy. The LDL FCR fell from a state of hypercatabolism to a value approximating that of the normal population (0.53 vs 0.27 pools/day, p=0.006). Changes in FCR correlated tightly with changes in serum LDL-c and C-reactive protein but not Clinical Disease Activity Index.Conclusions: Patients with RA have low serum LDL-c due to hypercatabolism of LDL particles. IL-6 blockade normalises this catabolism in a manner associating with the acute phase response (and thus hepatic IL-6 signalling) but not with RA disease activity as measured clinically. We demonstrate that IL-6 is one of the key drivers of inflammation-driven dyslipidaemia. [ABSTRACT FROM AUTHOR]

Published
2017
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48. Genetic invalidation of Lp-PLA2 as a therapeutic target: Large-scale study of five functional Lp-PLA2-lowering alleles.

Author

Gregson, John M, Freitag, Daniel F, Surendran, Praveen, Stitziel, Nathan O, Chowdhury, Rajiv, Burgess, Stephen, Kaptoge, Stephen, Gao, Pei, Staley, James R, Willeit, Peter, Nielsen, Sune F, Caslake, Muriel, Trompet, Stella, Polfus, Linda M, Kuulasmaa, Kari, Kontto, Jukka, Perola, Markus, Blankenberg, Stefan, Veronesi, Giovanni, and Gianfagna, Francesco

Published
2017
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49. The association of circulating microRNA-30c with atherogenic lipoprotein subfractions and composition.

Author

Eastwood, Jarlath, Caslake, Muriel J, and Sodi, Ravinder

Subjects
*LIPOPROTEINS, *MICRORNA genetics, *POLYMERASE chain reaction, *NUCLEIC acid amplification techniques, *PHOSPHOLIPID analysis
Abstract

Circulating miR-30c has been linked to various aspects of cholesterol homeostasis. The aim of this study was to determine the association of circulating miR-30c with the atherogenic lipoprotein subfractions. Samples from subjects who were given placebo ( n = 22) in a randomised, double-blind crossover study were used. Subjects were divided into non-atherogenic lipoprotein phenotype (Non-ALP; n = 12; triglycerides < 2.0 mmol/L) and atherogenic lipoprotein phenotype (ALP; n = 10; triglycerides ≥ 2.0 mmol/L) groups. All lipid and lipoprotein measurements, RNA extraction and reverse transcription-quantitative real-time polymerase chain reaction were undertaken using standard procedures. Subjects with ALP weighed significantly more than their non-ALP counterparts ( p = 0.023). In the non-ALP group there was significant correlation between miR-30c and components within VLDL1, namely triglyceride which showed a negative association ( p = 0.035) whereas phospholipids and cholesterol-ester were both positively correlated ( p = 0.025 and 0.014, respectively). In contrast, in the ALP group there was a significant correlation between the expression of miR-30c and components within VLDL2, namely triglyceride, which was positively associated ( p = 0.013). This study reveals specificity with regards to the effect of miR-30c on VLDL subfractions based on the individual's lipoprotein phenotype and implicates roles for microsomal-triglyceride transfer-protein and cholesteryl-ester-transfer-protein in LDL and VLDL metabolism, respectively. [ABSTRACT FROM AUTHOR]

Published
2016
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50. miR-34a(-/-) mice are susceptible to diet-induced obesity.

Author

Lavery, Christopher A., Kurowska‐Stolarska, Mariola, Holmes, William M., Donnelly, Iona, Caslake, Muriel, Collier, Andrew, Baker, Andrew H., Miller, Ashley M., and Kurowska-Stolarska, Mariola

Subjects
OBESITY, TYPE 2 diabetes, METABOLIC regulation, MICRORNA, MACROPHAGES, FAT cells, RNA metabolism, ADIPOSE tissues, ANIMAL experimentation, DIET, INTERLEUKINS, LIVER, MICE, TUMOR necrosis factors
Abstract

Objective: MicroRNA (miR)-34a regulates inflammatory pathways, and increased transcripts have been observed in serum and subcutaneous adipose of subjects who have obesity and type 2 diabetes. Therefore, the role of miR-34a in adipose tissue inflammation and lipid metabolism in murine diet-induced obesity was investigated.Methods: Wild-type (WT) and miR-34a(-/-) mice were fed chow or high-fat diet (HFD) for 24 weeks. WT and miR-34a(-/-) bone marrow-derived macrophages were cultured in vitro with macrophage colony-stimulating factor (M-CSF). Brown and white preadipocytes were cultured from the stromal vascular fraction (SVF) of intrascapular brown and epididymal white adipose tissue (eWAT), with rosiglitazone.Results: HFD-fed miR-34a(-/-) mice were significantly heavier with a greater increase in eWAT weight than WT. miR-34a(-/-) eWAT had a smaller adipocyte area, which significantly increased with HFD. miR-34a(-/-) eWAT showed basal increases in Cd36, Hmgcr, Lxrα, Pgc1α, and Fasn. miR-34a(-/-) intrascapular brown adipose tissue had basal reductions in c/ebpα and c/ebpβ, with in vitro miR-34a(-/-) white adipocytes showing increased lipid content. An F4/80(high) macrophage population was present in HFD miR-34a(-/-) eWAT, with increased IL-10 transcripts and serum IL-5 protein. Finally, miR-34a(-/-) bone marrow-derived macrophages showed an ablated CXCL1 response to tumor necrosis factor-α.Conclusions: These findings suggest a multifactorial role of miR-34a in controlling susceptibility to obesity, by regulating inflammatory and metabolic pathways. [ABSTRACT FROM AUTHOR]

Published
2016
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