Author: "Packard, C." / Publication Type: Electronic Resources - Searchworks@Jio Institute Digital Library Search Results

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23 results on '"Packard, C."'

1. SCORE2 risk prediction algorithms: new models to estimate 10-year risk of cardiovascular disease in Europe

Author: Achenbach, S, Aleksandrova, K, Amiano, P, San Sebastian, D, Amouyel, P, Andersson, J, Bakker, S, Da Providencia Costa, R, Beulens, J, Blaha, M, Bobak, M, Boer, J, Bonet, C, Bonnet, F, Boutron-Ruault, M, Braaten, T, Brenner, H, Brunner, F, Brunner, E, Brunström, M, Buring, J, Butterworth, A, Capkova, N, Cesana, G, Chrysohoou, C, Colorado-Yohar, S, Cook, N, Cooper, C, Dahm, C, Davidson, K, Dennison, E, Di Castelnuovo, A, Donfrancesco, C, Dörr, M, Doryńska, A, Eliasson, M, Engström, G, Ferrari, P, Ferrario, M, Ford, I, Fu, M, Gansevoort, R, Giampaoli, S, Gillum, R, Gómez de la Cámara, A, Grassi, G, Hansson, P, Huculeci, R, Hveem, K, Iacoviello, L, Ikram, M, Jørgensen, T, Joseph, B, Jousilahti, P, Wouter Jukema, J, Kaaks, R, Katzke, V, Kavousi, M, Kiechl, S, Klotsche, J, König, W, Kronmal, R, Kubinova, R, Kucharska-Newton, A, Läll, K, Lehmann, N, Leistner, D, Linneberg, A, Pablos, D, Lorenz, T, Lu, W, Luksiene, D, Lyngbakken, M, Magnussen, C, Malyutina, S, Ibañez, A, Masala, G, Mathiesen, E, Matsushita, K, Meade, T, Melander, O, Meyer, H, Moons, K, Moreno-Iribas, C, Muller, D, Münzel, T, Nikitin, Y, Nordestgaard, B, Omland, T, Onland, C, Overvad, K, Packard, C, Pająk, A, Palmieri, L, Panagiotakos, D, Panico, S, Perez-Cornago, A, Peters, A, Pietilä, A, Pikhart, H, Psaty, B, Quarti-Trevano, F, Garcia, J, Riboli, E, Ridker, P, Rodriguez, B, Rodriguez-Barranco, M, Rosengren, A, Roussel, R, Sacerdote, C, S, S, Sattar, N, Schiborn, C, Schmidt, B, Schöttker, B, Schulze, M, Schwartz, J, Selmer, R, Shea, S, Shipley, M, Sieri, S, Söderberg, S, Sofat, R, Tamosiunas, A, Thorand, B, Tillmann, T, Tjønneland, A, Tong, T, Trichopoulou, A, Tumino, R, Tunstall-Pedoe, H, Tybjaerg-Hansen, A, Tzoulaki, J, van der Heijden, A, van der Schouw, Y, Verschuren, W, Völzke, H, Waldeyer, C, Wareham, N, Weiderpass, E, Weidinger, F, Wild, P, Willeit, J, Willeit, P, Wilsgaard, T, Woodward, M, Zeller, T, Zhang, D, Zhou, B, Bakker, SJL, Da Providencia Costa, RB, Beulens, JWJ, Boer, JMA, Boutron-Ruault, MC, Brunner, EJ, Butterworth, AS, Cook, NR, Dahm, CC, Gansevoort, RT, Gillum, RF, Hansson, PO, Ikram, MK, Kronmal, RA, Pablos, DL, Malyutina, So, Ibañez, AM, Mathiesen, EB, Meade, TW, Meyer, HE, Moons, KGM, Nordestgaard, BG, Psaty, BM, Garcia, JRQ, Ridker, PM, C Sans, Schwartz, JE, Selmer, RM, Shipley, MJ, Tong, TYN, van der Schouw, YT, Verschuren, WMM, Wareham, NJ, Achenbach, S, Aleksandrova, K, Amiano, P, San Sebastian, D, Amouyel, P, Andersson, J, Bakker, S, Da Providencia Costa, R, Beulens, J, Blaha, M, Bobak, M, Boer, J, Bonet, C, Bonnet, F, Boutron-Ruault, M, Braaten, T, Brenner, H, Brunner, F, Brunner, E, Brunström, M, Buring, J, Butterworth, A, Capkova, N, Cesana, G, Chrysohoou, C, Colorado-Yohar, S, Cook, N, Cooper, C, Dahm, C, Davidson, K, Dennison, E, Di Castelnuovo, A, Donfrancesco, C, Dörr, M, Doryńska, A, Eliasson, M, Engström, G, Ferrari, P, Ferrario, M, Ford, I, Fu, M, Gansevoort, R, Giampaoli, S, Gillum, R, Gómez de la Cámara, A, Grassi, G, Hansson, P, Huculeci, R, Hveem, K, Iacoviello, L, Ikram, M, Jørgensen, T, Joseph, B, Jousilahti, P, Wouter Jukema, J, Kaaks, R, Katzke, V, Kavousi, M, Kiechl, S, Klotsche, J, König, W, Kronmal, R, Kubinova, R, Kucharska-Newton, A, Läll, K, Lehmann, N, Leistner, D, Linneberg, A, Pablos, D, Lorenz, T, Lu, W, Luksiene, D, Lyngbakken, M, Magnussen, C, Malyutina, S, Ibañez, A, Masala, G, Mathiesen, E, Matsushita, K, Meade, T, Melander, O, Meyer, H, Moons, K, Moreno-Iribas, C, Muller, D, Münzel, T, Nikitin, Y, Nordestgaard, B, Omland, T, Onland, C, Overvad, K, Packard, C, Pająk, A, Palmieri, L, Panagiotakos, D, Panico, S, Perez-Cornago, A, Peters, A, Pietilä, A, Pikhart, H, Psaty, B, Quarti-Trevano, F, Garcia, J, Riboli, E, Ridker, P, Rodriguez, B, Rodriguez-Barranco, M, Rosengren, A, Roussel, R, Sacerdote, C, S, S, Sattar, N, Schiborn, C, Schmidt, B, Schöttker, B, Schulze, M, Schwartz, J, Selmer, R, Shea, S, Shipley, M, Sieri, S, Söderberg, S, Sofat, R, Tamosiunas, A, Thorand, B, Tillmann, T, Tjønneland, A, Tong, T, Trichopoulou, A, Tumino, R, Tunstall-Pedoe, H, Tybjaerg-Hansen, A, Tzoulaki, J, van der Heijden, A, van der Schouw, Y, Verschuren, W, Völzke, H, Waldeyer, C, Wareham, N, Weiderpass, E, Weidinger, F, Wild, P, Willeit, J, Willeit, P, Wilsgaard, T, Woodward, M, Zeller, T, Zhang, D, Zhou, B, Bakker, SJL, Da Providencia Costa, RB, Beulens, JWJ, Boer, JMA, Boutron-Ruault, MC, Brunner, EJ, Butterworth, AS, Cook, NR, Dahm, CC, Gansevoort, RT, Gillum, RF, Hansson, PO, Ikram, MK, Kronmal, RA, Pablos, DL, Malyutina, So, Ibañez, AM, Mathiesen, EB, Meade, TW, Meyer, HE, Moons, KGM, Nordestgaard, BG, Psaty, BM, Garcia, JRQ, Ridker, PM, C Sans, Schwartz, JE, Selmer, RM, Shipley, MJ, Tong, TYN, van der Schouw, YT, Verschuren, WMM, and Wareham, NJ
Abstract: Aims: The aim of this study was to develop, validate, and illustrate an updated prediction model (SCORE2) to estimate 10-year fatal and non-fatal cardiovascular disease (CVD) risk in individuals without previous CVD or diabetes aged 40-69 years in Europe. Methods and results : We derived risk prediction models using individual-participant data from 45 cohorts in 13 countries (677 684 individuals, 30 121 CVD events). We used sex-specific and competing risk-adjusted models, including age, smoking status, systolic blood pressure, and total- and HDL-cholesterol. We defined four risk regions in Europe according to country-specific CVD mortality, recalibrating models to each region using expected incidences and risk factor distributions. Region-specific incidence was estimated using CVD mortality and incidence data on 10 776 466 individuals. For external validation, we analysed data from 25 additional cohorts in 15 European countries (1 133 181 individuals, 43 492 CVD events). After applying the derived risk prediction models to external validation cohorts, C-indices ranged from 0.67 (0.65-0.68) to 0.81 (0.76-0.86). Predicted CVD risk varied several-fold across European regions. For example, the estimated 10-year CVD risk for a 50-year-old smoker, with a systolic blood pressure of 140 mmHg, total cholesterol of 5.5 mmol/L, and HDL-cholesterol of 1.3 mmol/L, ranged from 5.9% for men in low-risk countries to 14.0% for men in very high-risk countries, and from 4.2% for women in low-risk countries to 13.7% for women in very high-risk countries. Conclusion : SCORE2-a new algorithm derived, calibrated, and validated to predict 10-year risk of first-onset CVD in European populations-enhances the identification of individuals at higher risk of developing CVD across Europe.
Published: 2021

2. Discovery of rare variants associated with blood pressure regulation through meta-analysis of 1.3 million individuals

Author: Surendran, P. (Praveen), Feofanova, E. V. (Elena, V), Lahrouchi, N. (Najim), Ntalla, I. (Ioanna), Karthikeyan, S. (Savita), Cook, J. (James), Chen, L. (Lingyan), Mifsud, B. (Borbala), Yao, C. (Chen), Kraja, A. T. (Aldi T.), Cartwright, J. H. (James H.), Hellwege, J. N. (Jacklyn N.), Giri, A. (Ayush), Tragante, V. (Vinicius), Thorleifsson, G. (Gudmar), Liu, D. J. (Dajiang J.), Prins, B. P. (Bram P.), Stewart, I. D. (Isobel D.), Cabrera, C. P. (Claudia P.), Eales, J. M. (James M.), Akbarov, A. (Artur), Auer, P. L. (Paul L.), Bielak, L. F. (Lawrence F.), Bis, J. C. (Joshua C.), Braithwaite, V. S. (Vickie S.), Brody, J. A. (Jennifer A.), Daw, E. W. (E. Warwick), Warren, H. R. (Helen R.), Drenos, F. (Fotios), Nielsen, S. F. (Sune Fallgaard), Faul, J. D. (Jessica D.), Fauman, E. B. (Eric B.), Fava, C. (Cristiano), Ferreira, T. (Teresa), Foley, C. N. (Christopher N.), Franceschini, N. (Nora), Gao, H. (He), Giannakopoulou, O. (Olga), Giulianini, F. (Franco), Gudbjartsson, D. F. (Daniel F.), Guo, X. (Xiuqing), Harris, S. E. (Sarah E.), Havulinna, A. S. (Aki S.), Helgadottir, A. (Anna), Huffman, J. E. (Jennifer E.), Hwang, S.-J. (Shih-Jen), Kanoni, S. (Stavroula), Kontto, J. (Jukka), Larson, M. G. (Martin G.), Li-Gao, R. (Ruifang), Lindstrom, J. (Jaana), Lotta, L. A. (Luca A.), Lu, Y. (Yingchang), Luan, J. (Jian'an), Mahajan, A. (Anubha), Malerba, G. (Giovanni), Masca, N. G. (Nicholas G. D.), Mei, H. (Hao), Menni, C. (Cristina), Mook-Kanamori, D. O. (Dennis O.), Mosen-Ansorena, D. (David), Muller-Nurasyid, M. (Martina), Pare, G. (Guillaume), Paul, D. S. (Dirk S.), Perola, M. (Markus), Poveda, A. (Alaitz), Rauramaa, R. (Rainer), Richard, M. (Melissa), Richardson, T. G. (Tom G.), Sepulveda, N. (Nuno), Sim, X. (Xueling), Smith, A. V. (Albert, V), Smith, J. A. (Jennifer A.), Staley, J. R. (James R.), Stanakova, A. (Alena), Sulem, P. (Patrick), Theriault, S. (Sebastien), Thorsteinsdottir, U. (Unnur), Trompet, S. (Stella), Varga, T. V. (Tibor V.), Edwards, D. R. (Digna R. Velez), Veronesi, G. (Giovanni), Weiss, S. (Stefan), Willems, S. M. (Sara M.), Yao, J. (Jie), Young, R. (Robin), Yu, B. (Bing), Zhang, W. (Weihua), Zhao, J.-H. (Jing-Hua), Zhao, W. (Wei), Evangelou, E. (Evangelos), Aeschbacher, S. (Stefanie), Asllanaj, E. (Eralda), Blankenberg, S. (Stefan), Bonnycastle, L. L. (Lori L.), Bork-Jensen, J. (Jette), Brandslund, I. (Ivan), Braund, P. S. (Peter S.), Burgess, S. (Stephen), Cho, K. (Kelly), Christensen, C. (Cramer), Connell, J. (John), de Mutsert, R. (Renee), Dominiczak, A. F. (Anna F.), Dorr, M. (Marcus), Eiriksdottir, G. (Gudny), Farmaki, A.-E. (Aliki-Eleni), Gaziano, J. M. (J. Michael), Grarup, N. (Niels), Grove, M. L. (Megan L.), Hallmans, G. (Goran), Hansen, T. (Torben), Have, C. T. (Christian T.), Heiss, G. (Gerardo), Jorgensen, M. E. (Marit E.), Jousilahti, P. (Pekka), Kajantie, E. (Eero), Kamat, M. (Mihir), Karajamaki, A. (AnneMari), Karpe, F. (Fredrik), Koistinen, H. A. (Heikki A.), Kovesdy, C. P. (Csaba P.), Kuulasmaa, K. (Kari), Laatikainen, T. (Tiina), Lannfelt, L. (Lars), Lee, I.-T. (I-Te), Lee, W.-J. (Wen-Jane), Linneberg, A. (Allan), Martin, L. W. (Lisa W.), Moitry, M. (Marie), Nadkarni, G. (Girish), Neville, M. J. (Matt J.), Palmer, C. N. (Colin N. A.), Papanicolaou, G. J. (George J.), Pedersen, O. (Oluf), Peters, J. (James), Poulter, N. (Neil), Rasheed, A. (Asif), Rasmussen, K. L. (Katrine L.), Rayner, N. W. (N. William), Magi, R. (Reedik), Renstrom, F. (Frida), Rettig, R. (Rainer), Rossouw, J. (Jacques), Schreiner, P. J. (Pamela J.), Sever, P. S. (Peter S.), Sigurdsson, E. L. (Emil L.), Skaaby, T. (Tea), Sun, Y. V. (Yan, V), Sundstrom, J. (Johan), Thorgeirsson, G. (Gudmundur), Esko, T. (Tonu), Trabetti, E. (Elisabetta), Tsao, P. S. (Philip S.), Tuomi, T. (Tiinamaija), Turner, S. T. (Stephen T.), Tzoulaki, I. (Ioanna), Vaartjes, I. (Ilonca), Vergnaud, A.-C. (Anne-Claire), Willer, C. J. (Cristen J.), Wilson, P. W. (Peter W. F.), Witte, D. R. (Daniel R.), Yonova-Doing, E. (Ekaterina), Zhang, H. (He), Aliya, N. (Naheed), Almgren, P. (Peter), Amouyel, P. (Philippe), Asselbergs, F. W. (Folkert W.), Barnes, M. R. (Michael R.), Blakemore, A. I. (Alexandra, I), Boehnke, M. (Michael), Bots, M. L. (Michiel L.), Bottinger, E. P. (Erwin P.), Buring, J. E. (Julie E.), Chambers, J. C. (John C.), Chen, Y. I. (Yii-Der Ida), Chowdhury, R. (Rajiv), Conen, D. (David), Correa, A. (Adolfo), Smith, G. D. (George Davey), de Boer, R. A. (Rudolf A.), Deary, I. J. (Ian J.), Dedoussis, G. (George), Deloukas, P. (Panos), Di Angelantonio, E. (Emanuele), Elliott, P. (Paul), Felix, S. B. (Stephan B.), Ferrieres, J. (Jean), Ford, I. (Ian), Fornage, M. (Myriam), Franks, P. W. (Paul W.), Franks, S. (Stephen), Frossard, P. (Philippe), Gambaro, G. (Giovanni), Gaunt, T. R. (Tom R.), Groop, L. (Leif), Gudnason, V. (Vilmundur), Harris, T. B. (Tamara B.), Hayward, C. (Caroline), Hennig, B. J. (Branwen J.), Herzig, K.-H. (Karl-Heinz), Ingelsson, E. (Erik), Tuomilehto, J. (Jaakko), Järvelin, M.-R. (Marjo-Riitta), Jukema, J. W. (J. Wouter), Kardia, S. L. (Sharon L. R.), Kee, F. (Frank), Kooner, J. S. (Jaspal S.), Kooperberg, C. (Charles), Launer, L. J. (Lenore J.), Lind, L. (Lars), Loos, R. J. (Ruth J. F.), Majumder, A. A. (Abdulla Al Shafi), Laakso, M. (Markku), McCarthy, M. I. (Mark, I), Melander, O. (Olle), Mohlke, K. L. (Karen L.), Murray, A. D. (Alison D.), Nordestgaard, B. G. (Borge Gronne), Orho-Melander, M. (Marju), Packard, C. J. (Chris J.), Padmanabhan, S. (Sandosh), Palmas, W. (Walter), Polasek, O. (Ozren), Porteous, D. J. (David J.), Prentice, A. M. (Andrew M.), Province, M. A. (Michael A.), Relton, C. L. (Caroline L.), Rice, K. (Kenneth), Ridker, P. M. (Paul M.), Rolandsson, O. (Olov), Rosendaal, F. R. (Frits R.), Rotter, J. I. (Jerome, I), Rudan, I. (Igor), Salomaa, V. (Veikko), Samani, N. J. (Nilesh J.), Sattar, N. (Naveed), Sheu, W. H. (Wayne H-H), Smith, B. H. (Blair H.), Soranzo, N. (Nicole), Spector, T. D. (Timothy D.), Starr, J. M. (John M.), Sebert, S. (Sylvain), Taylor, K. D. (Kent D.), Lakka, T. A. (Timo A.), Timpson, N. J. (Nicholas J.), Tobin, M. D. (Martin D.), van der Harst, P. (Pim), van der Meer, P. (Peter), Ramachandran, V. S. (Vasan S.), Verweij, N. (Niek), Virtamo, J. (Jarmo), Volker, U. (Uwe), Weir, D. R. (David R.), Zeggini, E. (Eleftheria), Charchar, F. J. (Fadi J.), Wareham, N. J. (Nicholas J.), Langenberg, C. (Claudia), Tomaszewski, M. (Maciej), Butterworth, A. S. (Adam S.), Caulfield, M. J. (Mark J.), Danesh, J. (John), Edwards, T. L. (Todd L.), Holm, H. (Hilma), Hung, A. M. (Adriana M.), Lindgren, C. M. (Cecilia M.), Liu, C. (Chunyu), Manning, A. K. (Alisa K.), Morris, A. P. (Andrew P.), Morrison, A. C. (Alanna C.), O'Donnell, C. J. (Christopher J.), Psaty, B. M. (Bruce M.), Saleheen, D. (Danish), Stefansson, K. (Kari), Boerwinkle, E. (Eric), Chasman, D. I. (Daniel, I), Levy, D. (Daniel), Newton-Cheh, C. (Christopher), Munroe, P. B. (Patricia B.), Howson, J. M. (Joanna M. M.), Surendran, P. (Praveen), Feofanova, E. V. (Elena, V), Lahrouchi, N. (Najim), Ntalla, I. (Ioanna), Karthikeyan, S. (Savita), Cook, J. (James), Chen, L. (Lingyan), Mifsud, B. (Borbala), Yao, C. (Chen), Kraja, A. T. (Aldi T.), Cartwright, J. H. (James H.), Hellwege, J. N. (Jacklyn N.), Giri, A. (Ayush), Tragante, V. (Vinicius), Thorleifsson, G. (Gudmar), Liu, D. J. (Dajiang J.), Prins, B. P. (Bram P.), Stewart, I. D. (Isobel D.), Cabrera, C. P. (Claudia P.), Eales, J. M. (James M.), Akbarov, A. (Artur), Auer, P. L. (Paul L.), Bielak, L. F. (Lawrence F.), Bis, J. C. (Joshua C.), Braithwaite, V. S. (Vickie S.), Brody, J. A. (Jennifer A.), Daw, E. W. (E. Warwick), Warren, H. R. (Helen R.), Drenos, F. (Fotios), Nielsen, S. F. (Sune Fallgaard), Faul, J. D. (Jessica D.), Fauman, E. B. (Eric B.), Fava, C. (Cristiano), Ferreira, T. (Teresa), Foley, C. N. (Christopher N.), Franceschini, N. (Nora), Gao, H. (He), Giannakopoulou, O. (Olga), Giulianini, F. (Franco), Gudbjartsson, D. F. (Daniel F.), Guo, X. (Xiuqing), Harris, S. E. (Sarah E.), Havulinna, A. S. (Aki S.), Helgadottir, A. (Anna), Huffman, J. E. (Jennifer E.), Hwang, S.-J. (Shih-Jen), Kanoni, S. (Stavroula), Kontto, J. (Jukka), Larson, M. G. (Martin G.), Li-Gao, R. (Ruifang), Lindstrom, J. (Jaana), Lotta, L. A. (Luca A.), Lu, Y. (Yingchang), Luan, J. (Jian'an), Mahajan, A. (Anubha), Malerba, G. (Giovanni), Masca, N. G. (Nicholas G. D.), Mei, H. (Hao), Menni, C. (Cristina), Mook-Kanamori, D. O. (Dennis O.), Mosen-Ansorena, D. (David), Muller-Nurasyid, M. (Martina), Pare, G. (Guillaume), Paul, D. S. (Dirk S.), Perola, M. (Markus), Poveda, A. (Alaitz), Rauramaa, R. (Rainer), Richard, M. (Melissa), Richardson, T. G. (Tom G.), Sepulveda, N. (Nuno), Sim, X. (Xueling), Smith, A. V. (Albert, V), Smith, J. A. (Jennifer A.), Staley, J. R. (James R.), Stanakova, A. (Alena), Sulem, P. (Patrick), Theriault, S. (Sebastien), Thorsteinsdottir, U. (Unnur), Trompet, S. (Stella), Varga, T. V. (Tibor V.), Edwards, D. R. (Digna R. Velez), Veronesi, G. (Giovanni), Weiss, S. (Stefan), Willems, S. M. (Sara M.), Yao, J. (Jie), Young, R. (Robin), Yu, B. (Bing), Zhang, W. (Weihua), Zhao, J.-H. (Jing-Hua), Zhao, W. (Wei), Evangelou, E. (Evangelos), Aeschbacher, S. (Stefanie), Asllanaj, E. (Eralda), Blankenberg, S. (Stefan), Bonnycastle, L. L. (Lori L.), Bork-Jensen, J. (Jette), Brandslund, I. (Ivan), Braund, P. S. (Peter S.), Burgess, S. (Stephen), Cho, K. (Kelly), Christensen, C. (Cramer), Connell, J. (John), de Mutsert, R. (Renee), Dominiczak, A. F. (Anna F.), Dorr, M. (Marcus), Eiriksdottir, G. (Gudny), Farmaki, A.-E. (Aliki-Eleni), Gaziano, J. M. (J. Michael), Grarup, N. (Niels), Grove, M. L. (Megan L.), Hallmans, G. (Goran), Hansen, T. (Torben), Have, C. T. (Christian T.), Heiss, G. (Gerardo), Jorgensen, M. E. (Marit E.), Jousilahti, P. (Pekka), Kajantie, E. (Eero), Kamat, M. (Mihir), Karajamaki, A. (AnneMari), Karpe, F. (Fredrik), Koistinen, H. A. (Heikki A.), Kovesdy, C. P. (Csaba P.), Kuulasmaa, K. (Kari), Laatikainen, T. (Tiina), Lannfelt, L. (Lars), Lee, I.-T. (I-Te), Lee, W.-J. (Wen-Jane), Linneberg, A. (Allan), Martin, L. W. (Lisa W.), Moitry, M. (Marie), Nadkarni, G. (Girish), Neville, M. J. (Matt J.), Palmer, C. N. (Colin N. A.), Papanicolaou, G. J. (George J.), Pedersen, O. (Oluf), Peters, J. (James), Poulter, N. (Neil), Rasheed, A. (Asif), Rasmussen, K. L. (Katrine L.), Rayner, N. W. (N. William), Magi, R. (Reedik), Renstrom, F. (Frida), Rettig, R. (Rainer), Rossouw, J. (Jacques), Schreiner, P. J. (Pamela J.), Sever, P. S. (Peter S.), Sigurdsson, E. L. (Emil L.), Skaaby, T. (Tea), Sun, Y. V. (Yan, V), Sundstrom, J. (Johan), Thorgeirsson, G. (Gudmundur), Esko, T. (Tonu), Trabetti, E. (Elisabetta), Tsao, P. S. (Philip S.), Tuomi, T. (Tiinamaija), Turner, S. T. (Stephen T.), Tzoulaki, I. (Ioanna), Vaartjes, I. (Ilonca), Vergnaud, A.-C. (Anne-Claire), Willer, C. J. (Cristen J.), Wilson, P. W. (Peter W. F.), Witte, D. R. (Daniel R.), Yonova-Doing, E. (Ekaterina), Zhang, H. (He), Aliya, N. (Naheed), Almgren, P. (Peter), Amouyel, P. (Philippe), Asselbergs, F. W. (Folkert W.), Barnes, M. R. (Michael R.), Blakemore, A. I. (Alexandra, I), Boehnke, M. (Michael), Bots, M. L. (Michiel L.), Bottinger, E. P. (Erwin P.), Buring, J. E. (Julie E.), Chambers, J. C. (John C.), Chen, Y. I. (Yii-Der Ida), Chowdhury, R. (Rajiv), Conen, D. (David), Correa, A. (Adolfo), Smith, G. D. (George Davey), de Boer, R. A. (Rudolf A.), Deary, I. J. (Ian J.), Dedoussis, G. (George), Deloukas, P. (Panos), Di Angelantonio, E. (Emanuele), Elliott, P. (Paul), Felix, S. B. (Stephan B.), Ferrieres, J. (Jean), Ford, I. (Ian), Fornage, M. (Myriam), Franks, P. W. (Paul W.), Franks, S. (Stephen), Frossard, P. (Philippe), Gambaro, G. (Giovanni), Gaunt, T. R. (Tom R.), Groop, L. (Leif), Gudnason, V. (Vilmundur), Harris, T. B. (Tamara B.), Hayward, C. (Caroline), Hennig, B. J. (Branwen J.), Herzig, K.-H. (Karl-Heinz), Ingelsson, E. (Erik), Tuomilehto, J. (Jaakko), Järvelin, M.-R. (Marjo-Riitta), Jukema, J. W. (J. Wouter), Kardia, S. L. (Sharon L. R.), Kee, F. (Frank), Kooner, J. S. (Jaspal S.), Kooperberg, C. (Charles), Launer, L. J. (Lenore J.), Lind, L. (Lars), Loos, R. J. (Ruth J. F.), Majumder, A. A. (Abdulla Al Shafi), Laakso, M. (Markku), McCarthy, M. I. (Mark, I), Melander, O. (Olle), Mohlke, K. L. (Karen L.), Murray, A. D. (Alison D.), Nordestgaard, B. G. (Borge Gronne), Orho-Melander, M. (Marju), Packard, C. J. (Chris J.), Padmanabhan, S. (Sandosh), Palmas, W. (Walter), Polasek, O. (Ozren), Porteous, D. J. (David J.), Prentice, A. M. (Andrew M.), Province, M. A. (Michael A.), Relton, C. L. (Caroline L.), Rice, K. (Kenneth), Ridker, P. M. (Paul M.), Rolandsson, O. (Olov), Rosendaal, F. R. (Frits R.), Rotter, J. I. (Jerome, I), Rudan, I. (Igor), Salomaa, V. (Veikko), Samani, N. J. (Nilesh J.), Sattar, N. (Naveed), Sheu, W. H. (Wayne H-H), Smith, B. H. (Blair H.), Soranzo, N. (Nicole), Spector, T. D. (Timothy D.), Starr, J. M. (John M.), Sebert, S. (Sylvain), Taylor, K. D. (Kent D.), Lakka, T. A. (Timo A.), Timpson, N. J. (Nicholas J.), Tobin, M. D. (Martin D.), van der Harst, P. (Pim), van der Meer, P. (Peter), Ramachandran, V. S. (Vasan S.), Verweij, N. (Niek), Virtamo, J. (Jarmo), Volker, U. (Uwe), Weir, D. R. (David R.), Zeggini, E. (Eleftheria), Charchar, F. J. (Fadi J.), Wareham, N. J. (Nicholas J.), Langenberg, C. (Claudia), Tomaszewski, M. (Maciej), Butterworth, A. S. (Adam S.), Caulfield, M. J. (Mark J.), Danesh, J. (John), Edwards, T. L. (Todd L.), Holm, H. (Hilma), Hung, A. M. (Adriana M.), Lindgren, C. M. (Cecilia M.), Liu, C. (Chunyu), Manning, A. K. (Alisa K.), Morris, A. P. (Andrew P.), Morrison, A. C. (Alanna C.), O'Donnell, C. J. (Christopher J.), Psaty, B. M. (Bruce M.), Saleheen, D. (Danish), Stefansson, K. (Kari), Boerwinkle, E. (Eric), Chasman, D. I. (Daniel, I), Levy, D. (Daniel), Newton-Cheh, C. (Christopher), Munroe, P. B. (Patricia B.), and Howson, J. M. (Joanna M. M.)
Abstract: Genetic studies of blood pressure (BP) to date have mainly analyzed common variants (minor allele frequency > 0.05). In a meta-analysis of up to similar to 1.3 million participants, we discovered 106 new BP-associated genomic regions and 87 rare (minor allele frequency ≤ 0.01) variant BP associations (P < 5 x 10(⁻⁸)), of which 32 were in new BP-associated loci and 55 were independent BP-associated single-nucleotide variants within known BP-associated regions. Average effects of rare variants (44% coding) were similar to 8 times larger than common variant effects and indicate potential candidate causal genes at new and known loci (for example, GATA5 and PLCB3). BP-associated variants (including rare and common) were enriched in regions of active chromatin in fetal tissues, potentially linking fetal development with BP regulation in later life. Multivariable Mendelian randomization suggested possible inverse effects of elevated systolic and diastolic BP on large artery stroke. Our study demonstrates the utility of rare-variant analyses for identifying candidate genes and the results highlight potential therapeutic targets., Correction A Publisher Correction to this article was published on 16 March 2021.
Published: 2020

3. Rare variant in scavenger receptor BI raises HDL cholesterol and increases risk of coronary heart disease

Author: Zanoni, P, Khetarpal, S, Larach, D, Hancock Cerutti, W, Millar, J, Cuchel, M, Derohannessian, S, Kontush, A, Surendran, P, Saleheen, D, Trompet, S, Wouter Jukema, J, De Craen, A, Deloukas, P, Sattar, N, Ford, I, Packard, C, Majumder, A, Alam, D, Di Angelantonio, E, Abecasis, G, Chowdhury, R, Erdmann, J, Nordestgaard, B, Nielsen, S, Tybjærg Hansen, A, Ruth Frikke Schmidt, N, Kuulasmaa, K, Liu, D, Perola, M, Blankenberg, S, Salomaa, V, Männistö, S, Amouyel, P, Arveiler, D, Ferrieres, J, Möller Nurasyid, M, Ferrario, M, Kee, F, Willer, C, Samani, N, Schunkert, H, Butterworth, A, Howson, J, Peloso, G, Stitziel, N, Danesh, J, Kathiresan, S, Rader, D, Brambilla, P, BRAMBILLA, PAOLO, Zanoni, P, Khetarpal, S, Larach, D, Hancock Cerutti, W, Millar, J, Cuchel, M, Derohannessian, S, Kontush, A, Surendran, P, Saleheen, D, Trompet, S, Wouter Jukema, J, De Craen, A, Deloukas, P, Sattar, N, Ford, I, Packard, C, Majumder, A, Alam, D, Di Angelantonio, E, Abecasis, G, Chowdhury, R, Erdmann, J, Nordestgaard, B, Nielsen, S, Tybjærg Hansen, A, Ruth Frikke Schmidt, N, Kuulasmaa, K, Liu, D, Perola, M, Blankenberg, S, Salomaa, V, Männistö, S, Amouyel, P, Arveiler, D, Ferrieres, J, Möller Nurasyid, M, Ferrario, M, Kee, F, Willer, C, Samani, N, Schunkert, H, Butterworth, A, Howson, J, Peloso, G, Stitziel, N, Danesh, J, Kathiresan, S, Rader, D, Brambilla, P, and BRAMBILLA, PAOLO
Abstract: Scavenger receptor BI (SR-BI) is the major receptor for high-density lipoprotein (HDL) cholesterol (HDL-C). In humans, high amounts of HDL-C in plasma are associated with a lower risk of coronary heart disease (CHD). Mice that have depleted Scarb1 (SR-BI knockout mice) have markedly elevated HDL-C levels but, paradoxically, increased atherosclerosis. The impact of SR-BI on HDL metabolism and CHD risk in humans remains unclear. Through targeted sequencing of coding regions of lipid-modifying genes in 328 individuals with extremely high plasma HDL-C levels, we identified a homozygote for a lossof-function variant, in which leucine replaces proline 376 (P376L), in SCARB1, the gene encoding SR-BI. The P376L variant impairs posttranslational processing of SR-BI and abrogates selective HDL cholesterol uptake in transfected cells, in hepatocyte-like cells derived from induced pluripotent stem cells from the homozygous subject, and in mice. Large population-based studies revealed that subjects who are heterozygous carriers of the P376L variant have significantly increased levels of plasma HDL-C. P376L carriers have a profound HDL-related phenotype and an increased risk of CHD (odds ratio = 1.79, which is statistically significant).
Published: 2016

4. Lack of effect of lowering LDL cholesterol on cancer: Meta-analysis of individual data from 175,000 people in 27 randomised trials of statin therapy

Author: Emberson, JR, Kearney, PM, Blackwell, L, Newman, C, Reith, C, Bhala, N, Holland, L, Peto, R, Keech, A, Collins, R, Simes, J, Baigent, C, De Lemos, J, Braunwald, E, Blazing, M, Murphy, S, Downs, JR, Gotto, A, Clearfield, M, Holdaas, H, Gordon, D, Davis, B, Koren, M, Dahlof, B, Poulter, N, Sever, P, Knopp, RH, Fellström, B, Jardine, A, Schmieder, R, Zannad, F, Goldbourt, U, Kaplinsky, E, Colhoun, HM, Betteridge, DJ, Durrington, PN, Hitman, GA, Fuller, J, Neil, A, Wanner, C, Krane, V, Sacks, F, Moyé, L, Pfeffer, M, Hawkins, CM, Kjekshus, J, Wedel, H, Wikstrand, J, Tavazzi, L, Maggioni, A, Marchioli, R, Tognoni, G, Franzosi, MG, Armitage, J, Parish, S, Sleight, P, Pedersen, TR, Ridker, PM, MacMahon, S, Marschner, I, Tonkin, A, Shaw, J, Serruys, PW, Nakamura, H, Knatterud, G, Furberg, C, Byington, R, Macfarlane, P, Cobbe, S, Ford, I, Murphy, M, Blauw, GJ, Packard, C, Shepherd, J, Wilhelmsen, L, Cannon, C, Bowman, L, La Rosa, J, Flather, M, Kastelein, J, Shear, C, Tobert, J, Varigos, J, White, H, Yusuf, S, Baxter, A, Barnes, EH, Buck, G, Herrington, WG, Kirby, A, Lewis, DA, Mellies, M, McGovern, M, Barclay, J, Belder, R, Mitchell, Y, Musliner, T, Ansquer, JC, Llewellyn, M, Bortolini, M, Emberson, JR, Kearney, PM, Blackwell, L, Newman, C, Reith, C, Bhala, N, Holland, L, Peto, R, Keech, A, Collins, R, Simes, J, Baigent, C, De Lemos, J, Braunwald, E, Blazing, M, Murphy, S, Downs, JR, Gotto, A, Clearfield, M, Holdaas, H, Gordon, D, Davis, B, Koren, M, Dahlof, B, Poulter, N, Sever, P, Knopp, RH, Fellström, B, Jardine, A, Schmieder, R, Zannad, F, Goldbourt, U, Kaplinsky, E, Colhoun, HM, Betteridge, DJ, Durrington, PN, Hitman, GA, Fuller, J, Neil, A, Wanner, C, Krane, V, Sacks, F, Moyé, L, Pfeffer, M, Hawkins, CM, Kjekshus, J, Wedel, H, Wikstrand, J, Tavazzi, L, Maggioni, A, Marchioli, R, Tognoni, G, Franzosi, MG, Armitage, J, Parish, S, Sleight, P, Pedersen, TR, Ridker, PM, MacMahon, S, Marschner, I, Tonkin, A, Shaw, J, Serruys, PW, Nakamura, H, Knatterud, G, Furberg, C, Byington, R, Macfarlane, P, Cobbe, S, Ford, I, Murphy, M, Blauw, GJ, Packard, C, Shepherd, J, Wilhelmsen, L, Cannon, C, Bowman, L, La Rosa, J, Flather, M, Kastelein, J, Shear, C, Tobert, J, Varigos, J, White, H, Yusuf, S, Baxter, A, Barnes, EH, Buck, G, Herrington, WG, Kirby, A, Lewis, DA, Mellies, M, McGovern, M, Barclay, J, Belder, R, Mitchell, Y, Musliner, T, Ansquer, JC, Llewellyn, M, and Bortolini, M
Abstract: © 2012 CTT Collaboration. Background: Statin therapy reduces the risk of occlusive vascular events, but uncertainty remains about potential effects on cancer. We sought to provide a detailed assessment of any effects on cancer of lowering LDL cholesterol (LDL-C) with a statin using individual patient records from 175,000 patients in 27 large-scale statin trials. Methods and Findings: Individual records of 134,537 participants in 22 randomised trials of statin versus control (median duration 4.8 years) and 39,612 participants in 5 trials of more intensive versus less intensive statin therapy (median duration 5.1 years) were obtained. Reducing LDL-C with a statin for about 5 years had no effect on newly diagnosed cancer or on death from such cancers in either the trials of statin versus control (cancer incidence: 3755 [1.4% per year [py]] versus 3738 [1.4% py], RR 1.00 [95% CI 0.96-1.05]; cancer mortality: 1365 [0.5% py] versus 1358 [0.5% py], RR 1.00 [95% CI 0.93-1.08]) or in the trials of more versus less statin (cancer incidence: 1466 [1.6% py] vs 1472 [1.6% py], RR 1.00 [95% CI 0.93-1.07]; cancer mortality: 447 [0.5% py] versus 481 [0.5% py], RR 0.93 [95% CI 0.82-1.06]). Moreover, there was no evidence of any effect of reducing LDL-C with statin therapy on cancer incidence or mortality at any of 23 individual categories of sites, with increasing years of treatment, for any individual statin, or in any given subgroup. In particular, among individuals with low baseline LDL-C (<2 mmol/L), there was no evidence that further LDL-C reduction (from about 1.7 to 1.3 mmol/L) increased cancer risk (381 [1.6% py] versus 408 [1.7% py]; RR 0.92 [99% CI 0.76-1.10]). Conclusions: In 27 randomised trials, a median of five years of statin therapy had no effect on the incidence of, or mortality from, any type of cancer (or the aggregate of all cancer).
Published: 2012

5. Lipid-related markers and cardiovascular disease prediction

Author: Angelantonio, E. (Emanuele) di, Gao, P. (Pei), Pennells, L. (Lisa), Kaptoge, S. (Stephen), Caslake, M. (Muriel), Thompson, A. (Alexander), Butterworth, A.S. (Adam), Sarwar, S. (Sheryar), Wormser, D. (David), Saleheen, D., Ballantyne, C. (Christie), Psaty, B.M. (Bruce), Sundstrom, J. (Johan), Ridker, P.M. (Paul), Nagel, D. (Dorothea), Gillum, R.F. (Richard), Ford, I. (Ian), Ducimetiere, P. (Pierre), Kiechl, S. (Stefan), Koenig, W. (Wolfgang), Dullaart, R.P.F. (Robin), Assmann, G. (Gerd), D'Agostino, R.B. (Ralph), Dagenais, G.R. (Gilles R), Cooper, J.A. (Jackie), Kromhout, D. (Daan), Onat, A. (Altan), Tipping, A. (Alex), Gómez-de-la-Cámara, A. (Agustín), Rosengren, A. (Annika), Sutherland, S.E. (Susan), Gallacher, J. (John), Fowkes, F.G.R. (F. Gerald R.), Casiglia, E. (Edoardo), Hofman, A. (Albert), Salomaa, V. (Veikko), Barrett-Connor, E. (Elizabeth), Clarke, R. (Robert), Brunner, E. (Eric), Jukema, J.W. (Jan Wouter), Simons, L.A. (Leon), Sandhu, M.S. (Manjinder), Wareham, N.J. (Nick), Khaw, K-T. (Kay-Tee), Kauhanen, J. (Jussi), Salonen, J.T., Howard, W.J. (William), Nordestgaard, B.G. (Børge), Wood, A.M. (Angela), Thompson, S.G. (Simon), Boekholdt, S.M. (Matthijs), Sattar, N. (Naveed), Packard, C. (Chris), Gudnason, V. (Vilmundur), Danesh, J. (John), Angelantonio, E. (Emanuele) di, Gao, P. (Pei), Pennells, L. (Lisa), Kaptoge, S. (Stephen), Caslake, M. (Muriel), Thompson, A. (Alexander), Butterworth, A.S. (Adam), Sarwar, S. (Sheryar), Wormser, D. (David), Saleheen, D., Ballantyne, C. (Christie), Psaty, B.M. (Bruce), Sundstrom, J. (Johan), Ridker, P.M. (Paul), Nagel, D. (Dorothea), Gillum, R.F. (Richard), Ford, I. (Ian), Ducimetiere, P. (Pierre), Kiechl, S. (Stefan), Koenig, W. (Wolfgang), Dullaart, R.P.F. (Robin), Assmann, G. (Gerd), D'Agostino, R.B. (Ralph), Dagenais, G.R. (Gilles R), Cooper, J.A. (Jackie), Kromhout, D. (Daan), Onat, A. (Altan), Tipping, A. (Alex), Gómez-de-la-Cámara, A. (Agustín), Rosengren, A. (Annika), Sutherland, S.E. (Susan), Gallacher, J. (John), Fowkes, F.G.R. (F. Gerald R.), Casiglia, E. (Edoardo), Hofman, A. (Albert), Salomaa, V. (Veikko), Barrett-Connor, E. (Elizabeth), Clarke, R. (Robert), Brunner, E. (Eric), Jukema, J.W. (Jan Wouter), Simons, L.A. (Leon), Sandhu, M.S. (Manjinder), Wareham, N.J. (Nick), Khaw, K-T. (Kay-Tee), Kauhanen, J. (Jussi), Salonen, J.T., Howard, W.J. (William), Nordestgaard, B.G. (Børge), Wood, A.M. (Angela), Thompson, S.G. (Simon), Boekholdt, S.M. (Matthijs), Sattar, N. (Naveed), Packard, C. (Chris), Gudnason, V. (Vilmundur), and Danesh, J. (John)
Abstract: Context: The value of assessing various emerging lipid-related markers for prediction of first cardiovascular events is debated. Objective: To determine whether adding information on apolipoprotein B and apolipoprotein A-I, lipoprotein(a), or lipoprotein-associated phospholipase A2 to total cholesterol and high-density lipoprotein cholesterol (HDL-C) improves cardiovascular disease (CVD) risk prediction. Design, Setting, and Participants: Individual records were available for 165 544 participants without baseline CVD in 37 prospective cohorts (calendar years of recruitment: 1968-2007) with up to 15 126 incident fatal or nonfatal CVD outcomes (1
Published: 2012
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6. C-reactive protein, fibrinogen, and cardiovascular disease prediction

Author: Kaptoge, S. (Stephen), Angelantonio, E. (Emanuele) di, Pennells, L. (Lisa), Wood, A.M. (Angela), White, I.R. (Ian), Gao, P. (Pei), Walker, M. (Mark), Thompson, A. (Alexander), Sarwar, S. (Sheryar), Caslake, M. (Muriel), Butterworth, A.S. (Adam), Amouyel, P. (Philippe), Assmann, G. (Gerd), Bakker, S.J.L. (Stephan), Barr, E.L.M., Barrett-Connor, E. (Elizabeth), Benjamin, E.J. (Emelia), Björkelund, C. (Cecilia), Brenner, H. (Hermann), Brunner, E. (Eric), Clarke, R. (Robert), Cooper, J.A. (Jackie), Cremer, P., Cushman, M. (Mary Ann), Dagenais, G.R. (Gilles R), D'Agostino, R.B. (Ralph), Dankner, R. (Rachel), Davey-Smith, G. (George), Deeg, D.J.H. (Dorly), Dekker, J.M. (Jacqueline), Engström, G., Folsom, A.R. (Aaron), Fowkes, F.G.R. (F. Gerald R.), Gallacher, J. (John), Gaziano, J.M. (J. Michael), Giampaoli, S. (Simona), Gillum, R.F. (Richard), Hofman, A. (Albert), Howard, B.V. (Barbara), Ingelsson, E. (Erik), Iso, H. (Hiroyasu), Jorgensen, T. (Torben), Kiechl, S. (Stefan), Kitamura, A., Kiyohara, Y. (Yutaka), Koenig, W. (Wolfgang), Kromhout, D. (Daan), Kuller, L.H. (Lewis), Lawlor, D.A. (Debbie), Meade, T. (Tom), Nissinen, A. (Aulikki), Nordestgaard, B.G. (Børge), Onat, A. (Altan), Panagiotakos, D.B. (Demosthenes), Psaty, B.M. (Bruce), Rodriguez, B. (Beatriz), Rosengren, A. (Annika), Salomaa, V. (Veikko), Kauhanen, J. (Jussi), Salonen, J.T., Shaffer, J.A. (Jonathan), Shea, S. (Steven), Ford, I. (Ian), Stehouwer, C.D. (Coen), Strandberg, T.E. (Timo), Tipping, A. (Alex), Tosetto, A. (Alberto), Wassertheil-Smoller, S. (Sylvia), Wennberg, P. (Patrik), Westendorp, R.G.J. (Rudi), Whincup, P.H. (Peter), Wilhelmsen, L. (Lars), Woodward, M. (Mark), Lowe, G.D.O. (Gordon), Wareham, N.J. (Nick), Khaw, K-T. (Kay-Tee), Sattar, N. (Naveed), Packard, C. (Chris), Gudnason, V. (Vilmundur), Ridker, P.M. (Paul), Pepys, M.B. (Mark), Thompson, S.G. (Simon), Danesh, J. (John), Kaptoge, S. (Stephen), Angelantonio, E. (Emanuele) di, Pennells, L. (Lisa), Wood, A.M. (Angela), White, I.R. (Ian), Gao, P. (Pei), Walker, M. (Mark), Thompson, A. (Alexander), Sarwar, S. (Sheryar), Caslake, M. (Muriel), Butterworth, A.S. (Adam), Amouyel, P. (Philippe), Assmann, G. (Gerd), Bakker, S.J.L. (Stephan), Barr, E.L.M., Barrett-Connor, E. (Elizabeth), Benjamin, E.J. (Emelia), Björkelund, C. (Cecilia), Brenner, H. (Hermann), Brunner, E. (Eric), Clarke, R. (Robert), Cooper, J.A. (Jackie), Cremer, P., Cushman, M. (Mary Ann), Dagenais, G.R. (Gilles R), D'Agostino, R.B. (Ralph), Dankner, R. (Rachel), Davey-Smith, G. (George), Deeg, D.J.H. (Dorly), Dekker, J.M. (Jacqueline), Engström, G., Folsom, A.R. (Aaron), Fowkes, F.G.R. (F. Gerald R.), Gallacher, J. (John), Gaziano, J.M. (J. Michael), Giampaoli, S. (Simona), Gillum, R.F. (Richard), Hofman, A. (Albert), Howard, B.V. (Barbara), Ingelsson, E. (Erik), Iso, H. (Hiroyasu), Jorgensen, T. (Torben), Kiechl, S. (Stefan), Kitamura, A., Kiyohara, Y. (Yutaka), Koenig, W. (Wolfgang), Kromhout, D. (Daan), Kuller, L.H. (Lewis), Lawlor, D.A. (Debbie), Meade, T. (Tom), Nissinen, A. (Aulikki), Nordestgaard, B.G. (Børge), Onat, A. (Altan), Panagiotakos, D.B. (Demosthenes), Psaty, B.M. (Bruce), Rodriguez, B. (Beatriz), Rosengren, A. (Annika), Salomaa, V. (Veikko), Kauhanen, J. (Jussi), Salonen, J.T., Shaffer, J.A. (Jonathan), Shea, S. (Steven), Ford, I. (Ian), Stehouwer, C.D. (Coen), Strandberg, T.E. (Timo), Tipping, A. (Alex), Tosetto, A. (Alberto), Wassertheil-Smoller, S. (Sylvia), Wennberg, P. (Patrik), Westendorp, R.G.J. (Rudi), Whincup, P.H. (Peter), Wilhelmsen, L. (Lars), Woodward, M. (Mark), Lowe, G.D.O. (Gordon), Wareham, N.J. (Nick), Khaw, K-T. (Kay-Tee), Sattar, N. (Naveed), Packard, C. (Chris), Gudnason, V. (Vilmundur), Ridker, P.M. (Paul), Pepys, M.B. (Mark), Thompson, S.G. (Simon), and Danesh, J. (John)
Abstract: BACKGROUND: There is debate about the value of assessing levels of C-reactive protein (CRP) and other biomarkers of inflammation for the prediction of first cardiovascular events. METHODS: We analyzed data from 52 prospective studies that included 246,669 participants without a history of cardiovascular disease to investigate the value of adding CRP or fibrinogen levels to conventional risk factors for the prediction of cardiovascular risk. We calculated measures of discrimination and reclassification during follow-up and modeled the clinical implications of initiation of statin therapy after the assessment of CRP or fibrinogen. RESULTS: The addition of information on high-density lipoprotein cholesterol to a prognostic model for cardiovascular disease that included age, sex, smoking status, blood pressure, history of diabetes, and total cholesterol level increased the C-index, a measure of risk discrimination, by 0.0050. The further addition to this model of information on CRP or fibrinogen increased the C-index by 0.0039 and 0.0027, respectively (P<0.001), and yielded a net reclassification improvement of 1.52% and 0.83%, respectively, for the predicted 10-year risk categories of "low" (<10%), "intermediate" (10% to <20%), and "high" (≥20%) (P<0.02 for both comparisons). We estimated that among 100,000 adults 40 years of age or older, 15,025 persons would initially be classified as being at intermediate risk for a cardiovascular event if conventional risk factors alone were used to calculate risk. Assuming that statin therapy would be initiated in accordance with Adult Treatment Panel III guidelines (i.e., for persons with a predicted risk of ≥20% and for those with certain other risk factors, such as diabetes, irrespective of their 10-year predicted risk), additional targeted assessment of CRP or fibrinogen levels in the 13,199 remaining participants at intermediate risk could help prevent approximately 30 additional cardiovascular events over the course of 10 ye
Published: 2012
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7. An Evaluation of the Arctic - Will it Become an Area of Cooperation or Conflict?

Author: NAVAL POSTGRADUATE SCHOOL MONTEREY CA, Trent, Packard C., NAVAL POSTGRADUATE SCHOOL MONTEREY CA, and Trent, Packard C.
Abstract: Climate change and the vast amount of natural resources in the Arctic region have prompted awareness of the need for new policies among Arctic states, including the U.S., and stimulated throughout the entire international community a critical assessment of the issues regarding the Arctic region. All of this could result in potential conflict in this critical region of the world. The Arctic's ice cover as of spring 2010 was the lowest it has ever been at that time of year, and it is melting faster than once thought, making it possible for the Arctic to have an ice free summer by 2013. Due to the increase of yearly ice melt, the race to extract the natural resources will speed up tremendously in future years. Research shows that the Arctic nations strongly encourage cooperation and are currently abiding by the international laws, treaties, and infrastructures in place that allow them the most potential to benefit from the Arctic resources. However, although the Arctic nations stress cooperation in their official statements and diplomatic overtures, they are actually preparing for conflict. There are many potential flashpoints that could cause the Arctic to end in conflict, such as territorial disputes, Russia's dependency on the Arctic, and the militarization of the Arctic. The Arctic region has long been neglected by the U.S; however, due to the current situation in the Arctic and the potential for new threats to the U.S. homeland, the region is becoming a far more important issue and is gaining the attention of the U.S. government. The major question this thesis will examine concerns the future of the Arctic: is it heading for conflict, or for cooperation? In addition, the state of U.S. security with respect to the Arctic will be evaluated, and recommendations for U.S. national and homeland security policy will be provided., The original document contains color images.
Published: 2011

8. Association between C reactive protein and coronary heart disease : mendelian randomisation analysis based on individual participant data

Author: Wensley, Frances, Gao, Pei, Burgess, Stephen, Kaptoge, Stephen, Di Angelantonio, Emanuele, Shah, Tina, Engert, James C., Clarke, Robert, Davey-Smith, George, Nordestgaard, Borge G., Saleheen, Danish, Samani, Nilesh J., Sandhu, Manjinder, Anand, Sonia, Pepys, Mark B., Smeeth, Liam, Whittaker, John, Casas, Juan Pablo, Thompson, Simon G., Hingorani, Aroon D., Danesh, John, Eiriksdottir, G., Harris, T. B., Launer, L. J., Gudnason, V., Folsom, A. R., Andrews, G., Ballantyne, C. M., Samani, N. J., Hall, A. S., Braund, P. S., Balmforth, A. J., Whincup, P. H., Morris, R., Lawlor, D. A., Lowe, G. D. O., Timpson, N., Ebrahim, S., Ben-Shlomo, Y., Davey-Smith, G., Nordestgaard, B. G., Tybjaerg-Hansen, A., Zacho, J., Brown, M., Sandhu, M., Ricketts, S. L., Ashford, S., Lange, L., Reiner, A., Cushman, M., Tracy, R., Wu, C., Ge, J., Zou, Y., Sun, A., Hung, J., McQuillan, B., Thompson, P., Beilby, J., Warrington, N., Palmer, L. J., Wanner, C., Drechsler, C., Hoffmann, M. M., Fowkes, F. G. R., Tzoulaki, I., Kumari, M., Miller, M., Marmot, M., Onland-Moret, C., van der Schouw, Y. T., Boer, J. M., Wijmenga, C., Khaw, K-T, Vasan, R. S., Schnabel, R. B., Yamamoto, J. F., Benjamin, E. J., Schunkert, H., Erdmann, J., Koenig, I. R., Hengstenberg, C., Chiodini, B., Franzosi, M. G., Pietri, S., Gori, F., Rudock, M., Liu, Y., Lohman, K., Humphries, S. E., Hamsten, A., Norman, P. E., Hankey, G. J., Jamrozik, K., Rimm, E. B., Pai, J. K., Psaty, B. M., Heckbert, S. R., Bis, J. C., Yusuf, S., Anand, S., Engert, J. C., Xie, C., Collins, R., Clarke, R., Bennett, D., Kooner, J., Chambers, J., Elliott, P., Maerz, W., Kleber, M. E., Boehm, B. O., Winkelmann, B. R., Melander, O., Berglund, G., Koenig, W., Thorand, B., Baumert, J., Peters, A., Manson, J., Cooper, J. A., Talmud, P. J., Ladenvall, P., Johansson, L., Jansson, Jan-Håkan, Hallmans, Göran, Reilly, M. P., Qu, L., Li, M., Rader, D. J., Watkins, H., Hopewell, J., Saleheen, D., Danesh, J., Frossard, P., Sattar, N., Robertson, M., Shepherd, J., Schaefer, E., Hofman, A., Witteman, J. C. M., Kardys, I., Dehghan, A., de Faire, U., Bennet, A., Gigante, B., Leander, K., Peters, B., Maitland-van der Zee, A. H., de Boer, A., Klungel, O., Greenland, P., Dai, J., Liu, S., Brunner, E., Kivimaki, M., O'Reilly, D., Ford, I., Packard, C. J., Wensley, Frances, Gao, Pei, Burgess, Stephen, Kaptoge, Stephen, Di Angelantonio, Emanuele, Shah, Tina, Engert, James C., Clarke, Robert, Davey-Smith, George, Nordestgaard, Borge G., Saleheen, Danish, Samani, Nilesh J., Sandhu, Manjinder, Anand, Sonia, Pepys, Mark B., Smeeth, Liam, Whittaker, John, Casas, Juan Pablo, Thompson, Simon G., Hingorani, Aroon D., Danesh, John, Eiriksdottir, G., Harris, T. B., Launer, L. J., Gudnason, V., Folsom, A. R., Andrews, G., Ballantyne, C. M., Samani, N. J., Hall, A. S., Braund, P. S., Balmforth, A. J., Whincup, P. H., Morris, R., Lawlor, D. A., Lowe, G. D. O., Timpson, N., Ebrahim, S., Ben-Shlomo, Y., Davey-Smith, G., Nordestgaard, B. G., Tybjaerg-Hansen, A., Zacho, J., Brown, M., Sandhu, M., Ricketts, S. L., Ashford, S., Lange, L., Reiner, A., Cushman, M., Tracy, R., Wu, C., Ge, J., Zou, Y., Sun, A., Hung, J., McQuillan, B., Thompson, P., Beilby, J., Warrington, N., Palmer, L. J., Wanner, C., Drechsler, C., Hoffmann, M. M., Fowkes, F. G. R., Tzoulaki, I., Kumari, M., Miller, M., Marmot, M., Onland-Moret, C., van der Schouw, Y. T., Boer, J. M., Wijmenga, C., Khaw, K-T, Vasan, R. S., Schnabel, R. B., Yamamoto, J. F., Benjamin, E. J., Schunkert, H., Erdmann, J., Koenig, I. R., Hengstenberg, C., Chiodini, B., Franzosi, M. G., Pietri, S., Gori, F., Rudock, M., Liu, Y., Lohman, K., Humphries, S. E., Hamsten, A., Norman, P. E., Hankey, G. J., Jamrozik, K., Rimm, E. B., Pai, J. K., Psaty, B. M., Heckbert, S. R., Bis, J. C., Yusuf, S., Anand, S., Engert, J. C., Xie, C., Collins, R., Clarke, R., Bennett, D., Kooner, J., Chambers, J., Elliott, P., Maerz, W., Kleber, M. E., Boehm, B. O., Winkelmann, B. R., Melander, O., Berglund, G., Koenig, W., Thorand, B., Baumert, J., Peters, A., Manson, J., Cooper, J. A., Talmud, P. J., Ladenvall, P., Johansson, L., Jansson, Jan-Håkan, Hallmans, Göran, Reilly, M. P., Qu, L., Li, M., Rader, D. J., Watkins, H., Hopewell, J., Saleheen, D., Danesh, J., Frossard, P., Sattar, N., Robertson, M., Shepherd, J., Schaefer, E., Hofman, A., Witteman, J. C. M., Kardys, I., Dehghan, A., de Faire, U., Bennet, A., Gigante, B., Leander, K., Peters, B., Maitland-van der Zee, A. H., de Boer, A., Klungel, O., Greenland, P., Dai, J., Liu, S., Brunner, E., Kivimaki, M., O'Reilly, D., Ford, I., and Packard, C. J.
Abstract: Objective To use genetic variants as unconfounded proxies of C reactive protein concentration to study its causal role in coronary heart disease. Design Mendelian randomisation meta-analysis of individual participant data from 47 epidemiological studies in 15 countries. Participants 194 418 participants, including 46 557 patients with prevalent or incident coronary heart disease. Information was available on four CRP gene tagging single nucleotide polymorphisms (rs3093077, rs1205, rs1130864, rs1800947), concentration of C reactive protein, and levels of other risk factors. Main outcome measures Risk ratios for coronary heart disease associated with genetically raised C reactive protein versus risk ratios with equivalent differences in C reactive protein concentration itself, adjusted for conventional risk factors and variability in risk factor levels within individuals. Results CRP variants were each associated with up to 30% per allele difference in concentration of C reactive protein (P<10(-34)) and were unrelated to other risk factors. Risk ratios for coronary heart disease per additional copy of an allele associated with raised C reactive protein were 0.93 (95% confidence interval 0.87 to 1.00) for rs3093077; 1.00 (0.98 to 1.02) for rs1205; 0.98 (0.96 to 1.00) for rs1130864; and 0.99 (0.94 to 1.03) for rs1800947. In a combined analysis, the risk ratio for coronary heart disease was 1.00 (0.90 to 1.13) per 1 SD higher genetically raised natural log (ln) concentration of C reactive protein. The genetic findings were discordant with the risk ratio observed for coronary heart disease of 1.33 (1.23 to 1.43) per 1 SD higher circulating ln concentration of C reactive protein in prospective studies (P=0.001 for difference). Conclusion Human genetic data indicate that C reactive protein concentration itself is unlikely to be even a modest causal factor in coronary heart disease.
Published: 2011
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9. An evaluation of the Arctic--will it become an area of cooperation or conflict?

Author: Dahl, Erik J., Boulton, John W., National Security Affairs, Trent, Packard C., Dahl, Erik J., Boulton, John W., National Security Affairs, and Trent, Packard C.
Abstract: Climate change and the vast amount of natural resources in the Arctic region have prompted awareness of the need for new policies among Arctic states, including the U.S., and stimulated throughout the entire international community a critical assessment of the issues regarding the Arctic region. All of this could result in potential conflict in this critical region of the world. The Arctic's ice cover as of spring 2010 was the lowest it has ever been at that time of year, and it is melting faster than once thought, making it possible for the Arctic to have an ice free summer by 2013. Due to the increase of yearly ice melt, the race to extract the natural resources will speed up tremendously in future years. Research shows that the Arctic nations strongly encourage cooperation and are currently abiding by the international laws, treaties, and infrastructures in place that allow them the most potential to benefit from the Arctic resources. However, although the Arctic nations stress cooperation in their official statements and diplomatic overtures, they are actually preparing for conflict. There are many potential flashpoints that could cause the Arctic to end in conflict, such as territorial disputes, Russia's dependency on the Arctic, and the militarization of the Arctic. The Arctic region has long been neglected by the U.S; however, due to the current situation in the Arctic and the potential for new threats to the U.S. homeland, the region is becoming a far more important issue and is gaining the attention of the U.S. government. The major question this thesis will examine concerns the future of the Arctic: is it heading for conflict, or for cooperation? In addition, the state of U.S. security with respect to the Arctic will be evaluated, and recommendations for U.S. national and homeland security policy will be provided.
Published: 2011

10. Obesity is associated with fatal coronary heart disease independently of traditional risk factors and deprivation

Author: Logue, J, Murray, HM, Welsh, P, Shepherd, J, Packard, C, Macfarlane, P, Cobbe, S, Ford, I, Sattar, N, Logue, J, Murray, HM, Welsh, P, Shepherd, J, Packard, C, Macfarlane, P, Cobbe, S, Ford, I, and Sattar, N
Abstract: Background The effect of body mass index (BMI) on coronary heart disease (CHD) risk is attenuated when mediators of this risk (such as diabetes, hypertension and hyperlipidaemia) are accounted for. However, there is now evidence of a differential effect of risk factors on fatal and non-fatal CHD events, with markers of inflammation more strongly associated with fatal than non-fatal events. Objective To describe the association with BMI separately for both fatal and non-fatal CHD risk after accounting for classical risk factors and to assess any independent effects of obesity on CHD risk. Methods and results In the West of Scotland Coronary Prevention Study BMI in 6082 men (mean age 55 years) with hypercholesterolaemia, but no history of diabetes or CVD, was related to the risk of fatal and non-fatal CHD events. After excluding participants with any event in the first 2 years, 1027 non-fatal and 214 fatal CHD events occurred during 14.7 years of follow-up. A minimally adjusted model (age, sex, statin treatment) and a maximally adjusted model (including known CVD risk factors and deprivation) were compared, with BMI 25–27.4 kg/m2 as referent. The risk of non-fatal events was similar across all BMI categories in both models. The risk of fatal CHD events was increased in men with BMI 30.0–39.9 kg/m2 in both the minimally adjusted model (HR=1.75 (95% CI 1.12 to 2.74)) and the maximally adjusted model (HR=1.60 (95% CI 1.02 to 2.53)). Conclusions These hypothesis generating data suggest that obesity is associated with fatal, but not non-fatal, CHD after accounting for known cardiovascular risk factors and deprivation.
Published: 2011

11. Obesity is associated with fatal coronary heart disease independently of traditional risk factors and deprivation

Author: Logue, J, Murray, HM, Welsh, P, Shepherd, J, Packard, C, Macfarlane, P, Cobbe, S, Ford, I, Sattar, N, Logue, J, Murray, HM, Welsh, P, Shepherd, J, Packard, C, Macfarlane, P, Cobbe, S, Ford, I, and Sattar, N
Abstract: Background The effect of body mass index (BMI) on coronary heart disease (CHD) risk is attenuated when mediators of this risk (such as diabetes, hypertension and hyperlipidaemia) are accounted for. However, there is now evidence of a differential effect of risk factors on fatal and non-fatal CHD events, with markers of inflammation more strongly associated with fatal than non-fatal events. Objective To describe the association with BMI separately for both fatal and non-fatal CHD risk after accounting for classical risk factors and to assess any independent effects of obesity on CHD risk. Methods and results In the West of Scotland Coronary Prevention Study BMI in 6082 men (mean age 55 years) with hypercholesterolaemia, but no history of diabetes or CVD, was related to the risk of fatal and non-fatal CHD events. After excluding participants with any event in the first 2 years, 1027 non-fatal and 214 fatal CHD events occurred during 14.7 years of follow-up. A minimally adjusted model (age, sex, statin treatment) and a maximally adjusted model (including known CVD risk factors and deprivation) were compared, with BMI 25–27.4 kg/m2 as referent. The risk of non-fatal events was similar across all BMI categories in both models. The risk of fatal CHD events was increased in men with BMI 30.0–39.9 kg/m2 in both the minimally adjusted model (HR=1.75 (95% CI 1.12 to 2.74)) and the maximally adjusted model (HR=1.60 (95% CI 1.02 to 2.53)). Conclusions These hypothesis generating data suggest that obesity is associated with fatal, but not non-fatal, CHD after accounting for known cardiovascular risk factors and deprivation.
Published: 2011

12. Bayesian methods for meta-analysis of causal relationships estimated using genetic instrumental variables

Author: Burgess, Stephen, Thompson, Simon G, Andrews, G, Samani, N J, Hall, A, Whincup, P, Morris, R, Lawlor, D A, Davey Smith, G, Timpson, N, Ebrahim, S, Ben-Shlomo, Y, Brown, M, Ricketts, S, Sandhu, M, Reiner, A, Psaty, B, Lange, L, Cushman, M, Hung, J, Thompson, P, Beilby, J, Warrington, N, Palmer, L J, Nordestgaard, B G, Tybjaerg-Hansen, A, Zacho, J, Wu, C, Lowe, G, Tzoulaki, I, Kumari, M, Yamamoto, J F, Chiodini, B, Franzosi, M, Hankey, G J, Jamrozik, K, Palmer, L, Rimm, E, Pai, J, Heckbert, S, Bis, J, Anand, S, Engert, J, Collins, R, Clarke, R, Melander, O, Berglund, G, Ladenvall, P, Johansson, L, Jansson, Jan-Håkan, Hallmans, Göran, Hingorani, A, Humphries, S, Manson, J, Watkins, H, Hopewell, J, Saleheen, D, Frossard, R, Danesh, J, Sattar, N, Robertson, M, Shepherd, J, Schaefer, E, Hofman, A, Witteman, J C M, Kardys, I, de Faire, U, Bennet, A, Ford, I, Packard, C, Lawlor, Debbie A, Davey Smith, George, Casas, J P, Smeeth, L, Wensley, F, Bowden, J, Burgess, S, Di Angelantonio, E, Gao, P, Shah, T, Thompson, S G, Verzilli, C, Walker, M, Whittaker, J, Burgess, Stephen, Thompson, Simon G, Andrews, G, Samani, N J, Hall, A, Whincup, P, Morris, R, Lawlor, D A, Davey Smith, G, Timpson, N, Ebrahim, S, Ben-Shlomo, Y, Brown, M, Ricketts, S, Sandhu, M, Reiner, A, Psaty, B, Lange, L, Cushman, M, Hung, J, Thompson, P, Beilby, J, Warrington, N, Palmer, L J, Nordestgaard, B G, Tybjaerg-Hansen, A, Zacho, J, Wu, C, Lowe, G, Tzoulaki, I, Kumari, M, Yamamoto, J F, Chiodini, B, Franzosi, M, Hankey, G J, Jamrozik, K, Palmer, L, Rimm, E, Pai, J, Heckbert, S, Bis, J, Anand, S, Engert, J, Collins, R, Clarke, R, Melander, O, Berglund, G, Ladenvall, P, Johansson, L, Jansson, Jan-Håkan, Hallmans, Göran, Hingorani, A, Humphries, S, Manson, J, Watkins, H, Hopewell, J, Saleheen, D, Frossard, R, Danesh, J, Sattar, N, Robertson, M, Shepherd, J, Schaefer, E, Hofman, A, Witteman, J C M, Kardys, I, de Faire, U, Bennet, A, Ford, I, Packard, C, Lawlor, Debbie A, Davey Smith, George, Casas, J P, Smeeth, L, Wensley, F, Bowden, J, Burgess, S, Di Angelantonio, E, Gao, P, Shah, T, Thompson, S G, Verzilli, C, Walker, M, and Whittaker, J
Abstract: Genetic markers can be used as instrumental variables, in an analogous way to randomization in a clinical trial, to estimate the causal relationship between a phenotype and an outcome variable. Our purpose is to extend the existing methods for such Mendelian randomization studies to the context of multiple genetic markers measured in multiple studies, based on the analysis of individual participant data. First, for a single genetic marker in one study, we show that the usual ratio of coefficients approach can be reformulated as a regression with heterogeneous error in the explanatory variable. This can be implemented using a Bayesian approach, which is next extended to include multiple genetic markers. We then propose a hierarchical model for undertaking a meta-analysis of multiple studies, in which it is not necessary that the same genetic markers are measured in each study. This provides an overall estimate of the causal relationship between the phenotype and the outcome, and an assessment of its heterogeneity across studies. As an example, we estimate the causal relationship of blood concentrations of C-reactive protein on fibrinogen levels using data from 11 studies. These methods provide a flexible framework for efficient estimation of causal relationships derived from multiple studies. Issues discussed include weak instrument bias, analysis of binary outcome data such as disease risk, missing genetic data, and the use of haplotypes.
Published: 2010
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13. Separating the mechanism-based and off-target actions of cholesteryl ester transfer protein inhibitors with CETP gene polymorphisms

Author: Sofat, R. (Reecha), Hingorani, A. (Aroon), Smeeth, L. (Liam), Humphries, S.E. (Steve), Talmud, P.J., Cooper, J. (Jim), Shah, T. (Tina), Sandhu, M.S. (Manjinder), Ricketts, S.L. (Sally), Boekholdt, S.M. (Matthijs), Wareham, N.J. (Nick), Khaw, K-T. (Kay-Tee), Kumari, M. (Meena), Kivimaki, M. (Mika), Marmot, M. (Michael), Asselbergs, F.W. (Folkert), Harst, P. (Pim) van der, Dullaart, R.P.F. (Robin), Navis, G. (Gerjan), Veldhuisen, D.J. (Dirk) van, Gilst, W.H. (Wiek) van, Thompson, J.F. (John), McCaskie, P. (Pamela), Palmer, C. (Cameron), Arca, M. (Marcello), Quagliarini, F. (Fabiana), Gaudio, C. (Carlo), Cambien, F. (François), Nicaud, V., Poirer, O. (Odette), Gudnason, V. (Vilmundur), Isaacs, A.J. (Aaron), Witteman, J.C.M. (Jacqueline), Tikka-Kleemola, P. (Päivi), Pencina, M. (Michael), Vasan, R.S. (Ramachandran Srini), D'Agostino, R.B. (Ralph), Ordovas, J.M. (Jose), Li, T.Y. (Tricia), Kakko, S. (Sakari), Kauma, H. (Heikki), Savolainen, M.J. (Markku), Kesäniemi, Y.A. (Antero), Sandhofer, A. (Anton), Paulweber, B. (Bernhard), Sorli, J.V. (Jose), Goto, A. (Akimoto), Yokoyama, S. (Shinji), Okumura, K. (Kenji), Horne, B.D. (Benjamin), Packard, C. (Chris), Freeman, D. (Dilys), Ford, I. (Ian), Sattar, N. (Naveed), McCormack, V. (Valerie), Lawlor, D.A. (Debbie), Ebrahim, S. (Shanil), Smith, A.V. (Davey), Kastelein, J.J.P. (John), Deanfield, J. (John), Casas, J.P. (Juan), Sofat, R. (Reecha), Hingorani, A. (Aroon), Smeeth, L. (Liam), Humphries, S.E. (Steve), Talmud, P.J., Cooper, J. (Jim), Shah, T. (Tina), Sandhu, M.S. (Manjinder), Ricketts, S.L. (Sally), Boekholdt, S.M. (Matthijs), Wareham, N.J. (Nick), Khaw, K-T. (Kay-Tee), Kumari, M. (Meena), Kivimaki, M. (Mika), Marmot, M. (Michael), Asselbergs, F.W. (Folkert), Harst, P. (Pim) van der, Dullaart, R.P.F. (Robin), Navis, G. (Gerjan), Veldhuisen, D.J. (Dirk) van, Gilst, W.H. (Wiek) van, Thompson, J.F. (John), McCaskie, P. (Pamela), Palmer, C. (Cameron), Arca, M. (Marcello), Quagliarini, F. (Fabiana), Gaudio, C. (Carlo), Cambien, F. (François), Nicaud, V., Poirer, O. (Odette), Gudnason, V. (Vilmundur), Isaacs, A.J. (Aaron), Witteman, J.C.M. (Jacqueline), Tikka-Kleemola, P. (Päivi), Pencina, M. (Michael), Vasan, R.S. (Ramachandran Srini), D'Agostino, R.B. (Ralph), Ordovas, J.M. (Jose), Li, T.Y. (Tricia), Kakko, S. (Sakari), Kauma, H. (Heikki), Savolainen, M.J. (Markku), Kesäniemi, Y.A. (Antero), Sandhofer, A. (Anton), Paulweber, B. (Bernhard), Sorli, J.V. (Jose), Goto, A. (Akimoto), Yokoyama, S. (Shinji), Okumura, K. (Kenji), Horne, B.D. (Benjamin), Packard, C. (Chris), Freeman, D. (Dilys), Ford, I. (Ian), Sattar, N. (Naveed), McCormack, V. (Valerie), Lawlor, D.A. (Debbie), Ebrahim, S. (Shanil), Smith, A.V. (Davey), Kastelein, J.J.P. (John), Deanfield, J. (John), and Casas, J.P. (Juan)
Abstract: Background: Cholesteryl ester transfer protein (CETP) inhibitors raise high-density lipoprotein (HDL) cholesterol, but torcetrapib, the first-in-class inhibitor tested in a large outcome trial, caused an unexpected blood pressure elevation and increased cardiovascular events. Whether the hypertensive effect resulted from CETP inhibition or an off-target action of torcetrapib has been debated. We hypothesized that common single-nucleotide polymorphisms in the CETP gene could help distinguish mechanism-based from off-target actions of CETP inhibitors to inform on the validity of CETP as a therapeutic target. Methods and Results: We compared the effect of CETP single-nucleotide polymorphisms and torcetrapib treatment on lipid fractions, blood pressure, and electrolytes in up to 67 687 individuals from genetic studies and 17 911 from randomized trials. CETP single-nucleotide polymorphisms and torcetrapib treatment reduced CETP activity and had a directionally concordant effect on 8 lipid and lipoprotein traits (total, low-density lipoprotein, and HDL cholesterol; HDL2; HDL3; apolipoproteins A-I and B; and triglycerides), with the genetic effect on HDL cholesterol (0.13 mmol/L, 95% confidence interval [CI] 0.11 to 0.14 mmol/L) being consistent with that expected of a 10-mg dose of torcetrapib (0.13 mmol/L, 95% CI 0.10 to 0.15). In trials, 60 mg of torcetrapib elevated systolic and diastolic blood pressure by 4.47 mm Hg (95% CI 4.10 to 4.84 mm Hg) and 2.08 mm Hg (95% CI 1.84 to 2.31 mm Hg), respectively. However, the effect of CETP single-nucleotide polymorphisms on systolic blood pressure (0.16 mm Hg, 95% CI-0.28 to 0.60 mm Hg) and diastolic blood pressure (-0.04 mm Hg, 95% CI-0.36 to 0.28 mm Hg) was null and significantly different from that expected of 10 mg of torcetrapib. Conclusions: Discordance in the effects of CETP single-nucleotide polymorphisms and torcetrapib treatment on blood pressure despite the concordant effects on lipids indicates the hypertensive action
Published: 2010
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14. Lipoprotein-associated phospholipase A2 and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies

Author: Thompson, A. (Alexander), Gao, P. (Pei), Orfei, L. (Lia), Watson, S. (Sarah), Angelantonio, E. (Emanuele) di, Kaptoge, S. (Stephen), Ballantyne, C. (Christie), Cannon, C.P., Criqui, M. (Michael), Cushman, M. (Mary Ann), Hofman, A. (Albert), Packard, C. (Chris), Collins, R. (Rory), Danesh, J. (John), Thompson, A. (Alexander), Gao, P. (Pei), Orfei, L. (Lia), Watson, S. (Sarah), Angelantonio, E. (Emanuele) di, Kaptoge, S. (Stephen), Ballantyne, C. (Christie), Cannon, C.P., Criqui, M. (Michael), Cushman, M. (Mary Ann), Hofman, A. (Albert), Packard, C. (Chris), Collins, R. (Rory), and Danesh, J. (John)
Abstract: Background: Lipoprotein-associated phospholipase A2(Lp-PLA2), an inflammatory enzyme expressed in atherosclerotic plaques, is a therapeutic target being assessed in trials of vascular disease prevention. We investigated associations of circulating Lp-PLA2mass and activity with risk of coronary heart disease, stroke, and mortality under different circumstances. Methods: With use of individual records from 79 036 participants in 32 prospective studies (yielding 17 722 incident fatal or non-fatal outcomes during 474 976 person-years at risk), we did a meta-analysis of within-study regressions to calculate risk ratios (RRs) per 1 SD higher value of Lp-PLA2or other risk factor. The primary outcome was coronary heart disease. Findings: Lp-PLA2activity and mass were associated with each other (r=0·51, 95% CI 0·47-0·56) and proatherogenic lipids. We noted roughly log-linear associations of Lp-PLA2activity and mass with risk of coronary heart disease and vascular death. RRs, adjusted for conventional risk factors, were: 1·10 (95% CI 1·05-1·16) with Lp-PLA2activity and 1·11 (1·07-1·16) with Lp-PLA2mass for coronary heart disease; 1·08 (0·97-1·20) and 1·14 (1·02-1·27) for ischaemic stroke; 1·16 (1·09-1·24) and 1·13 (1·05-1·22) for vascular mortality; and 1·10 (1·04-1·17) and 1·10 (1·03-1·18) for non-vascular mortality, respectively. RRs with Lp-PLA2did not differ significantly in people with and without initial stable vascular disease, apart from for vascular death with Lp-PLA2mass. Adjusted RRs for coronary heart disease were 1·10 (1·02-1·18) with non-HDL cholesterol and 1·10 (1·00-1·21) with systolic blood pressure. Interpretation: Lp-PLA2activity and mass each show continuous associations with risk of coronary heart disease, similar in magnitude to that with non-HDL cholesterol or systolic blood pressure in this population. Associations of Lp-PLA2mass and activity are not exclusive to vascular outcomes, and the vascular associations depend at least partly on lipids. Funding
Published: 2010
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15. Collaborative pooled analysis of data on C-reactive protein gene variants and coronary disease: judging causality by Mendelian randomisation

Author: Danesh, J., Hingorani, A., Wensley, F., Casas, J.P., Smeeth, N.J., Samani, N.J., Whincup, P., Morris, R., Lawlor, D.A., Smith, G.D., Ebrahim, S., Brown, M., Sandhu, M., Reiner, A., Psaty, B., Lange, L., Cusman, M., Tracy, R., Nordestgaard, B.G., Tybjearg-Hansen, A., Zacho, J., Hung, J., Thompson, P., Beilby, J., Palmer, L.J., Fowkes, G., Lowe, G., Tzoulaki, I., Kumani, M., Overvad, K., Khaw, K.T., Benjamin, E., Chiodoini, B., Franzosi, M., Norman, P.E., Hankey, G.J., Jamrozik, K., Rimm, E., Pai, J., Heckbert, S., Bis, J., Yusuf, S., Anand, S., Engort, J., Collins, R., Melander, O., berglund, G., Ladenvall, P., Johansson, L., Jansson, J.H., Hallmans, G., Humphries, S., Manson, J., Saleheen, D., Frossard, P., Robertson, M, Shepherd, J, Svhaefer, E, Hofman, A, Witteman, J.C, Kardys, I, Faire, U de, Bennet, A, O'Reilly, D, McMahon, A, Packard, C, Clarke, R, Greenland, P, Bowden, J, Angelantonio, E Di, Shah, T, Thompson, S, Verzilli, C, Walker, M, Wensley, F, Whittaker, J, Danesh, J., Hingorani, A., Wensley, F., Casas, J.P., Smeeth, N.J., Samani, N.J., Whincup, P., Morris, R., Lawlor, D.A., Smith, G.D., Ebrahim, S., Brown, M., Sandhu, M., Reiner, A., Psaty, B., Lange, L., Cusman, M., Tracy, R., Nordestgaard, B.G., Tybjearg-Hansen, A., Zacho, J., Hung, J., Thompson, P., Beilby, J., Palmer, L.J., Fowkes, G., Lowe, G., Tzoulaki, I., Kumani, M., Overvad, K., Khaw, K.T., Benjamin, E., Chiodoini, B., Franzosi, M., Norman, P.E., Hankey, G.J., Jamrozik, K., Rimm, E., Pai, J., Heckbert, S., Bis, J., Yusuf, S., Anand, S., Engort, J., Collins, R., Melander, O., berglund, G., Ladenvall, P., Johansson, L., Jansson, J.H., Hallmans, G., Humphries, S., Manson, J., Saleheen, D., Frossard, P., Robertson, M, Shepherd, J, Svhaefer, E, Hofman, A, Witteman, J.C, Kardys, I, Faire, U de, Bennet, A, O'Reilly, D, McMahon, A, Packard, C, Clarke, R, Greenland, P, Bowden, J, Angelantonio, E Di, Shah, T, Thompson, S, Verzilli, C, Walker, M, Wensley, F, and Whittaker, J
Abstract: Many prospective studies have reported associations between circulating C-reactive protein (CRP) levels and risk of coronary heart disease (CHD), but causality remains uncertain. Studies of CHD are being conducted that involve measurement of common polymorphisms of the CRP gene known to be associated with circulating concentrations, thereby utilising these variants as proxies for circulating CRP levels. By analysing data from several studies examining the association between relevant CRP polymorphisms and CHD risk, the present collaboration will undertake a Mendelian randomisation analysis to help assess the likelihood of any causal relevance of CRP levels to CHD risk. A central database is being established containing individual data on CRP polymorphisms, circulating CRP levels, and major coronary outcomes as well as age, sex and other relevant characteristics. Associations between CRP polymorphisms or haplotypes and CHD will be evaluated under different circumstances. This collaboration comprises, at present, about 37,000 CHD outcomes and about 120,000 controls, which should yield suitably precise findings to help judge causality. This work should advance understanding of the relevance of low-grade inflammation to CHD and indicate whether or not CRP itself is involved in long-term pathogenesis Udgivelsesdato: 2008
Published: 2008

16. Collaborative pooled analysis of data on C-reactive protein gene variants and coronary disease: judging causality by Mendelian randomisation

Author: Danesh, J., Hingorani, A., Wensley, F., Casas, J.P., Smeeth, N.J., Samani, N.J., Whincup, P., Morris, R., Lawlor, D.A., Smith, G.D., Ebrahim, S., Brown, M., Sandhu, M., Reiner, A., Psaty, B., Lange, L., Cusman, M., Tracy, R., Nordestgaard, B.G., Tybjearg-Hansen, A., Zacho, J., Hung, J., Thompson, P., Beilby, J., Palmer, L.J., Fowkes, G., Lowe, G., Tzoulaki, I., Kumani, M., Overvad, K., Khaw, K.T., Benjamin, E., Chiodoini, B., Franzosi, M., Norman, P.E., Hankey, G.J., Jamrozik, K., Rimm, E., Pai, J., Heckbert, S., Bis, J., Yusuf, S., Anand, S., Engort, J., Collins, R., Melander, O., berglund, G., Ladenvall, P., Johansson, L., Jansson, J.H., Hallmans, G., Humphries, S., Manson, J., Saleheen, D., Frossard, P., Robertson, M, Shepherd, J, Svhaefer, E, Hofman, A, Witteman, J.C, Kardys, I, Faire, U de, Bennet, A, O'Reilly, D, McMahon, A, Packard, C, Clarke, R, Greenland, P, Bowden, J, Angelantonio, E Di, Shah, T, Thompson, S, Verzilli, C, Walker, M, Wensley, F, Whittaker, J, Danesh, J., Hingorani, A., Wensley, F., Casas, J.P., Smeeth, N.J., Samani, N.J., Whincup, P., Morris, R., Lawlor, D.A., Smith, G.D., Ebrahim, S., Brown, M., Sandhu, M., Reiner, A., Psaty, B., Lange, L., Cusman, M., Tracy, R., Nordestgaard, B.G., Tybjearg-Hansen, A., Zacho, J., Hung, J., Thompson, P., Beilby, J., Palmer, L.J., Fowkes, G., Lowe, G., Tzoulaki, I., Kumani, M., Overvad, K., Khaw, K.T., Benjamin, E., Chiodoini, B., Franzosi, M., Norman, P.E., Hankey, G.J., Jamrozik, K., Rimm, E., Pai, J., Heckbert, S., Bis, J., Yusuf, S., Anand, S., Engort, J., Collins, R., Melander, O., berglund, G., Ladenvall, P., Johansson, L., Jansson, J.H., Hallmans, G., Humphries, S., Manson, J., Saleheen, D., Frossard, P., Robertson, M, Shepherd, J, Svhaefer, E, Hofman, A, Witteman, J.C, Kardys, I, Faire, U de, Bennet, A, O'Reilly, D, McMahon, A, Packard, C, Clarke, R, Greenland, P, Bowden, J, Angelantonio, E Di, Shah, T, Thompson, S, Verzilli, C, Walker, M, Wensley, F, and Whittaker, J
Abstract: Many prospective studies have reported associations between circulating C-reactive protein (CRP) levels and risk of coronary heart disease (CHD), but causality remains uncertain. Studies of CHD are being conducted that involve measurement of common polymorphisms of the CRP gene known to be associated with circulating concentrations, thereby utilising these variants as proxies for circulating CRP levels. By analysing data from several studies examining the association between relevant CRP polymorphisms and CHD risk, the present collaboration will undertake a Mendelian randomisation analysis to help assess the likelihood of any causal relevance of CRP levels to CHD risk. A central database is being established containing individual data on CRP polymorphisms, circulating CRP levels, and major coronary outcomes as well as age, sex and other relevant characteristics. Associations between CRP polymorphisms or haplotypes and CHD will be evaluated under different circumstances. This collaboration comprises, at present, about 37,000 CHD outcomes and about 120,000 controls, which should yield suitably precise findings to help judge causality. This work should advance understanding of the relevance of low-grade inflammation to CHD and indicate whether or not CRP itself is involved in long-term pathogenesis Udgivelsesdato: 2008
Published: 2008

17. Collaborative meta-analysis of individual participant data from observational studies of Lp-PLA2 and cardiovascular diseases

Author: Ballantyne, C., Cushman, M., Psaty, B., Furberg, C., Khaw, K. T., Sandhu, M., Oldgren, J., Rossi, G. P., Maiolino, G., Cesari, M., Lenzini, L., James, Stefan, Rimm, E., Collins, R., Anderson, J., Koenig, W., Brenner, H., Rothenbacher, D., Berglund, G., Persson, M., Berger, P., Brilakis, E., McConnell, J. P., Sacco, R., Elkind, M., Talmud, P., Cannon, C. P., Packard, C., Barrett-Connor, E., Hofman, A., Kardys, I., Witteman, J. C., Criqui, M., Corsetti, J. P., Rainwater, D. L., Moss, A. J., Robins, S., Bloomfield, H., Collins, D., Wassertheil-Smoller, S., Ridker, P., Danesh, J., Gu, D., Nelson, J. J., Thompson, S., Zalewski, A., Zariffa, N., Di Angelantonio, E., Kaptoge, S., Thompson, A., Walker, M., Watson, S., Wood, A, Ballantyne, C., Cushman, M., Psaty, B., Furberg, C., Khaw, K. T., Sandhu, M., Oldgren, J., Rossi, G. P., Maiolino, G., Cesari, M., Lenzini, L., James, Stefan, Rimm, E., Collins, R., Anderson, J., Koenig, W., Brenner, H., Rothenbacher, D., Berglund, G., Persson, M., Berger, P., Brilakis, E., McConnell, J. P., Sacco, R., Elkind, M., Talmud, P., Cannon, C. P., Packard, C., Barrett-Connor, E., Hofman, A., Kardys, I., Witteman, J. C., Criqui, M., Corsetti, J. P., Rainwater, D. L., Moss, A. J., Robins, S., Bloomfield, H., Collins, D., Wassertheil-Smoller, S., Ridker, P., Danesh, J., Gu, D., Nelson, J. J., Thompson, S., Zalewski, A., Zariffa, N., Di Angelantonio, E., Kaptoge, S., Thompson, A., Walker, M., Watson, S., and Wood, A
Abstract: BACKGROUND: A large number of observational epidemiological studies have reported generally positive associations between circulating mass and activity levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) and the risk of cardiovascular diseases. Few studies have been large enough to provide reliable estimates in different circumstances, such as in different subgroups (e.g., by age group, sex, or smoking status) or at different Lp-PLA2 levels. Moreover, most published studies have related disease risk only to baseline values of Lp-PLA2 markers (which can lead to substantial underestimation of any risk relationships because of within-person variability over time) and have used different approaches to adjustment for possible confounding factors. OBJECTIVES: By combination of data from individual participants from all relevant observational studies in a systematic 'meta-analysis', with correction for regression dilution (using available data on serial measurements of Lp-PLA2), the Lp-PLA2 Studies Collaboration will aim to characterize more precisely than has previously been possible the strength and shape of the age and sex-specific associations of plasma Lp-PLA2 with coronary heart disease (and, where data are sufficient, with other vascular diseases, such as ischaemic stroke). It will also help to determine to what extent such associations are independent of possible confounding factors and to explore potential sources of heterogeneity among studies, such as those related to assay methods and study design. It is anticipated that the present collaboration will serve as a framework to investigate related questions on Lp-PLA2 and cardiovascular outcomes. METHODS: A central database is being established containing data on circulating Lp-PLA2 values, sex and other potential confounding factors, age at baseline Lp-PLA2 measurement, age at event or at last follow-up, major vascular morbidity and cause-specific mortality. Information about any repeat measurements of Lp
Published: 2007
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18. Management of hypercholesterol - aemia in the patient with diabetes

Author: Packard, C, Olsson, Anders, Packard, C, and Olsson, Anders
Abstract: Coronary heart disease (CHD) is the leading cause of death in patients with type 2 diabetes. The hyperglycaemia that characterises this disease is often accompanied by a cluster of other risk factors, such as dyslipidaemia and hypertension, and effective management of the patient with diabetes requires treatment directed at correcting all of the abnormalities that increase cardiovascular risk. Approximately 90% of patients with diabetes have type 2 disease, and dyslipidaemia in these patients is characterised by elevated plasma triglycerides and very-low-density lipoproteins (VLDL), by reduced high-density lipoprotein cholesterol (HDL-C), and by a shift in LDL distribution towards small, dense particles. All of these lipid abnormalities are important risk factors for CHD. Retrospective subgroup analysis and prospective studies have shown that lipid-lowering therapy can slow the progression of atherosclerosis and reduce the risk for cardiovascular events in patients with diabetes, and both the National Cholesterol Education Program Adult Treatment Panel III and American Diabetes Association have established aggressive treatment goals for lipid-lowering therapy in these patients. All of the major medications used to treat hyperlipidaemia in other populations (niacin, fibrates, bile acid sequestrants and statins) have been used effectively to improve the plasma lipid profile in patients with diabetes. Statins are generally accepted as first-line treatment for these patients, although fibrates also have an important role in patients with pronounced hypertriglyceridaemia. Statins significantly reduce low-density lipoprotein cholesterol (LDL-C) in a broad range of patients. These agents also have substantial effects on plasma triglycerides and, in patients with hypertriglyceridaemia, lower very-low-density lipoprotein cholesterol (VLDL-C) to approximately the same extent as LDLC. In this regard, the new agent rosuvastatin has been shown, in recent trials, to produce great
Published: 2002

19. New global standards in lipid lowering : a review of emerging evidence and concepts.

Author: Olsson, Anders, Packard, C, Olsson, Anders, and Packard, C
Published: 2002

20. Yours all the time, Frank N. Dix.

Author: Packard, C. C. (Cullen Channing), 1839-1898 photographer., Packard, C. C. (Cullen Channing), 1839-1898 photographer., Packard, C. C. (Cullen Channing), 1839-1898 photographer., and Packard, C. C. (Cullen Channing), 1839-1898 photographer.
Abstract: Head and shoulders portrait of man with thin mustache, wearing long tie.; Title from ms. note below image.; Photographer's imprint on verso., William L. Clements Library, http://name.umdl.umich.edu/IC-WCL1IC-X-5032%5DWCL005119, https://quod.lib.umich.edu/cgi/i/image/api/thumb/wcl1ic/5032/WCL005119/!250,250, The University of Michigan Library provides access to these materials for educational and research purposes. These materials may be under copyright. If you decide to use any of these materials, you are responsible for making your own legal assessment and securing any necessary permission. If you have questions about the collection, please contact the William L. Clements Library: icwcl1ic-umdl-help@umich.edu. If you have concerns about the inclusion of an item in this collection, please contact Library IT: libraryit-info@umich.edu., https://www.lib.umich.edu/about-us/policies/copyright-policy

21. The Hessian Fly in California.

Author: Packard, C. M., Packard, C. M., Packard, C. M., and Packard, C. M.
Abstract: 26 p., Includes: line drawings; tables, 12 references, 17038117 Historic Organic Production Research Database., Later this year, we will begin redirecting users to these reports on the National Agricultural Library site at https://naldc.nal.usda.gov/organic_roots, Organic Agriculture Information Access, (dlps) 17038117.0081.001, (nal) https://naldc.nal.usda.gov/catalog/CAT86200076, https://www.lib.umich.edu/about-us/policies/copyright-policy, Works produced by employees of the U.S. Government as part of their official duties are not copyrighted within the U.S. National Agricultural Library call no.: 1 Ag84Te no.81

22. Notes on Development Type Materiel for Rifle, Caliber 7.62mm, T44E5 (M15)

Author: SPRINGFIELD ARMORY MA, Packard,C F, SPRINGFIELD ARMORY MA, and Packard,C F
Abstract: This report is directed to personnel charged with the use, care, and maintenance of the Caliber 7.62mm t44E5 (M15) Rifle. The subject rifle is a heavy barrel version of the Caliber 7.62mm T44E4 (M14) Rifle, designed to permit sustained full automatic fire. The caliber 7.62mm, T44E5 (M15) rifle is a heavy barreled, aircooled, gas-operated, magazine-fed, shoulder weapon, designed for selective semiautomatic fire. In principle of operation, it is similar to the M1 rifle. The T44E5 is chambered for the NATO caliber 7.62mm cartridge, and a 20-round box magazine has been added.
Published: 1958

23. An evaluation of the Arctic--will it become an area of cooperation or conflict?

Author: Dahl, Erik J., Boulton, John W., National Security Affairs, Trent, Packard C., Dahl, Erik J., Boulton, John W., National Security Affairs, and Trent, Packard C.
Abstract: Climate change and the vast amount of natural resources in the Arctic region have prompted awareness of the need for new policies among Arctic states, including the U.S., and stimulated throughout the entire international community a critical assessment of the issues regarding the Arctic region. All of this could result in potential conflict in this critical region of the world. The Arctic's ice cover as of spring 2010 was the lowest it has ever been at that time of year, and it is melting faster than once thought, making it possible for the Arctic to have an ice free summer by 2013. Due to the increase of yearly ice melt, the race to extract the natural resources will speed up tremendously in future years. Research shows that the Arctic nations strongly encourage cooperation and are currently abiding by the international laws, treaties, and infrastructures in place that allow them the most potential to benefit from the Arctic resources. However, although the Arctic nations stress cooperation in their official statements and diplomatic overtures, they are actually preparing for conflict. There are many potential flashpoints that could cause the Arctic to end in conflict, such as territorial disputes, Russia's dependency on the Arctic, and the militarization of the Arctic. The Arctic region has long been neglected by the U.S; however, due to the current situation in the Arctic and the potential for new threats to the U.S. homeland, the region is becoming a far more important issue and is gaining the attention of the U.S. government. The major question this thesis will examine concerns the future of the Arctic: is it heading for conflict, or for cooperation? In addition, the state of U.S. security with respect to the Arctic will be evaluated, and recommendations for U.S. national and homeland security policy will be provided., http://archive.org/details/anevaluationofar1094510783, US Navy (USN) author

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23 results on '"Packard, C."'

1. SCORE2 risk prediction algorithms: new models to estimate 10-year risk of cardiovascular disease in Europe

2. Discovery of rare variants associated with blood pressure regulation through meta-analysis of 1.3 million individuals

3. Rare variant in scavenger receptor BI raises HDL cholesterol and increases risk of coronary heart disease

4. Lack of effect of lowering LDL cholesterol on cancer: Meta-analysis of individual data from 175,000 people in 27 randomised trials of statin therapy

5. Lipid-related markers and cardiovascular disease prediction

6. C-reactive protein, fibrinogen, and cardiovascular disease prediction

7. An Evaluation of the Arctic - Will it Become an Area of Cooperation or Conflict?

8. Association between C reactive protein and coronary heart disease : mendelian randomisation analysis based on individual participant data

9. An evaluation of the Arctic--will it become an area of cooperation or conflict?

10. Obesity is associated with fatal coronary heart disease independently of traditional risk factors and deprivation

11. Obesity is associated with fatal coronary heart disease independently of traditional risk factors and deprivation

12. Bayesian methods for meta-analysis of causal relationships estimated using genetic instrumental variables

13. Separating the mechanism-based and off-target actions of cholesteryl ester transfer protein inhibitors with CETP gene polymorphisms

14. Lipoprotein-associated phospholipase A2 and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies

15. Collaborative pooled analysis of data on C-reactive protein gene variants and coronary disease: judging causality by Mendelian randomisation

16. Collaborative pooled analysis of data on C-reactive protein gene variants and coronary disease: judging causality by Mendelian randomisation

17. Collaborative meta-analysis of individual participant data from observational studies of Lp-PLA2 and cardiovascular diseases

18. Management of hypercholesterol - aemia in the patient with diabetes

19. New global standards in lipid lowering : a review of emerging evidence and concepts.

20. Yours all the time, Frank N. Dix.

21. The Hessian Fly in California.

22. Notes on Development Type Materiel for Rifle, Caliber 7.62mm, T44E5 (M15)

23. An evaluation of the Arctic--will it become an area of cooperation or conflict?

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