24 results on '"T. Lehtimaki"'
Search Results
2. P5 First screening round results of the ProScreen trial with PSA, kallikrein panel and MRI
- Author
-
A.S. Rannikko, T.L.J. Tammela, T. Mirtti, H. Lilja, T. Tolonen, A. Kenttämies, I. Rinta-Kiikka, T. Lehtimäki, K. Natunen, J. Nevalainen, J. Raitanen, J. Ronkainen, T. van der Kwast, J. Riikonen, A. Petas, M. Matikainen, K. Taari, and T. Kilpeläinen
- Subjects
Diseases of the genitourinary system. Urology ,RC870-923 ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Published
- 2024
- Full Text
- View/download PDF
3. Poster session 1
- Author
-
J. Schlueter, T. Brand, D. J. Henderson, V. Boczonadi, P. Humbert, B. Chaudhry, D. Sedmera, J. Svatunkova, R. Kockova, B. Sankova, C. Lopez Sanchez, D. Franco, A. Aranega, V. Garcia-Martinez, E. Demina, V. Miroshikova, A. Denisenko, A. Schwarzman, F. Sanchez-Cabo, C. Torroja, A. Benguria, R. Buchan, P. Srivastava, F. Martinez, P. Barton, S. Cook, A. Dopazo, E. Lara-Pezzi, H. Rai, S. Kumar, A. K. Sharma, S. Mastana, A. Kapoor, C. M. Pandey, S. Agrawal, N. Sinha, J. Lipkova, M. Goldbergova, J. Parenica, J. Bienertova Vasku, A. Vasku, P. Kala, J. Spinar, L. Perez-Cabornero, D. Cantalapiedra, A. Forteza, R. Saez-Villaverde, J. Zumalde, V. Fernandez-Pedrosa, S. Zuniga-Trejos, M. Gil-Borja, M. Lazaro, S. Santillan, M. Costa, N. Cortez-Dias, P. Carrilho-Ferreira, D. Silva, C. Jorge, R. Placido, C. Calisto, M. Fiuza, A. Nunes Diogo, F. J. Enguita, H. H. W. Sillje, B. Lu, H. Yu, M. Zwartbol, W. P. Ruifrok, W. H. Van Gilst, R. A. De Boer, D. Zaliaduonyte-Peksiene, S. Simonyte, V. Lesauskaite, J. Vaskelyte, V. Mizariene, R. Zaliunas, W. Tigchelaar, E. Barlaka, A. Lazou, C. Del Giudice, E. Cipolletta, A. Anastasio, G. Santulli, M. Rusciano, A. S. Maione, P. Campiglia, M. Illario, B. Trimarco, G. Iaccarino, G. A. Frentzou, M. J. Drinkhill, N. A. Turner, S. G. Ball, J. F. X. Ainscough, L. Bertrand, F. Mailleux, J. Hammond, A. Ginion, L. Hue, J. L. Balligand, S. Horman, J. L. Vanoverschelde, C. Beauloye, B. Demeulder, S. L. Puhl, A. Mueller, Y. Devaux, D. R. Wagner, K. Roemer, M. Boehm, C. Maack, D. Miranda-Silva, I. Falcao-Pires, N. Goncalves, D. Moreira-Goncalves, A. F. Leite-Moreira, F. Mraiche, L. Fliegel, J. Xue, G. G. Haddad, L. C. Hsiao, C. Carr, Z. F. Cui, K. Clarke, M. A. D'amico, P. Izzicupo, A. Di Fonso, A. Bascelli, S. Gallina, A. Di Baldassarre, C. Silvestre, P. Fernandez, O. M. Pello, C. Indolfi, F. Civeira, R. Hutter, B. Ibanez, J. Chaves, J. Martinez-Gonzalez, V. Andres Garcia, A. Zabirnik, N. Smolina, A. Malashicheva, E. Omelchenko, T. Sejersen, A. Kostareva, C. Noack, M. P. Zafiriou, A. Renger, R. Dietz, H. J. Schaeffer, M. B. Bergmann, C. Zelarayan, S. Van Linthout, K. Miteva, M. P. Becher, M. Haag, J. Ringe, H.-P. schultheiss, M. Sittinger, C. Tschoepe, T. Kakuchaya, L. Bockeria, E. Golukhova, M. Eremeeva, N. Chigogidze, I. Aslanidi, I. Shurupova, A. Svobodov, A. A. Ramkisoensing, D. A. Pijnappels, J. Swildens, M. J. Goumans, M. J. Schalij, A. A. F. De Vries, D. E. Atsma, A. Gomes, G. M. Costa, C. A. Cordeiro, A. Matsuada, L. B. Rosario, A. P. Freire, M. Bousquenaud, M. Rolland-Turner, F. Maskali, L. Zhang, P. Y. Marie, F. Azuaje, A. J. Smith, G. M. Ellison, C. D. Waring, S. Purushothaman, D. Torella, B. Nadal-Ginard, M. H. Van Marion, D. W. J. Van Der Schaft, M.-J. Goumans, F. P. T. Baaijens, C. V. C. Bouten, N. Kraenkel, K. Kuschnerus, M. Mueller, T. Speer, S. Briand, M. Bader, P. Madeddu, T. F. Luescher, U. Landmesser, A. Papalamprou, C. Vicinanza, D. F. Goldspink, M. Noseda, S. J. Mcsweeney, T. Leja, E. Belian, I. Macaulay, F. Al-Beidh, S. Koenemann, M. S. Abreu Pavia, S. E. Jacobsen, M. D. Schneider, G. Foldes, Z. Bagyura, Z. Lendvai, D. Mathe, T. Nemeth, J. Skopal, I. Foldes, B. Merkely, S. E. Harding, A. J. Candasamy, R. S. Haworth, A. Boguslavsky, F. Cuello, M. J. Shattock, M. Mayr, M. Gautel, M. Avkiran, P. Leszek, B. Sochanowicz, M. Szperl, P. Kolsut, K. Brzoska, W. Piotrowski, T. Rywik, B. Danko, J. Rozanski, M. Kruszewski, N. Bouteldja, R. J. Woodman, C. L. Hewitson, E. Domingo, J. A. Barbara, A. A. Mangoni, R. Carnicer Hijazo, A. B. Hale, X. Liu, S. Suffredini, J. K. Bendall, G. B. S. Lim, N. J. Alp, K. M. Channon, B. Casadei, L. R. Moltzau, J. M. Aronsen, S. Meier, I. Sjaastad, T. Skomedal, J.-B. Osnes, F. O. Levy, E. Qvigstad, P. T. Wright, L. M. K. Pannell, A. R. Lyon, J. Gorelik, A. Guellich, S. F. Vatner, R. Fischmeister, B. Manoury, E. Dubois, J. Hamelet, A. Vanderper, P. Herijgers, D. Langin, F. Gartner, J. Gummert, H. Milting, G. Euler, M. Priess, J. Heger, T. Noll, R. Schulz, T. Doi, T. Akagami, T. Naka, T. Masuyama, M. Ohyanagi, M. Massaro, E. Scoditti, M. Pellegrino, M. A. Carluccio, C. Martines, C. Storelli, R. De Caterina, M. Falck-Hansen, M. E. Goddard, J. E. Cole, N. Astola, A. J. Cross, R. Krams, C. Monaco, M. F. Corsten, W. Verhesen, A. P. Papageorgiou, P. Carai, M. Lindow, S. Obad, G. Summer, L. De Rijck, S. Coort, M. Hazebroek, R. Van Leeuwen, M. Gijbels, M. P. J. De Winther, F. R. M. Stassen, S. Kauppinen, B. Schroen, S. Heymans, Z. Husti, V. Juhasz, L. Virag, A. Kristof, I. Koncz, T. Szel, I. Baczko, N. Jost, J. G. Y. Papp, A. Varro, A. Ghigo, A. Perino, F. Damilano, J. Leroy, V. O. Nikolaev, W. Richter, M. Conti, G. Vandecasteele, E. Hirsch, R. Ang, S. Sebastian, A. Ludwig, L. Birnbaumer, A. Tinker, E. A. Ertel, R. Sube, A. Opel, C. L-H Huang, A. Grace, N. Tribulova, J. Radosinska, B. Bacova, T. Benova, V. Knezl, J. Slezak, T. A. Matsuyama, T. Tanaka, T. Adachi, Y. Jiang, H. Ishibashi-Ueda, T. Takamatsu, J. Kornej, C. Reihardt, J. Kosiuk, A. Arya, G. Hindricks, V. Adams, D. Husser, A. Bollmann, S. Severi, M. Fantini, E. Ravagli, L. A. Charawi, D. Difrancesco, C. Poulet, L. Lu, U. R. Ravens, M. Hoch, T. Koenig, A. Gardiwal, B. Stapel, S. Erschow, A. Froese, B. Weinhold, R. Gerardy-Schahn, G. Klein, D. Hilfiker-Kleiner, K. Chinda, S. Palee, S. Surinkaew, M. Phornphutkul, S. Chattipakorn, N. Chattipakorn, B. Tuana, Z. Kohajda, A. A. Kristof, C. Corici, F. Fulop, N. L. Jost, V. Szuts, D. Menesi, G. L. Puskas, A. Zvara, N. Houshmand, J. G. Papp, N. Al-Shanti, M. Hancock, A. Venturini, C. Stewart, R. Ascione, G. Angelini, M.-S. Suleiman, A. Gonzalez-Tendero, I. Torre, F. Crispi, E. Gratacos, T. Tzanavari, E. Varela, A. Economides, S. Theocharis, C. Pantos, D. V. Cokkinos, A. Karalis, P. Hecker, V. Lionetti, W. C. Stanley, C. Ferrara, N. Piroddi, B. Scellini, C. Ferrantini, V. Sequiera, C. Remedios, L. Carrier, C. Tesi, J. Van Der Velden, C. Poggesi, V. Kooij, G. J. M. Stienen, D. Dooijes, s. Marston, C. Redwood, C. Dos Remedios, I. Diakonov, S. Tokar, M. Sikkel, S. Schlossarek, M. Sauer, A. Papageorgiou, S. Velthuis, E. Lutgens, M. Swinnen, N. Van Rooijen, J. Kzhyshkowska, P. Carmeliet, P. Garcia-Canadilla, F. Garcia-Garcia, I. Iruretagoiena, J. Dopazo, I. Amat-Roldan, M. H. Zhang, Y. H. Zhang, C. E. Sears, B. Wojtas, A. Llach, L. Hove-Madsen, V. Spinelli, L. Sartiani, M. Bucciantini, R. Coppini, E. Russo, A. Mugelli, E. Cerbai, M. Stefani, M. Ibrahim, P. Kukadia, M. Navaratnarajah, U. Siedlecka, C. Van Doorn, M. Yacoub, C. Terracciano, W. Song, N. Curtin, R. Woledge, S. Marston, M. Balteau, N. Tajeddine, G. Behets-Wydemans, C. Dessy, P. Gailly, W. J. Van Der Laarse, S. J. P. Bogaards, D. Van Groen, Y. Y. Wong, I. Schalij, A. Vonk Noordegraaf, F. M. Faz, B. Littlejohns, P. Pasdois, A. P. Halestrap, G. D. Angelini, S. Lemoine, V. Jaspard-Vinassa, F. Vigneron, P. Dos Santos, M. Popescu, A. Vlad, G. Isvoranu, L. Suciu, B. Marinescu, D. Dimulescu, L. Zagrean, P. W. M. Kleikers, K. Wingler, K. Radermacher, A. Sydykov, H. A. Ghofrani, N. Weissmann, H. H. W. Schmidt, A. Poddubnaya, K. E. M. Khurs, S. O. G. Smolenskaya, G. Szucs, Z. Murlasits, S. Torok, G. F. Kocsis, T. Csont, C. Csonka, P. Ferdinandy, R. Dongworth, D. M. Yellon, D. J. Hausenloy, Y. Y. Chen, W. S. Lian, C. F. Cheng, K. H. Khoo, T. C. Meng, G. Youcef, E. Belaidi, L. Fazal, M. P. Vinvent, D. De Paulis, G. Zadigue, C. Richer-Giudicelli, F. Alhenc-Gelas, M. Ovize, A. Pizard, R. Cal, J. Castellano, J. Farre, G. Vilahur, L. Badimon, V. Llorente-Cortes, H. Naz, M. Gharanei, C. Mee, H. Maddock, A. Hussain, O. Pisarenko, V. Shulzhenko, L. Serebryakova, I. Studneva, Y. Pelogeykina, D. Khatri, O. Tskitishvili, E. Barnucz, G. Veres, P. Hegedus, T. Radovits, S. Korkmaz, S. Klein, R. Zoller, M. Karck, G. Szabo, S. Morel, M. A. Frias, C. Rosker, R. W. James, S. Rohr, B. R. Kwak, V. Braunersreuther, B. Foglia, F. Mach, E. Shantsila, S. Montoro-Garcia, L. D. Tapp, S. Apostolakis, B. J. Wrigley, G. Y. H. Lip, E. Sokolowska, K. Przyborowski, K. Kramkowski, W. Buczko, A. Mogielnicki, U. Simonsen, E. R. Hedegaard, B. D. Nielsen, A. Kun, A. Hughes, C. Kroigaard, S. Mogensen, O. Frobert, K. Ait Aissa, J. P. Max, D. Wahl, T. Lecompte, P. Lacolley, V. Regnault, A. Novakovic, M. Pavlovic, A. Vranic, P. Milojevic, I. Stojanovic, M. Jovic, D. Nenezic, N. Ugresic, Q. Yang, G. W. He, L. Calvier, P. Reboul, B. Martin-Fernandez, V. Lahera, F. Zannad, V. Cachofeiro, P. Rossignol, N. Lopez-Andres, V. K. Pulakazhi Venu, R. Baetta, A. Bonomo, A. F. Muro, A. Corsini, A. L. Catapano, G. D. Norata, L. E. Viiri, L. E. Full, T. J. Navin, A. Didangelos, I. Seppala, T. Lehtimaki, A. H. Davies, R. Wait, D. Sedding, P. Stieger, C. Thoelen, S. Fischer, J. M. Daniel, R. Widmer-Teske, K. T. Preissner, N. Alenina, L. A. Rabelo, M. Todiras, V. N. Souza, J. M. Penninger, R. A. Santos, I. A. Leonova, S. A. Boldueva, V. S. Feoktistova, O. V. Sirotkina, M. G. Kolesnichenko, Z. Springo, P. Toth, P. Cseplo, G. Szijjarto, A. Koller, S. Puthenkalam, M. K. Frey, I. M. Lang, R. Madonna, H. Shelat, Y. J. Geng, T. Ziegler, V. Pfetsch, J. Horstkotte, C. Schwab, I. Rohwedde, R. Hinkel, Q. Di, S. Dietzel, U. Deutsch, C. Kupatt, I. Ernens, B. Lenoir, O. Fortunato, A. Caporali, E. Sangalli, D. Cordella, M. Marchetti, G. Spinetti, C. Emanueli, G. Arderiu, E. Pena, M. J. Forteza, V. Bodi, S. Novella, C. Alguero, I. Trapero, I. Benet, C. Hermenegildo, J. Sanchis, F. J. Chorro, A. Nemeth, S. Szabados, A. Cziraki, E. Sulyok, I. G. Horvath, M. Rauh, W. Rascher, I. Sikharulidze, I. B. Bakhlishvili, J. T. T. Laitinen, J. P. Hytonen, O. Leppanen, J. Taavitsainen, A. Partanen, P. Korpisalo, S. Yla-Herttuala, J. Lonn, J. Hallstrom, T. Bengtsson, M. C. Guisasola, E. Dulin, S. Stojkovic, C. Kaun, G. Maurer, K. Huber, J. Wojta, S. Demyanets, T. B. Opstad, A. Pettersen, S. Aakra, H. Arnesen, I. Seljeflot, M. Borrell-Pages, C. Romero, A. Toso, M. Leoncini, L. Tanini, T. Pizzetti, F. Tropeano, M. Maioli, P. Casprini, F. Bellandi, R. F. Antunes, J. C. Kaski, I. E. Dumitriu, E. Wu, A. A. L. Tareen, M. Udovychenko, I. Rudyk, K. Riches, L. Franklin, A. Maqbool, J. Bond, M. L. Koschinsky, D. J. O'regan, K. E. Porter, I. R. Parepa, A. I. Suceveanu, A. Suceveanu, L. Mazilu, L. Cojocaru, A. Rusali, L. A. Tuta, E. Craiu, D. Lindner, C. Zietsch, H.-P. Schultheiss, C. Tschope, D. Westermann, M. Miana, E. Martinez, R. Jurado, C. Delgado, N. Gomez-Hurtado, A. Briones, J. Young, T. J. Geng, A. Brodehl, T. Schmidt, O. Smolenskaya, C. Stegemann, D. Byzov, I. Mikhaylova, N. Chizh, E. Pushkova, O. Synchykova, B. Sandomirsky, O. Freylikhman, O. Rotar, N. Chromova, E. Moguchaya, V. Ivanenko, E. Kolesova, A. Erina, M. Boyarinova, A. Konradi, S. D. Preston, D. Baskaran, A. M. Plonczak, K. Norita, S. V. De Noronha, M. N. Sheppard, A. Haghikia, S. F. Hill, M. Hoepfner, B. Nitzsche, M. Schrader, F. Zengerling, B. Hoffmann, A. Pries, S. Gao, J. T. Laitinen, S. Laidinen, H. Markkanen, H. Karvinen, V. Marjomaki, I. Vajanto, T. T. Rissanen, K. Alitalo, P. Mello Ferrao, M. C. Waghabi, L. R. Garzoni, J. Ritterhoff, C. Weidenhammer, M. Voelkers, W. H. Zimmermann, J. Rabinowitz, P. Most, S. C. Gordts, I. Muthuramu, F. Jacobs, E. Van Craeyveld, E. Nefyodova, B. De Geest, D. R. Tribuddharat, D. R. Sathitkarnmanee, M. R. Buddhisa, M. S. Suwannasaen, D. R. Silarat, D. R. Ngamsangsirisup, D. R. Hawrylowicz, D. R. Lertmemongkolchai, S. Rain, M. L. Handoko, N. Westerhof, A. Vonk-Noordegraaf, F. S. De Man, A. S. Iakovleva, O. A. Mirolyubova, A. Berezin, T. A. Samura, Suwannasaen, Tippayawat, Ngamsangsirisup, D. R. Sutra, Hawrylowicz, Lertmemongkolchai, L. M. Lima, M. G. Carvalho, D. R. G. Junqueira, M. O. Sousa, A. Zampetaki, P. Willeit, L. Tilling, I. Drozdov, M. Prokopi, A. Shah, C. Boulanger, P. Chowienczyk, S. Kiechl, S. H. V. Oliveira, V. Kirillova, E. Prosviryakov, C. T. M. Van Der Pouw Kraan, F. J. P. Bernink, J. M. Baggen, L. Timmers, A. M. Beek, M. Diamant, A. C. Van Rossum, N. Van Royen, A. J. G. Horrevoets, J. E. A. Appelman, A. Zyatenkov, L. S. Kokov, Y. U. D. Volynskiy, M. Krestjyaninov, V. I. Ruzov, A. V. Villar, E. Martinez-Laorden, A. Almela, M. A. Hurle, M. L. Laorden, N. Apaijai, M. K. Mcmullen, J. M. Whitehouse, G. Shine, and A. Towell
- Subjects
Gerontology ,Physiology ,business.industry ,Physiology (medical) ,Cancer research ,Medicine ,SCRIB gene ,Cardiology and Cardiovascular Medicine ,business - Published
- 2012
4. Genome-wide association and longitudinal analyses reveal genetic loci linking pubertal height growth, pubertal timing and childhood adiposity
- Author
-
D. L. Cousminer, D. J. Berry, N. J. Timpson, W. Ang, E. Thiering, E. M. Byrne, H. R. Taal, V. Huikari, J. P. Bradfield, M. Kerkhof, M. M. Groen Blokhuis, E. Kreiner Moller, M. Marinelli, C. Holst, J. T. Leinonen, J. R. B. Perry, I. Surakka, O. Pietilainen, J. Kettunen, V. Anttila, M. Kaakinen, U. Sovio, A. Pouta, S. Das, V. Lagou, C. Power, I. Prokopenko, D. M. Evans, J. P. Kemp, B. St Pourcain, S. Ring, A. Palotie, E. Kajantie, C. Osmond, T. Lehtimaki, J. S. Viikari, M. Kahonen, N. M. Warrington, S. J. Lye, L. J. Palmer, C. M. T. Tiesler, C. Flexeder, G. W. Montgomery, S. E. Medland, A. Hofman, H. Hakonarson, M. Guxens, M. Bartels, V. Salomaa, J. M. Murabito, J. Kaprio, T. I. A. Sorensen, F. Ballester, H. Bisgaard, D. I. Boomsma, G. H. Koppelman, S. F. A. Grant, V. W. V. Jaddoe, N. G. Martin, J. Heinrich, C. E. Pennell, O. T. Raitakari, J. G. Eriksson, G. D. Smith, E. Hypponen, M. R. Jarvelin, M. I. McCarthy, S. Ripatti, E. Widen, Adair LS, Ang W, Atalay M, van Beijsterveldt T, Bergen N, Benke K, Berry DJ, Boomsma DI, Bradfield JP, Charoen P, Coin L, Cooper C, Cousminer DL, Das S, Davis OS, Dedoussis GV, Elliott P, Estivill X, Evans DM, Feenstra B, Flexeder C, Frayling T, Freathy RM, Gaillard R, Geller F, Gillman M, Grant SF, Groen Blokhuis M, Goh LK, Guxens M, Hakonarson H, Hattersley AT, Haworth CM, Hadley D, Hedebrand J, Heinrich J, Hinney A, Hirschhorn JN, Hocher B, Holloway JW, Holst C, Hottenga JJ, Horikoshi M, Huikari V, Hypponen E, Iñiguez C, Jaddoe VW, Jarvelin MR, Kaakinen M, Kilpeläinen TO, Kirin M, Kowgier M, Lakka HM, Lakka TA, Lange LA, Lawlor DA, Lehtimäki T, Lewin A, Lindgren C, Lindi V, Maggi R, Marsh J, McCarthy MI, Melbye M, Middeldorp C, Millwood I, Mohlke KL, Mook Kanamori DO, Murray JC, Nivard M, Nohr EA, Ntalla I, Oken E, Ong KK, O'Reilly PF, Palmer LJ, Panoutsopoulou K, Pararajasingham J, Pearson ER, Pennell CE, Power C, Price TS, Prokopenko I, Raitakari OT, Rodriguez A, Salem RM, Saw SM, Scherag A, Sebert S, Siitonen N, Simell O, Sørensen TI, Sovio U, Pourcain BS, Strachan DP, Sunyer J, Taal HR, Teo YY, Thiering E, Tiesler C, Timpson NJ, Uitterlinden AG, Valcárcel B, Warrington NM, White S, Widén E, Willemsen G, Wilson JF, Yaghootkar H, Zeggini E, Elks CE, Perry JR, Sulem P, Chasman DI, Franceschini N, He C, Lunetta KL, Visser JA, Byrne EM, Gudbjartsson DF, Esko T, Koller DL, Kutalik Z, Lin P, Mangino M, Marongiu M, McArdle PF, Smith AV, Stolk L, van Wingerden SH, Zhao JH, Albrecht E, Corre T, Ingelsson E, Hayward C, Magnusson PK, Smith EN, Ulivi S, Warrington M, Zgaga L, Alavere H, Amin N, Aspelund T, Bandinelli S, Barroso I, Berenson GS, Bergmann S, Blackburn H, Boerwinkle E, Buring JE, Busonero F, Campbell H, Chanock SJ, Chen W, Cornelis MC, Couper D, Coviello AD, de Faire U, de Geus EJ, Deloukas P, Döring A, Davey Smith G, Easton DF, Eiriksdottir G, Emilsson V, Eriksson J, Ferrucci L, Folsom AR, Foroud T, Garcia M, GASPARINI, PAOLO, Gieger C, Gudnason V, Hall P, Hankinson SE, Ferreli L, Heath AC, Hernandez DG, Hofman A, Hu FB, Illig T, Järvelin MR, Johnson AD, Karasik D, Khaw KT, Kiel DP, Kolcic I, Kraft P, Launer LJ, Laven JS, Li S, Liu J, Levy D, Martin NG, McArdle WL, Mooser V, Murray SS, Nalls MA, Navarro P, Nelis M, Ness AR, Northstone K, Oostra BA, Peacock M, Palotie A, Paré G, Parker AN, Pedersen NL, Peltonen L, Pharoah P, Polasek O, Plump AS, Pouta A, Porcu E, Rafnar T, Rice JP, Ring SM, Rivadeneira F, Rudan I, Sala C, Salomaa V, Sanna S, Schlessinger D, Schork NJ, Scuteri A, Segrè AV, Shuldiner AR, Soranzo N, Srinivasan SR, Tammesoo ML, Tikkanen E, Toniolo D, Tsui K, Tryggvadottir L, Tyrer J, Uda M, van Dam RM, van Meurs JB, Vollenweider P, Waeber G, Wareham NJ, Waterworth DM, Weedon MN, Wichmann HE, Wright AF, Young L, Zhai G, Zhuang WV, Bierut LJ, Boyd HA, Crisponi L, Demerath EW, van Duijn CM, Econs MJ, Harris TB, Hunter DJ, Loos RJ, Metspalu A, Montgomery GW, Ridker PM, Spector TD, Streeten EA, Stefansson K, Thorsteinsdottir U, Widen E, Murabito JM, Murray A., D'ADAMO, ADAMO PIO, Cousminer, Diana L, Berry, Diane J, Timpson, Nicholas J, Ang, Wei, Hyppönen, Elina, Widen, Elisabéth, ReproGen Consortium, Early Growth Genetics (EGG) Consortium, Pediatrics, Epidemiology, Internal Medicine, D. L., Cousminer, D. J., Berry, N. J., Timpson, W., Ang, E., Thiering, E. M., Byrne, H. R., Taal, V., Huikari, J. P., Bradfield, M., Kerkhof, M. M., Groen Blokhui, E., Kreiner Moller, M., Marinelli, C., Holst, J. T., Leinonen, J. R. B., Perry, I., Surakka, O., Pietilainen, J., Kettunen, V., Anttila, M., Kaakinen, U., Sovio, A., Pouta, S., Da, V., Lagou, C., Power, I., Prokopenko, D. M., Evan, J. P., Kemp, B., St Pourcain, S., Ring, A., Palotie, E., Kajantie, C., Osmond, T., Lehtimaki, J. S., Viikari, M., Kahonen, N. M., Warrington, S. J., Lye, L. J., Palmer, C. M. T., Tiesler, C., Flexeder, G. W., Montgomery, S. E., Medland, A., Hofman, H., Hakonarson, M., Guxen, M., Bartel, V., Salomaa, J. M., Murabito, J., Kaprio, T. I. A., Sorensen, F., Ballester, H., Bisgaard, D. I., Boomsma, G. H., Koppelman, S. F. A., Grant, V. W. V., Jaddoe, N. G., Martin, J., Heinrich, C. E., Pennell, O. T., Raitakari, J. G., Eriksson, G. D., Smith, E., Hypponen, M. R., Jarvelin, M. I., Mccarthy, S., Ripatti, E., Widen, Adair, L, Ang, W, Atalay, M, van Beijsterveldt, T, Bergen, N, Benke, K, Berry, Dj, Boomsma, Di, Bradfield, Jp, Charoen, P, Coin, L, Cooper, C, Cousminer, Dl, Das, S, Davis, O, Dedoussis, Gv, Elliott, P, Estivill, X, Evans, Dm, Feenstra, B, Flexeder, C, Frayling, T, Freathy, Rm, Gaillard, R, Geller, F, Gillman, M, Grant, Sf, Groen Blokhuis, M, Goh, Lk, Guxens, M, Hakonarson, H, Hattersley, At, Haworth, Cm, Hadley, D, Hedebrand, J, Heinrich, J, Hinney, A, Hirschhorn, Jn, Hocher, B, Holloway, Jw, Holst, C, Hottenga, Jj, Horikoshi, M, Huikari, V, Hypponen, E, Iñiguez, C, Jaddoe, Vw, Jarvelin, Mr, Kaakinen, M, Kilpeläinen, To, Kirin, M, Kowgier, M, Lakka, Hm, Lakka, Ta, Lange, La, Lawlor, Da, Lehtimäki, T, Lewin, A, Lindgren, C, Lindi, V, Maggi, R, Marsh, J, Mccarthy, Mi, Melbye, M, Middeldorp, C, Millwood, I, Mohlke, Kl, Mook Kanamori, Do, Murray, Jc, Nivard, M, Nohr, Ea, Ntalla, I, Oken, E, Ong, Kk, O'Reilly, Pf, Palmer, Lj, Panoutsopoulou, K, Pararajasingham, J, Pearson, Er, Pennell, Ce, Power, C, Price, T, Prokopenko, I, Raitakari, Ot, Rodriguez, A, Salem, Rm, Saw, Sm, Scherag, A, Sebert, S, Siitonen, N, Simell, O, Sørensen, Ti, Sovio, U, Pourcain, B, Strachan, Dp, Sunyer, J, Taal, Hr, Teo, Yy, Thiering, E, Tiesler, C, Timpson, Nj, Uitterlinden, Ag, Valcárcel, B, Warrington, Nm, White, S, Widén, E, Willemsen, G, Wilson, Jf, Yaghootkar, H, Zeggini, E, Elks, Ce, Perry, Jr, Sulem, P, Chasman, Di, Franceschini, N, He, C, Lunetta, Kl, Visser, Ja, Byrne, Em, Gudbjartsson, Df, Esko, T, Koller, Dl, Kutalik, Z, Lin, P, Mangino, M, Marongiu, M, Mcardle, Pf, Smith, Av, Stolk, L, van Wingerden, Sh, Zhao, Jh, Albrecht, E, Corre, T, Ingelsson, E, Hayward, C, Magnusson, Pk, Smith, En, Ulivi, S, Warrington, M, Zgaga, L, Alavere, H, Amin, N, Aspelund, T, Bandinelli, S, Barroso, I, Berenson, G, Bergmann, S, Blackburn, H, Boerwinkle, E, Buring, Je, Busonero, F, Campbell, H, Chanock, Sj, Chen, W, Cornelis, Mc, Couper, D, Coviello, Ad, D'Adamo, ADAMO PIO, de Faire, U, de Geus, Ej, Deloukas, P, Döring, A, Davey Smith, G, Easton, Df, Eiriksdottir, G, Emilsson, V, Eriksson, J, Ferrucci, L, Folsom, Ar, Foroud, T, Garcia, M, Gasparini, Paolo, Gieger, C, Gudnason, V, Hall, P, Hankinson, Se, Ferreli, L, Heath, Ac, Hernandez, Dg, Hofman, A, Hu, Fb, Illig, T, Järvelin, Mr, Johnson, Ad, Karasik, D, Khaw, Kt, Kiel, Dp, Kolcic, I, Kraft, P, Launer, Lj, Laven, J, Li, S, Liu, J, Levy, D, Martin, Ng, Mcardle, Wl, Mooser, V, Murray, S, Nalls, Ma, Navarro, P, Nelis, M, Ness, Ar, Northstone, K, Oostra, Ba, Peacock, M, Palotie, A, Paré, G, Parker, An, Pedersen, Nl, Peltonen, L, Pharoah, P, Polasek, O, Plump, A, Pouta, A, Porcu, E, Rafnar, T, Rice, Jp, Ring, Sm, Rivadeneira, F, Rudan, I, Sala, C, Salomaa, V, Sanna, S, Schlessinger, D, Schork, Nj, Scuteri, A, Segrè, Av, Shuldiner, Ar, Soranzo, N, Srinivasan, Sr, Tammesoo, Ml, Tikkanen, E, Toniolo, D, Tsui, K, Tryggvadottir, L, Tyrer, J, Uda, M, van Dam, Rm, van Meurs, Jb, Vollenweider, P, Waeber, G, Wareham, Nj, Waterworth, Dm, Weedon, Mn, Wichmann, He, Wright, Af, Young, L, Zhai, G, Zhuang, Wv, Bierut, Lj, Boyd, Ha, Crisponi, L, Demerath, Ew, van Duijn, Cm, Econs, Mj, Harris, Tb, Hunter, Dj, Loos, Rj, Metspalu, A, Montgomery, Gw, Ridker, Pm, Spector, Td, Streeten, Ea, Stefansson, K, Thorsteinsdottir, U, Widen, E, Murabito, Jm, Murray, A., Hedebrand, Johannes (Beitragende*r), Hinney, Anke (Beitragende*r), Biological Psychology, Neuroscience Campus Amsterdam - Neurobiology of Mental Health, EMGO+ - Lifestyle, Overweight and Diabetes, Neuroscience Campus Amsterdam - Brain Imaging Technology, Neuroscience Campus Amsterdam - Brain Mechanisms in Health & Disease, Faculteit Medische Wetenschappen/UMCG, Groningen Research Institute of Pharmacy, and Groningen Research Institute for Asthma and COPD (GRIAC)
- Subjects
Male ,Netherlands Twin Register (NTR) ,Genetic Linkage ,Medizin ,Gene Expression ,Genome-wide association study ,VARIANTS ,Body Mass Index ,0302 clinical medicine ,genetic linkage ,Transforming Growth Factor beta ,Neoplasms ,molecular biology ,genetics ,Child ,Genetics (clinical) ,Adiposity ,2. Zero hunger ,0303 health sciences ,adiposity ,Mitogen-Activated Protein Kinase 3 ,Association Studies Articles ,Age Factors ,ACHONDROPLASIA ,General Medicine ,Genome-Wide Association Study ,pubertal height growth ,pubertal timing ,Phenotype ,OBESITY ,Menarche ,body height ,Female ,Signal Transduction ,medicine.medical_specialty ,age factors ,CHROMOSOME 16P11.2 ,Adolescent ,BIRTH ,Quantitative Trait Loci ,030209 endocrinology & metabolism ,Context (language use) ,Biology ,Childhood obesity ,MENARCHE ,Young Adult ,03 medical and health sciences ,AGE ,SDG 3 - Good Health and Well-being ,Prepuberty ,Internal medicine ,Genetics ,medicine ,Humans ,Molecular Biology ,030304 developmental biology ,Sign ,FACTOR RECEPTOR-3 ,MUTATIONS ,Puberty ,ta3121 ,medicine.disease ,Obesity ,Body Height ,Genetic architecture ,Endocrinology ,POPULATION COHORT ,gene expression ,Body mass index ,Follow-Up Studies - Abstract
The pubertal height growth spurt is a distinctive feature of childhood growth reflecting both the central onset of puberty and local growth factors. Although little is known about the underlying genetics, growth variability during puberty correlates with adult risks for hormone-dependent cancer and adverse cardiometabolic health. The only gene so far associated with pubertal height growth, LIN28B, pleiotropically influences childhood growth, puberty and cancer progression, pointing to shared underlying mechanisms. To discover genetic loci influencing pubertal height and growth and to place them in context of overall growth and maturation, we performed genome-wide association meta-analyses in 18 737 European samples utilizing longitudinally collected height measurements. We found significant associations (P
- Published
- 2013
5. Changes in BMI and physical activity from youth to adulthood distinguish normal-weight, metabolically obese adults from those who remain healthy
- Author
-
A. Viitasalo, K. Pahkala, T. Lehtimäki, JSA. Viikari, TH. Tammelin, O. Raitakari, and TO. Kilpeläinen
- Subjects
child ,normal weight ,metabolic risk ,obesity ,physical activity ,BMI ,Diseases of the endocrine glands. Clinical endocrinology ,RC648-665 - Abstract
HighlightsAdults with MONW have a lower BMI during youth until young adulthood, but higher BMI after this than adults with metabolically healthy normal weight. Adults with MONW have a greater decrease in physical activity from youth to adulthood than other adults. Healthy lifestyle is important in the prevention of metabolic disorders, particularly in individuals who are slim in childhood.BackgroundIndividuals with metabolically obese normal-weight (MONW) have higher risk of cardiovascular events than those with obesity but a metabolically healthy status. Etiological factors leading to MONW are not well known. We hypothesized distinct trajectories of changes in BMI and physical activity may modify metabolic risk and distinguish individuals with MONW from those who remain healthy.MethodsWe compared the mean levels of BMI and physical activity at eight time points (1980, 1983, 1986, 1989, 1992, 2001, 2007, 2011) between MONW and healthy normal-weight adults using linear mixed-model analysis. The analyses included 1180 participants of the Cardiovascular Risk in Young Finns study, a population-based study that represents six different age cohorts 3, 6, 9, 12, 15 and 18 years of age at baseline.ResultsIndividuals with adult MONW had significantly lower BMI in childhood and young adulthood, but their BMI increased more than in other adults after this age (p
- Published
- 2022
- Full Text
- View/download PDF
6. Polymorphism in high density lipoprotein paraoxonase gene and risk of acute myocardial infarction in men: prospective nested case-control study Commentary: Causality---the Achilles' heel of observational studies Commentary: How high density lipoprotein protects against heart disease
- Author
-
J. T Salonen, R. Malin, T.-P. Tuomainen, K. Nyyssonen, T. A Lakka, T. Lehtimaki, and M. D Flather
- Subjects
medicine.medical_specialty ,biology ,business.industry ,General Engineering ,Paraoxonase ,Case-control study ,Infarction ,General Medicine ,medicine.disease ,chemistry.chemical_compound ,Endocrinology ,High-density lipoprotein ,chemistry ,Internal medicine ,Nested case-control study ,medicine ,biology.protein ,General Earth and Planetary Sciences ,Myocardial infarction ,Prospective cohort study ,business ,General Environmental Science ,Cohort study - Abstract
Increased lipid peroxidation is associated with accelerated progression of atherosclerosis.1 Paraoxonase (paraoxonase/arylesterase) is an antioxidative enzyme in high density lipoproteins, which protect against coronary disease2 3 It eliminates organophosphorus pesticides but also the products of lipid peroxidation2 4 The mutation at position 54 of the paraoxonase gene in which methionine is substituted by leucine (Met54Leu) has an effect on paraoxonase, increasing its activity; people who have the methionine allele show decreased paraoxonase activity.4 Only a few studies have looked at the association of the Met54Leu polymorphism with coronary disease,2 5 and the findings are inconclusive. Thus we carried out a prospective study of the role of this polymorphism on the risk of acute myocardial infarction in healthy men from eastern Finland. Our prospective nested case-control study was carried out among participants in the Kuopio ischaemic heart disease risk factor study We examined 2682 (83%) of 3235 invited men aged 42, 48, 54 or 60 during 1984-9. Blood samples were collected and risk factors assessed at baseline. A DNA sample was available for this study for 1137 men who were free of coronary disease. We registered and verified all myocardial infarctions—definite or possible—between the baseline examinations and the end of 1995.3 The mean follow up time was 8.5 years, and in patients who had had multiple infarctions we considered only the first. The cases were all 55 men (among the 1137) who had had an infarction by 1995. The controls were drawn from the remaining members of the same cohort. Two controls for each case (110 men) were matched …
- Published
- 1999
7. Mineral resource evaluation based on AHP
- Author
-
K Brahma, B Pal, C Das, T Cichon, J Chen, J Li, T Golosinski, B Ding, C Pelley, J de Ruiter, U Dzharlkaganov, D Bukeikhanov, M Zhanasov, M Heidari, F Rashidinejad, M Heriawan, J Rivoirard, null Syafrizal, S Jalali, M Ataee-pour, W Kawalec, M Mukalay, K Mboko, M Kamulete, S Ngoie, R Prissang, P Hella, T Lehtimki, P Saksa, J Nummela, A Vuento, T Lehtimaki, J Toran˜ o, R Rodr_´guez, J Rivas, A Pelegry, X Li, and Y Zhang
- Published
- 2004
8. T-wave alternans during exercise testing calculated by the method of 'modified moving average': reply
- Author
-
T. Nieminen, T. Lehtimaki, J. Viik, R. Lehtinen, K. Nikus, T. Koobi, K. Niemela, V. Turjanmaa, W. Kaiser, H. Huhtala, R. L. Verrier, H. Huikuri, and M. Kahonen
- Subjects
Cardiology and Cardiovascular Medicine - Published
- 2007
9. Vascular fibrosis and calcification in the hippocampus in aging, Alzheimer disease, and Down syndrome
- Author
-
J., Wegiel, primary, I., Kuchna, additional, T., Wisniewski, additional, Leon, M. de, additional, B., Reisberg, additional, T., Pirttila, additional, T., Kivimaki, additional, and T., Lehtimaki, additional
- Published
- 2002
- Full Text
- View/download PDF
10. 3.4 Endogenous nitric oxide synthase inhibitors modulate the effect of pravastatin on coronary artery reactivity
- Author
-
J KNUUTI, T LEHTIMAKI, T JANATUINEN, I LAAKSO, R VESALALINEN, and R LAAKSONEN
- Subjects
Radiology, Nuclear Medicine and imaging ,Cardiology and Cardiovascular Medicine - Published
- 2001
11. Genome-wide meta-analysis of common variant differences between men and women
- Author
-
Igor Rudan, Nora Franceschini, Sheila Ulivi, Maja Barbalić, Gérard Waeber, Jouke-Jan Hottenga, Jian'an Luan, James F. Wilson, Veikko Salomaa, Jacqueline M. Vink, Juan R. González, Aarno Palotie, Elisabeth Widen, Johan G. Eriksson, Alan F. Wright, Michael Stumvoll, Zoltán Kutalik, Caroline Hayward, Mathieu Lemire, Thomas J. Hudson, Johannes H. Smit, Gonneke Willemsen, Daniela Toniolo, Michael Boehnke, Olli T. Raitakari, Tanguy Corre, Dorret I. Boomsma, Harry Campbell, Stefania Bandinelli, Wiek H. van Gilst, Nigel W. Rayner, Kalliope Panoutsopoulou, Albert Hofman, Vasiliki Lagou, Alexander Teumer, Nicholas G. Martin, Dorine W. Swinkels, Jorma Viikari, Tamara B. Harris, Momoko Horikoshi, Massimo Mangino, Nicole M. Warrington, Kay-Tee Khaw, Adamo Pio D'Adamo, Lambertus A. Kiemeney, Tim D. Spector, Martin den Heijer, Evelin Mihailov, Wei Ang, Samuli Ripatti, Markus Perola, Nicola Pirastu, Ozren Polasek, Mika Kähönen, Albert V. Smith, Anke Tönjes, Michela Traglia, Jing Hua Zhao, Gerjan Navis, Christian Gieger, Stefan Schreiber, André G. Uitterlinden, Eva Albrecht, Inês Barroso, Marja-Liisa Lokki, Andrew C. Heath, Eco J. C. de Geus, H.-Erich Wichmann, Grant W. Montgomery, Armand Valsesia, Marjo-Riitta Järvelin, Reiner Biffar, Krista Fischer, Markku S. Nieminen, Jacques S. Beckmann, Ellen W. Demerath, Fernando Rivadeneira, Yali Xue, Vilmundur Gudnason, Christina Loley, Graham R. S. Ritchie, Giorgia Girotto, Lisette Stolk, Terho Lehtimäki, Annette Peters, Jeanette Erdmann, Lorraine Southam, Vincenza Colonna, So-Youn Shin, Andres Metspalu, Tõnu Esko, Craig E. Pennell, Jaakko Tuomilehto, Vesna Boraska, Nilesh J. Samani, Karola Rehnström, Antonietta Robino, Anne U. Jackson, Irene Mateo Leach, Nicholas J. Wareham, Manolis Kogevinas, Toshiko Tanaka, Heribert Schunkert, Sarah E. Medland, Juha Sinisalo, Wolfgang Hoffmann, John P. Newnham, Peter Vollenweider, Dale R. Nyholt, Lenore J. Launer, Luigi Ferrucci, Brent W. Zanke, Pim van der Harst, Ana Jerončić, Nicole Soranzo, Joyce B. J. van Meurs, Lina Zgaga, Christian Hengstenberg, Timothy M. Frayling, Eleftheria Zeggini, Iris M. Heid, Brenda W.J.H. Penninx, Norman Klopp, Ruth J. F. Loos, Antti Jula, Henry Völzke, John R. B. Perry, V., Boraska, A., Jeroncic, V., Colonna, L., Southam, D. R., Nyholt, N., William Rayner, J. R. B., Perry, D., Toniolo, E., Albrecht, W., Ang, S., Bandinelli, M., Barbalic, I., Barroso, J. S., Beckmann, R., Biffar, D., Boomsma, H., Campbell, T., Corre, J., Erdmann, T., Esko, K., Fischer, N., Franceschini, T. M., Frayling, Girotto, Giorgia, J. R., Gonzalez, T. B., Harri, A. C., Heath, I. M., Heid, W., Hoffmann, A., Hofman, M., Horikoshi, J., Hua Zhao, A. U., Jackson, J. J., Hottenga, A., Jula, M., Kahonen, K. T., Khaw, L. A., Kiemeney, N., Klopp, Z., Kutalik, V., Lagou, L. J., Launer, T., Lehtimaki, M., Lemire, M. L., Lokki, C., Loley, J., Luan, M., Mangino, I., Mateo Leach, S. E., Medland, E., Mihailov, G. W., Montgomery, G., Navi, J., Newnham, M. S., Nieminen, A., Palotie, K., Panoutsopoulou, A., Peter, Pirastu, Nicola, O., Polasek, K., Rehnstrom, S., Ripatti, G. R. S., Ritchie, F., Rivadeneira, Robino, Antonietta, N. J., Samani, S. Y., Shin, J., Sinisalo, J. H., Smit, N., Soranzo, L., Stolk, D. W., Swinkel, T., Tanaka, A., Teumer, A., Tonje, Traglia, Michela, J., Tuomilehto, A., Valsesia, W. H., van Gilst, J. B. J., van Meur, A. V., Smith, J., Viikari, J. M., Vink, G., Waeber, N. M., Warrington, E., Widen, G., Willemsen, A. F., Wright, B. W., Zanke, L., Zgaga, M., Boehnke, D'Adamo, ADAMO PIO, E., de Geu, E. W., Demerath, M., den Heijer, J. G., Eriksson, L., Ferrucci, C., Gieger, V., Gudnason, C., Hayward, C., Hengstenberg, T. J., Hudson, M. R., Jarvelin, M., Kogevina, R. J. F., Loo, N. G., Martin, A., Metspalu, C. E., Pennell, B. W., Penninx, M., Perola, O., Raitakari, V., Salomaa, S., Schreiber, H., Schunkert, T. D., Spector, M., Stumvoll, A. G., Uitterlinden, S., Ulivi, P., van der Harst, P., Vollenweider, H., Volzke, N. J., Wareham, H. E., Wichmann, J. F., Wilson, I., Rudan, Y., Xue, E., Zeggini, Biological Psychology, EMGO+ - Musculoskeletal Health, Medical Research Council (MRC), Psychiatry, Internal medicine, EMGO - Musculoskeletal health, Cardiovascular Centre (CVC), Lifestyle Medicine (LM), Groningen Kidney Center (GKC), Vascular Ageing Programme (VAP), Wellcome Trust Case Control Consortium, Surgery, Epidemiology, Medical Oncology, Internal Medicine, Hematology, Immunology, and Clinical Genetics
- Subjects
Male ,Netherlands Twin Register (NTR) ,sex differences ,Iron metabolism Pathogenesis and modulation of inflammation [IGMD 7] ,Genome-wide association study ,Aetiology, screening and detection [ONCOL 5] ,DISEASE ,meta-analysi ,0302 clinical medicine ,5. Gender equality ,Gene Frequency ,Gender differences ,GWAS ,Genetics (clinical) ,SEX-RATIO ,11 Medical and Health Sciences ,Genetics ,Genetics & Heredity ,0303 health sciences ,Association Studies Articles ,General Medicine ,ASSOCIATION ,male-to-female sex ratio ,meta-analysis ,TIME ,HUMAN SEX-RATIO ,030220 oncology & carcinogenesis ,SIMULATION ,Female ,Wellcome Trust Case Control Consortium ,Life Sciences & Biomedicine ,Sex ratio ,Biochemistry & Molecular Biology ,GENES ,BIRTH ,European Continental Ancestry Group ,Sexism ,Single-nucleotide polymorphism ,Biology ,Human sex ratio ,Polymorphism, Single Nucleotide ,White People ,03 medical and health sciences ,Sex Factors ,Humans ,Sex Ratio ,Allele ,Molecular Biology ,Allele frequency ,Health aging / healthy living Cardiovascular diseases [IGMD 5] ,030304 developmental biology ,Genetic association ,Molecular epidemiology Aetiology, screening and detection [NCEBP 1] ,Science & Technology ,Models, Genetic ,ta3121 ,06 Biological Sciences ,Minor allele frequency ,Genome-Wide Association Study - Abstract
Item does not contain fulltext The male-to-female sex ratio at birth is constant across world populations with an average of 1.06 (106 male to 100 female live births) for populations of European descent. The sex ratio is considered to be affected by numerous biological and environmental factors and to have a heritable component. The aim of this study was to investigate the presence of common allele modest effects at autosomal and chromosome X variants that could explain the observed sex ratio at birth. We conducted a large-scale genome-wide association scan (GWAS) meta-analysis across 51 studies, comprising overall 114 863 individuals (61 094 women and 53 769 men) of European ancestry and 2 623 828 common (minor allele frequency >0.05) single-nucleotide polymorphisms (SNPs). Allele frequencies were compared between men and women for directly-typed and imputed variants within each study. Forward-time simulations for unlinked, neutral, autosomal, common loci were performed under the demographic model for European populations with a fixed sex ratio and a random mating scheme to assess the probability of detecting significant allele frequency differences. We do not detect any genome-wide significant (P < 5 x 10(-8)) common SNP differences between men and women in this well-powered meta-analysis. The simulated data provided results entirely consistent with these findings. This large-scale investigation across approximately 115 000 individuals shows no detectable contribution from common genetic variants to the observed skew in the sex ratio. The absence of sex-specific differences is useful in guiding genetic association study design, for example when using mixed controls for sex-biased traits.
- Published
- 2012
12. Cardiorespiratory fitness and heart rate recovery predict sudden cardiac death independent of ejection fraction.
- Author
-
Hernesniemi JA, Sipilä K, Tikkakoski A, Tynkkynen JT, Mishra PP, Lyytikäinen LP, Nikus K, Nieminen T, Lehtimaki T, and Kähönen M
- Subjects
- Female, Humans, Male, Middle Aged, Prognosis, Prospective Studies, Risk Assessment, Risk Factors, Cardiorespiratory Fitness, Death, Sudden, Cardiac epidemiology, Heart Rate, Stroke Volume
- Abstract
Objective: To evaluate whether cardiorespiratory fitness (CRF) and heart rate recovery (HRR) associate with the risk of sudden cardiac death (SCD) independently of left ventricular ejection fraction (LVEF)., Methods: The Finnish Cardiovascular Study is a prospective clinical study of patients referred to clinical exercise testing in 2001-2008 and follow-up until December 2013. Patients without pacemakers undergoing first maximal or submaximal exercise testing with cycle ergometer were included (n=3776). CRF in metabolic equivalents (METs) was estimated by achieving maximal work level. HRR was defined as the reduction in heart rate 1 min after maximal exertion. Adjudication of SCD was based on death certificates. LVEF was measured for clinical indications in 71.4% of the patients (n=2697)., Results: Population mean age was 55.7 years (SD 13.1; 61% men). 98 SCDs were recorded during a median follow-up of 9.1 years (6.9-10.7). Mean CRF and HRR were 7.7 (SD 2.9) METs and 25 (SD 12) beats/min/min. Both CRF and HRR were associated with the risk of SCD in the entire study population (HR
CRF 0.47 (0.37-0.59), p<0.001 and HRHRR 0.57 (0.48-0.67), p<0.001 with HR estimates corresponding to one SD increase in the exposure variables) and with CRF, HRR and LVEF in the same model (HRCRF 0.60 (0.45-0.79), p<0.001, HRHRR 0.65 (0.51-0.82), p<0.001) or adjusting additionally for all significant risk factors for SCD (LVEF, sex, creatinine level, history of myocardial infarction and atrial fibrillation, corrected QT interval) (HRCRF 0.69 (0.52-0.93), p<0.01, HRHRR 0.74 (0.58-0.95) p=0.02)., Conclusions: CRF and HRR are significantly associated with the risk of SCD regardless of LVEF., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)- Published
- 2020
- Full Text
- View/download PDF
13. The Duke treadmill score with bicycle ergometer: Exercise capacity is the most important predictor of cardiovascular mortality.
- Author
-
Salokari E, Laukkanen JA, Lehtimaki T, Kurl S, Kunutsor S, Zaccardi F, Viik J, Lehtinen R, Nikus K, Kööbi T, Turjanmaa V, Kähönen M, and Nieminen T
- Subjects
- Adult, Aged, Cardiovascular Diseases physiopathology, Cause of Death, Female, Finland epidemiology, Humans, Male, Middle Aged, Predictive Value of Tests, Prognosis, Risk Assessment, Risk Factors, Time Factors, Bicycling, Cardiovascular Diseases diagnosis, Cardiovascular Diseases mortality, Exercise Test, Exercise Tolerance
- Abstract
Background: The Duke treadmill score, a widely used treadmill testing tool, is a weighted index combining exercise time or capacity, maximum ST-segment deviation and exercise-induced angina. No previous studies have investigated whether the Duke treadmill score and its individual components based on bicycle exercise testing predict cardiovascular death., Design: Two populations with a standard bicycle testing were used: 3936 patients referred for exercise testing (2371 men, age 56 ± 13 years) from the Finnish Cardiovascular Study (FINCAVAS) and a population-based sample of 2683 men (age 53 ± 5.1 years) from the Kuopio Ischaemic Heart Disease study (KIHD)., Methods: Cox regression was applied for risk prediction with cardiovascular mortality as the primary endpoint., Results: In FINCAVAS, during a median 6.3-year (interquartile range (IQR) 4.5-8.2) follow-up period, 180 patients (4.6%) experienced cardiovascular mortality. In KIHD, 562 patients (21.0%) died from cardiovascular causes during the median follow-up of 24.1 (IQR 18.0-26.2) years. The Duke treadmill score was associated with cardiovascular mortality in both populations (FINCAVAS, adjusted hazard ratio (HR) 3.15 for highest vs. lowest Duke treadmill score tertile, 95% confidence interval (CI) 1.83-5.42, P < 0.001; KIHD, adjusted HR 1.71, 95% CI 1.34-2.18, P < 0.001). However, after progressive adjustment for the Duke treadmill score components, the score was not associated with cardiovascular mortality in either study population, as exercise capacity in metabolic equivalents of task was the dominant harbinger of poor prognosis., Conclusions: The Duke treadmill score is associated with cardiovascular mortality among patients who have undergone bicycle exercise testing, but metabolic equivalents of task, a component of the Duke treadmill score, proved to be a superior predictor.
- Published
- 2019
- Full Text
- View/download PDF
14. Childhood adiposity, adult adiposity, and the ACE gene insertion/deletion polymorphism: evidence of gene-environment interaction effects on adult blood pressure and hypertension status in adulthood.
- Author
-
Sun C, Ponsonby AL, Carlin JB, Bui M, Magnussen CG, Burns TL, Lehtimaki T, Wardrop NH, Juonala M, Viikari JSA, Venn AJ, Raitakari OT, and Dwyer T
- Subjects
- Adult, Body Mass Index, Child, Genotype, Humans, INDEL Mutation, Polymorphism, Genetic, Prospective Studies, Skinfold Thickness, Waist Circumference, Waist-Hip Ratio, Adiposity, Blood Pressure genetics, Gene-Environment Interaction, Hypertension etiology, Pediatric Obesity complications, Peptidyl-Dipeptidase A genetics
- Abstract
Background: Genetic variants may modify the associations of adiposity measures with blood pressure (BP) and hypertension. The insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene is an attractive candidate., Aims: To examine interaction effects between I/D polymorphism and adiposity measures (BMI, waist circumference, waist-to-hip ratio, and skinfold thickness) during childhood and adulthood in relation to adult BP and hypertension., Methods: Data were available for 4835 participants from three prospective cohort studies. Multivariable linear regression models for adult SBP and DBP, and multivariable logistic regression models for hypertension were fit that included interaction effects between child or adult adiposity and I/D polymorphism., Results: Evidence for interaction effects on BP/hypertension were found across the three studies. Compared with childhood measures, the effect modification appeared to be more consistent when using adult adiposity. In particular, the adverse effects of greater adult waist circumference on increasing adult SBP and DBP appeared to be larger among carriers of ACE DD (or GG) [adjusted linear regression coefficients 0.26, 95% CI (0.21-0.31) and 0.28 (0.24-0.32) for SBP and DBP, respectively] and ID (or AG) genotypes [0.25 (0.21-0.29) and 0.25 (0.21-0.28), respectively], whereas those with II (or AA) genotypes had smaller effects [0.15 (0.09-0.21) and 0.19 (0.13-0.23)]., Conclusion: ACE genetic variation may modify the effect of adult adiposity on increasing BP and risk of hypertension in adulthood. Individuals with ACE DD (or GG) and/or ID (or AG) genotypes, compared with those with II (or AA) genotype, appear more vulnerable to the impact of excess adiposity.
- Published
- 2018
- Full Text
- View/download PDF
15. Nine loci for ocular axial length identified through genome-wide association studies, including shared loci with refractive error.
- Author
-
Cheng CY, Schache M, Ikram MK, Young TL, Guggenheim JA, Vitart V, MacGregor S, Verhoeven VJ, Barathi VA, Liao J, Hysi PG, Bailey-Wilson JE, St Pourcain B, Kemp JP, McMahon G, Timpson NJ, Evans DM, Montgomery GW, Mishra A, Wang YX, Wang JJ, Rochtchina E, Polasek O, Wright AF, Amin N, van Leeuwen EM, Wilson JF, Pennell CE, van Duijn CM, de Jong PT, Vingerling JR, Zhou X, Chen P, Li R, Tay WT, Zheng Y, Chew M, Burdon KP, Craig JE, Iyengar SK, Igo RP Jr, Lass JH Jr, Chew EY, Haller T, Mihailov E, Metspalu A, Wedenoja J, Simpson CL, Wojciechowski R, Höhn R, Mirshahi A, Zeller T, Pfeiffer N, Lackner KJ, Bettecken T, Meitinger T, Oexle K, Pirastu M, Portas L, Nag A, Williams KM, Yonova-Doing E, Klein R, Klein BE, Hosseini SM, Paterson AD, Makela KM, Lehtimaki T, Kahonen M, Raitakari O, Yoshimura N, Matsuda F, Chen LJ, Pang CP, Yip SP, Yap MK, Meguro A, Mizuki N, Inoko H, Foster PJ, Zhao JH, Vithana E, Tai ES, Fan Q, Xu L, Campbell H, Fleck B, Rudan I, Aung T, Hofman A, Uitterlinden AG, Bencic G, Khor CC, Forward H, Pärssinen O, Mitchell P, Rivadeneira F, Hewitt AW, Williams C, Oostra BA, Teo YY, Hammond CJ, Stambolian D, Mackey DA, Klaver CC, Wong TY, Saw SM, and Baird PN
- Subjects
- Adolescent, Adult, Aged, Asian People, Axial Length, Eye pathology, Eye Proteins metabolism, Female, Gene Expression, Genome-Wide Association Study, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Refractive Errors ethnology, Refractive Errors pathology, Signal Transduction, White People, Axial Length, Eye metabolism, Eye Proteins genetics, Genetic Loci, Genetic Predisposition to Disease, Refractive Errors genetics
- Abstract
Refractive errors are common eye disorders of public health importance worldwide. Ocular axial length (AL) is the major determinant of refraction and thus of myopia and hyperopia. We conducted a meta-analysis of genome-wide association studies for AL, combining 12,531 Europeans and 8,216 Asians. We identified eight genome-wide significant loci for AL (RSPO1, C3orf26, LAMA2, GJD2, ZNRF3, CD55, MIP, and ALPPL2) and confirmed one previously reported AL locus (ZC3H11B). Of the nine loci, five (LAMA2, GJD2, CD55, ALPPL2, and ZC3H11B) were associated with refraction in 18 independent cohorts (n = 23,591). Differential gene expression was observed for these loci in minus-lens-induced myopia mouse experiments and human ocular tissues. Two of the AL genes, RSPO1 and ZNRF3, are involved in Wnt signaling, a pathway playing a major role in the regulation of eyeball size. This study provides evidence of shared genes between AL and refraction, but importantly also suggests that these traits may have unique pathways., (Copyright © 2013 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
16. Myocardial infarction induces early increased remote ADAM8 expression of rat hearts after cardiac arrest.
- Author
-
Vuohelainen V, Raitoharju E, Levula M, Lehtimaki T, Pelto-Huikko M, Honkanen T, Huovila A, Paavonen T, Tarkka M, and Mennander A
- Subjects
- ADAM Proteins genetics, Animals, Coronary Vessels pathology, Gene Expression, Heart Arrest pathology, Immunohistochemistry, Myocardial Infarction pathology, Myocardium pathology, Rats, Rats, Inbred F344, Real-Time Polymerase Chain Reaction, Reperfusion Injury pathology, Transplantation, Heterotopic, Ventricular Function, Left, ADAM Proteins metabolism, Coronary Vessels metabolism, Heart Arrest metabolism, Heart Transplantation, Myocardial Infarction metabolism, Myocardium metabolism, Reperfusion Injury metabolism, Ventricular Remodeling
- Abstract
Background: A disintegrin and metalloproteinase-8 (ADAM8) is a potential surrogate of inflammation which has recently been associated with myocardial infarction. We evaluated in a rat cardiac transplantation model whether ischemia-reperfusion injury alone (IRI) or with early regional myocardial infarction (MI) would suffice to induce inflammatory myocardial remodeling and ADAM8 expression., Material and Methods: Isogenic heterotopic cardiac transplantation after cardiac arrest was performed to 48 Fischer 344 rats to induce ischemia-reperfusion injury (IRI), of which 27 rats also underwent ligation of the left anterior coronary artery (LAD) of the heart to yield MI. Histology was performed at 0.5, 24 and 48 h after transplantation. ADAM8 was evaluated by qRT-PCR after graft harvesting., Results: After 0.5 and 48 h respectively, edematous intramyocardial artery nuclei and periadventitial inflammation were more prominent in MI after transplantation, as compared with IRI alone and Controls (57.0 vs 40.0 and 5.0; 1.9 vs 1.1 and 0.9, point score units, p < 0.05, respectively). The expression of ADAM-8 was increased in MI as compared with Controls (1.9 vs 1.0, 1.9 fold increase) at 48 h. In grafts with MI, ADAM8 was localized using immunohistochemistry to the vicinity of the area corresponding to the developing infarction as well as in intramyocardial arteries remote to the infarction area., Conclusions: Remote histopathological changes of ischemic cardiac grafts are associated with increased expression of ADAM8 thus emphasizing a global myocardial impact of MI.
- Published
- 2011
- Full Text
- View/download PDF
17. A disintegrin and metalloprotease -8 and -15 and susceptibility for ascending aortic dissection.
- Author
-
Levula M, Paavonen T, Valo T, Pelto-Huikko M, Laaksonen R, Kahonen M, Huovila A, Lehtimaki T, Tarkka M, and Mennander AA
- Subjects
- ADAM Proteins genetics, Aged, Aortic Dissection pathology, Aortic Dissection surgery, Aorta pathology, Aorta surgery, Aortic Aneurysm pathology, Aortic Aneurysm surgery, B-Lymphocytes pathology, Down-Regulation, Female, Humans, Male, Membrane Proteins genetics, Middle Aged, Real-Time Polymerase Chain Reaction, Transcription, Genetic, ADAM Proteins metabolism, Aortic Dissection enzymology, Aorta enzymology, Aortic Aneurysm enzymology, Membrane Proteins metabolism
- Abstract
BACKGROUND. Dilatation of the ascending aorta (AA) is affected by extra-cellular matrix modifications and inflammation. A disintegrin and metalloproteases (ADAMs) may reveal differences between AA and ascending aortic dissection (AD). We characterized the inflammatory histology of AD and AA and examined the role of ADAM8 and -15 in these diseases. MATERIAL AND METHODS. Aortic wall histology and immunohistochemistry for leukocytes, T- and B-lymphocytes, plasma cells, macrophages, endothelial cells, smooth muscle cells, cell proliferation, elastase and Van-Gieson-staining were performed to 40 consecutive patients that underwent surgery for AA or AD. The expressions of ADAM8 and -15 mRNA and proteins were evaluated using QRT-PCR and immunohistochemistry. RESULTS. Thirty-four patients were enrolled, of which 29 had AA and five had AD of the ascending aorta. B-cells throughout the aortic wall and intimal plasma cells were more numerous during AD as compared with AA (p < 0.05). The gene expressions for ADAM8 and -15 were notably lower in AA as compared with AD. The median for down-regulation of ADAM8 and -15 in AA was -2.7 and -1.8, respectively. ADAM8 and -15 were mainly found in the media layer in patients with AD. Two of the patients with AA and increased ADAMs developed AD of the remaining aorta. CONCLUSIONS. The involvement of ADAM8 and -15 together with inflammation consisting of B-cells may indicate active remodelling of the aortic wall leading to AD.
- Published
- 2011
- Full Text
- View/download PDF
18. Associations of apolipoprotein E gene with ischemic stroke and intracranial atherosclerosis.
- Author
-
Abboud S, Viiri LE, Lütjohann D, Goebeler S, Luoto T, Friedrichs S, Desfontaines P, Gazagnes MD, Laloux P, Peeters A, Seeldrayers P, Lehtimaki T, Karhunen P, Pandolfo M, and Laaksonen R
- Subjects
- Aged, Autopsy, Brain Ischemia pathology, Case-Control Studies, Genetic Variation, Humans, Intracranial Arteriosclerosis pathology, Male, Middle Aged, Stroke pathology, Apolipoproteins E genetics, Brain Ischemia genetics, Intracranial Arteriosclerosis genetics, Polymorphism, Single Nucleotide genetics, Promoter Regions, Genetic genetics, Stroke genetics
- Abstract
The apolipoprotein E (APOE) epsilon4 allele is associated with elevated cholesterol and risk of atherosclerosis. However, its role in ischemic stroke (IS) remains controversial. We investigated a possible link between IS or the severity of intracranial atherosclerosis and the APOE promoter polymorphisms -219G/T and +113G/C, involved in regulating APOE transcription. We genotyped subjects from a multicentric Belgian case-control study, including 237 middle-aged patients with IS due to small- or large-vessel atherosclerotic stroke and 326 ethnicity- and gender-matched controls and a Finnish autopsy series of 1004 non-stroke cases, who had received a quantitative score of atherosclerosis in the circle of Willis. The APOE epsilon4+ genotype did not associate with IS, but was related to more severe intracranial atherosclerosis score in men (5.4 vs 4.6, P=0.044). Within the most common APOE epsilon3/epsilon3 genotype group, the risk of IS associated with the G-allele of the tightly linked -219G/T (OR=6.2; 95% CI: 1.6-24.3, P=0.009) and +113G/C (OR=7.1; 95% CI: 1.7-29.9, P=0.007) promoter polymorphisms. There was no difference in the severity of intracranial atherosclerosis between -219G/G genotype carriers and non-carriers. This study suggests a multifaceted role of apoE on the risk of cerebrovascular diseases. The APOE epsilon4+ genotype did not predict the risk of IS but was associated with severity of subclinical intracranial atherosclerosis in men on the autopsy study. In contrast, the promoter variants were significant predictors of IS, suggesting that quantitative rather than qualitative variation of apoE is related to IS.
- Published
- 2008
- Full Text
- View/download PDF
19. Association of the apolipoprotein E gene, its promoter polymorphisms and haplotypes with depressive symptoms. The Cardiovascular Risk in Young Finns Study.
- Author
-
Elovainio M, Puttonen S, Pulkki-Råback L, Kivimaki M, Viiri LE, Lehtimaki T, Karhunen P, Viikari J, Raitakari OT, and Keltikangas-Jarvinen L
- Subjects
- Adult, Analysis of Variance, Cohort Studies, Community Health Planning, Female, Finland epidemiology, Humans, Male, Retrospective Studies, Risk Factors, Young Adult, Apolipoproteins E genetics, Depression genetics, Genetic Predisposition to Disease, Haplotypes genetics, Polymorphism, Genetic genetics, Promoter Regions, Genetic genetics
- Abstract
Objectives: Evidence on apolipoprotein E (APOE) gene as a vulnerability factor for depression is mixed. Polymorphisms of the APOE gene regulatory region may serve as additional explanatory factors, as they help in explaining variation of depressive symptoms within the APOE epsilon2/epsilon3/epsilon4 genotype groups. In this study, the associations of the APOE gene promoter polymorphisms -219G/T and +113G/C and their haplotypes with depressive symptoms were examined., Methods: The data is from a subpopulation of 660 young adults (24-39 years old) of the ongoing population-based Cardiovascular Risk in Young Finns Study. Depressive symptoms were assessed by a revised version of Beck's Depression Inventory. Clinical screening assessed lipid levels and other known physiological and behavioral risk factors for depressive symptoms., Results: The APOE epsilon4 allele was not related to depressive symptoms. Similarly, no statistically significant associations were found between the APOE gene promoter -219G/T and +113G/C polymorphisms and depressive symptoms. Within theAPOE epsilon3/epsilon3 genotype subgroup (n = 373), carriers of both -219G/+113C and -219T/+113G haplotypes (GC/TG) had higher depressive symptoms compared to noncarriers of these haplotypes (2.52 vs. 1.98; p = 0.002). This relationship persisted after separate adjustments for various risk factors including sex, age, LDL cholesterol, HDL cholesterol, triglycerides, total cholesterol, C-reactive protein, systolic blood pressure, body mass index and alcohol consumption., Conclusions: Our results suggest that the APOE gene does not predispose carriers to depressive symptoms among healthy young adults. However, the promoter haplotype GC/TG may elevate the risk of depressive symptoms., (Copyright 2008 S. Karger AG, Basel.)
- Published
- 2008
- Full Text
- View/download PDF
20. Proprotein convertase subtilisin/kexin type 9 (PCSK9) gene is a risk factor of large-vessel atherosclerosis stroke.
- Author
-
Abboud S, Karhunen PJ, Lütjohann D, Goebeler S, Luoto T, Friedrichs S, Lehtimaki T, Pandolfo M, and Laaksonen R
- Subjects
- Aged, Case-Control Studies, Cerebral Arteries pathology, Female, Humans, Male, Middle Aged, Polymorphism, Genetic, Proprotein Convertase 9, Proprotein Convertases, Risk, Risk Factors, Atherosclerosis genetics, Genetic Predisposition to Disease, Genetic Variation, Serine Endopeptidases genetics, Serine Endopeptidases physiology, Stroke genetics
- Abstract
Background/purpose: Genetic variation in proprotein convertase subtilisin/kexin type 9 (PCSK9) gene has been recently identified as an important determinant of plasma LDL-cholesterol and severity of coronary heart disease. We studied whether the PCSK9 gene is linked to the risk of ischemic stroke (IS) and with the development of intracranial atherosclerosis., Methods/results: The pivotal E670G polymorphism, tagging an important haplotype of the PCSK9 gene, was genotyped in two independent studies. The Belgium Stroke Study included 237 middle aged (45-60) Belgian patients, with small-vessel occlusion (SVO) and large-vessel atherosclerosis stroke (LVA), and 326 gender and ethnicity matched controls (>60 yrs) without a history of stroke. In multivariate analysis the minor allele (G) carriers appeared as a significant predictor of LVA (OR = 3.52, 95% CI 1.25-9.85; p = 0.017). In a Finnish crossectional population based consecutive autopsy series of 604 males and females (mean age 62.5 years), G-allele carriers tended to have more severe allele copy number-dependent (p = 0.095) atherosclerosis in the circle of Willis and in its branches., Conclusion: Our findings in this unique combination of clinical and autopsy data, provide evidence that PCSK9 gene associates with the risk of LVA stroke subtype, and suggest that the risk is mediated by the severity of intracranial atherosclerosis.
- Published
- 2007
- Full Text
- View/download PDF
21. Osteopontin levels are associated with cholesterol synthesis markers in mildly hypercholesterolaemic patients.
- Author
-
Luomala M, Päivä H, Thelen K, Laaksonen R, Saarela M, Mattila K, Lütjohann D, and Lehtimaki T
- Subjects
- Adult, Aged, Analysis of Variance, Apolipoprotein A-I blood, Apolipoproteins B blood, Biomarkers blood, Cholesterol biosynthesis, Cholesterol, HDL blood, Cholesterol, LDL blood, Enzyme-Linked Immunosorbent Assay, Female, Finland, Humans, Hydroxycholesterols blood, Hypercholesterolemia metabolism, Male, Middle Aged, Muscle, Skeletal metabolism, Phytosterols blood, Severity of Illness Index, Sex Factors, Triglycerides blood, Cholesterol blood, Hypercholesterolemia blood, Osteopontin blood
- Abstract
Objective: Atherosclerotic lesions are characterized by an accumulation of inflammatory cells and lipids. Osteopontin (OPN) is a cell-binding phosphoprotein, and it seems to promote the development of atherosclerosis. The purpose of our study was to find out whether plasma levels of OPN are associated with cholesterol metabolites in plasma or tissues., Methods and Results: Forty-three normal or mildly hypercholesterolaemic subjects, aged 31 to 69, were studied. The plasma level of OPN correlated negatively with muscle lathosterol (r = -0.52, P < 0.0001) and with the muscle lathosterol to muscle cholesterol ratio (r = -0.48, P = 0.001). Lathosterol concentrations in muscle (P = 0.003) and in relation to cholesterol (P = 0.005) were also significantly different among the OPN tertiles. OPN correlated negatively and significantly with muscle lathosterol in men (r = -0.58, P = 0.001, n = 29) but not in women (r = -0.21, P = 0.48, n = 14). Correspondingly, it also correlated negatively and significantly with the muscle lathosterol to muscle cholesterol ratio (r = -0.60, P = 0.001) in men but not in women (r = -0.13, P = 0.65). Plasma levels of OPN had a non-significant inverse correlation with plasma lathosterol and the plasma lathosterol to plasma cholesterol ratio. Plasma OPN concentrations were not related to plant sterols, cholesterol and 27-hydroxycholesterol., Conclusions: Tissue markers of cholesterol synthesis were related to plasma OPN, particularly in men. This suggests that there is interplay between OPN and cholesterol metabolism in human cells.
- Published
- 2007
- Full Text
- View/download PDF
22. No association between the brain-derived neurotrophic factor 196 G>A or 270 C>T polymorphisms and Alzheimer's or Parkinson's disease.
- Author
-
Saarela MS, Lehtimaki T, Rinne JO, Huhtala H, Rontu R, Hervonen A, Roytta M, Ahonen JP, and Mattila KM
- Subjects
- Aged, Apolipoproteins E genetics, Female, Gene Frequency, Genetic Predisposition to Disease, Genotype, Humans, Male, Polymerase Chain Reaction, Alzheimer Disease genetics, Brain-Derived Neurotrophic Factor genetics, Parkinson Disease genetics, Polymorphism, Genetic
- Abstract
The brain-derived neurotrophic factor (BDNF) promotes survival, differentiation and maintenance of neurons in the central nervous system. BDNF 196 G>A and 270 C>T polymorphisms have previously been associated with Alzheimer's disease (AD) and with Parkinson's disease (PD). To study the role of BDNF 196 G>A and 270 C>T polymorphisms in Finnish AD and PD patients we genotyped BDNF 196 G>A and 270 C>T polymorphisms in 97 sporadic AD patients, 52 PD patients and 101 control subjects with polymerase chain reaction. No associations were found between the genotypes studied and AD or PD in Finnish patients. Moreover, no interaction between either BDNF polymorphism and the epsilon 4 allele of apolipoprotein E was found. In conclusion, it seems that the BDNF gene does not contribute significantly to the risk of AD or PD in Finnish patients.
- Published
- 2006
23. Vascular fibrosis and calcification in the hippocampus in aging, Alzheimer disease, and Down syndrome.
- Author
-
Wegiel J, Kuchna I, Wisniewski T, de Leon MJ, Reisberg B, Pirttila T, Kivimaki T, and Lehtimaki T
- Subjects
- Adult, Aged, Aged, 80 and over, Alzheimer Disease pathology, Blood Vessels pathology, Brain Diseases physiopathology, Calcinosis physiopathology, Disease Progression, Down Syndrome pathology, Fibrosis, Hippocampus physiopathology, Humans, Middle Aged, Aging physiology, Alzheimer Disease complications, Brain Diseases etiology, Calcinosis etiology, Down Syndrome complications, Hippocampus blood supply
- Abstract
Study of the hippocampal formation of 82 subjects, including 25 control subjects from 33 to 83 years of age, 34 subjects with Alzheimer disease (AD) from 65 to 89 years of age, and 23 subjects with Down syndrome (DS) from 33 to 72 years of age, revealed hippocampal vasculopathy with fibrosis and calcification (VFC) in 40% of control, 59% of AD, and 4% of DS subjects. VFC starts in the precapillaries/capillaries in the molecular layer of the dentate gyrus (DG) and expands to the granule cell and polymorphic cell layer of the DG, and to the stratum lacunosum/molecular in the CA1 sector. Vasculopathy spreads from the tail to the body and, in a few cases, to the head of the hippocampal formation. Light and electron microscopy reveal thickening of the vascular wall with fibrosis, calcification, and enforcement of the astrocyte interface with vessels with anchorage densities associated with hemidesmosome-like structures. In moderately and severely affected cases, fragmentation and removal of calcified and occluded vessels result in local reduction of vascular network. In two AD subjects, severe vascular calcification extending from the tail to the head of the hippocampal formation was associated with loss of almost all neurons in the CA1 sector and in the subiculum proper, corresponding to hippocampal sclerosis. The topography of affected vessels and the patterns of neuronal loss reflect the middle hippocampal artery distribution with its precapillary/capillary network. The similar prevalence of vasculopathy in the AD group and in the age-matched control group, and the presence of hippocampal VFC in only one subject in the DS cohort, 96% of which is affected by Alzheimer-type pathology, oppose the link between AD and this form of vasculopathy. However, severe VFC affects the pattern of AD pathology locally by deletion of neurofibrillary degeneration and beta-amyloidosis in the CA1 sector, subiculum proper, and the molecular layer of the dentate gyrus. Hippocampal VFC appears to be a form of vascular pathology with a unique predilection for the middle hippocampal artery and corresponding capillary network, which results in patchy neuronal loss in moderately affected subjects and in almost total neuronal loss in the area of impaired blood supply in severely affected subjects. These observations suggest an etiologic link between hippocampal VFC and hippocampal sclerosis.
- Published
- 2002
- Full Text
- View/download PDF
24. Apolipoprotein E E4 allele and risk of dementia.
- Author
-
Pirttila T, Lehtimaki T, Nikkari T, Frey H, and Mattila K
- Subjects
- Humans, Alzheimer Disease genetics, Apolipoproteins E genetics, Dementia, Vascular genetics
- Published
- 1995
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.