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Christian Ehnholm

Bio: Christian Ehnholm is an academic researcher from University of Helsinki. The author has contributed to research in topics: Cholesterol & Phospholipid transfer protein. The author has an hindex of 70, co-authored 243 publications receiving 16443 citations. Previous affiliations of Christian Ehnholm include University of Tampere & National Institutes of Health.


Papers
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Journal ArticleDOI
TL;DR: It is concluded that high serum total cholesterol may be an independent risk factor for AD and some of the effect of the apoE σ4 allele on risk of AD might be mediated through high serum cholesterol.
Abstract: The σ4 allele of the apolipoprotein E (apoE) is associated with Alzheimer’s disease (AD) and also with elevated serum total cholesterol and low-density lipoprotein levels. However, the interrelationsh

636 citations

Journal ArticleDOI
TL;DR: The results of this prospective population-based study do not support the hypotheses that serum homocysteine or Lp(a) are risk factors for atherosclerotic disease and may be due to the exceptionally low gene frequency predisposing to homocysteinemia in Finland.

539 citations

Journal ArticleDOI
TL;DR: Metabolic syndrome components identify higher CVD risk in individuals with type 2 diabetes, so the absolute benefits of fenofibrate are likely to be greater when metabolic syndrome features are present.
Abstract: OBJECTIVE—We explored whether cardiovascular disease (CVD) risk and the effects of fenofibrate differed in subjects with and without metabolic syndrome and according to various features of metabolic syndrome defined by the Adult Treatment Panel III (ATP III) in subjects with type 2 diabetes in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study. RESEARCH DESIGN AND METHODS—The prevalence of metabolic syndrome and its features was calculated. Cox proportional models adjusted for age, sex, CVD status, and baseline A1C levels were used to determine the independent contributions of metabolic syndrome features to total CVD event rates and the effects of fenofibrate. RESULTS—More than 80% of FIELD participants met the ATP III criteria for metabolic syndrome. Each ATP III feature of metabolic syndrome, apart from increased waist circumference, increased the absolute risk of CVD events over 5 years by at least 3%. Those with marked dyslipidemia (elevated triglycerides ≥2.3 mmol/l and low HDL cholesterol) were at the highest risk of CVD (17.8% over 5 years). Fenofibrate significantly reduced CVD events in those with low HDL cholesterol or hypertension. The largest effect of fenofibrate to reduce CVD risk was observed in subjects with marked dyslipidemia in whom a 27% relative risk reduction (95% CI 9–42, P = 0.005; number needed to treat = 23) was observed. Subjects with no prior CVD had greater risk reductions than the entire group. CONCLUSIONS—Metabolic syndrome components identify higher CVD risk in individuals with type 2 diabetes, so the absolute benefits of fenofibrate are likely to be greater when metabolic syndrome features are present. The highest risk and greatest benefits of fenofibrate are seen among those with marked hypertriglyceridemia.

492 citations

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TL;DR: The data suggest that the apoE gene locus may be one factor responsible for the high LDL cholesterol concentrations in the Finnish population.

428 citations

Journal ArticleDOI
TL;DR: It is concluded that in the Helsinki Heart Study cohort the serum Lp(a) level was not a predictor of future coronary events.

365 citations


Cited by
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Journal ArticleDOI
TL;DR: The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations, permitting the differentiation of six stages.
Abstract: Eighty-three brains obtained at autopsy from nondemented and demented individuals were examined for extracellular amyloid deposits and intraneuronal neurofibrillary changes. The distribution pattern and packing density of amyloid deposits turned out to be of limited significance for differentiation of neuropathological stages. Neurofibrillary changes occurred in the form of neuritic plaques, neurofibrillary tangles and neuropil threads. The distribution of neuritic plaques varied widely not only within architectonic units but also from one individual to another. Neurofibrillary tangles and neuropil threads, in contrast, exhibited a characteristic distribution pattern permitting the differentiation of six stages. The first two stages were characterized by an either mild or severe alteration of the transentorhinal layer Pre-alpha (transentorhinal stages I-II). The two forms of limbic stages (stages III-IV) were marked by a conspicuous affection of layer Pre-alpha in both transentorhinal region and proper entorhinal cortex. In addition, there was mild involvement of the first Ammon's horn sector. The hallmark of the two isocortical stages (stages V-VI) was the destruction of virtually all isocortical association areas. The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations.

13,699 citations

Journal Article
TL;DR: For the next few weeks the course is going to be exploring a field that’s actually older than classical population genetics, although the approach it’ll be taking to it involves the use of population genetic machinery.
Abstract: So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

9,847 citations

Journal ArticleDOI
John W. Belmont1, Andrew Boudreau, Suzanne M. Leal1, Paul Hardenbol  +229 moreInstitutions (40)
27 Oct 2005
TL;DR: A public database of common variation in the human genome: more than one million single nucleotide polymorphisms for which accurate and complete genotypes have been obtained in 269 DNA samples from four populations, including ten 500-kilobase regions in which essentially all information about common DNA variation has been extracted.
Abstract: Inherited genetic variation has a critical but as yet largely uncharacterized role in human disease. Here we report a public database of common variation in the human genome: more than one million single nucleotide polymorphisms (SNPs) for which accurate and complete genotypes have been obtained in 269 DNA samples from four populations, including ten 500-kilobase regions in which essentially all information about common DNA variation has been extracted. These data document the generality of recombination hotspots, a block-like structure of linkage disequilibrium and low haplotype diversity, leading to substantial correlations of SNPs with many of their neighbours. We show how the HapMap resource can guide the design and analysis of genetic association studies, shed light on structural variation and recombination, and identify loci that may have been subject to natural selection during human evolution.

5,479 citations

Journal ArticleDOI
François Mach, Colin Baigent, Alberico L. Catapano, Konstantinos C. Koskinas1, Manuela Casula, Lina Badimon1, M. John Chapman, Guy De Backer, Victoria Delgado, Brian A. Ference, Ian D. Graham, Alison Halliday, Ulf Landmesser, Borislava Mihaylova, Terje R. Pedersen, Gabriele Riccardi, Dimitrios J. Richter, Marc S. Sabatine, Marja-Riitta Taskinen, Lale Tokgozoglu, Olov Wiklund, Christian Mueller, Heinz Drexel, Victor Aboyans, Alberto Corsini, Wolfram Doehner, Michel Farnier, Bruna Gigante, Meral Kayıkçıoğlu, Goran Krstacic, Ekaterini Lambrinou, Basil S. Lewis, Josep Masip, Philippe Moulin, Steffen E. Petersen, Anna Sonia Petronio, Massimo F Piepoli, Xavier Pintó, Lorenz Räber, Kausik K. Ray, Željko Reiner, Walter F Riesen, Marco Roffi, Jean-Paul Schmid, Evgeny Shlyakhto, Iain A. Simpson, Erik S.G. Stroes, Isabella Sudano, Alexandros D Tselepis, Margus Viigimaa, Cecile Vindis, Alexander Vonbank, Michal Vrablik, Mislav Vrsalovic, José Luis Zamorano, Jean-Philippe Collet, Stephan Windecker, Veronica Dean, Donna Fitzsimons, Chris P Gale, Diederick E. Grobbee, Sigrun Halvorsen, Gerhard Hindricks, Bernard Iung, Peter Jüni, Hugo A. Katus, Christophe Leclercq, Maddalena Lettino, Béla Merkely, Miguel Sousa-Uva, Rhian M. Touyz, Djamaleddine Nibouche, Parounak H. Zelveian, Peter Siostrzonek, Ruslan Najafov, Philippe van de Borne, Belma Pojskic, Arman Postadzhiyan, Lambros Kypris, Jindřich Špinar, Mogens Lytken Larsen, Hesham Salah Eldin, Timo E. Strandberg, Jean Ferrières, Rusudan Agladze, Ulrich Laufs, Loukianos S. Rallidis, Laszlo Bajnok, Thorbjorn Gudjonsson, Vincent Maher, Yaakov Henkin, Michele Massimo Gulizia, Aisulu Mussagaliyeva, Gani Bajraktari, Alina Kerimkulova, Gustavs Latkovskis, Omar Hamoui, Rimvydas Šlapikas, Laurent Visser, P. Dingli, Victoria Ivanov, Aneta Boskovic, Mbarek Nazzi, Frank L.J. Visseren, Irena Mitevska, Kjetil Retterstøl, Piotr Jankowski, Ricardo Fontes-Carvalho, Dan Gaita, Marat V. Ezhov, Marina Foscoli, Vojislav Giga, Daniel Pella, Zlatko Fras, Leopoldo Pérez de Isla, Emil Hagström, Roger Lehmann, Leila Abid, Oner Ozdogan, Olena Mitchenko, Riyaz S. Patel 

4,069 citations