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Search Results: 1 - 10 of 117935 matches for " Bastiaan T. Heijmans "
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Periconceptional Maternal Folic Acid Use of 400 μg per Day Is Related to Increased Methylation of the IGF2 Gene in the Very Young Child
Régine P. Steegers-Theunissen,Sylvia A. Obermann-Borst,Dennis Kremer,Jan Lindemans,Cissy Siebel,Eric A. Steegers,P. Eline Slagboom,Bastiaan T. Heijmans
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0007845
Abstract: Countries worldwide recommend women planning pregnancy to use daily 400 μg of synthetic folic acid in the periconceptional period to prevent birth defects in children. The underlying mechanisms of this preventive effect are not clear, however, epigenetic modulation of growth processes by folic acid is hypothesized. Here, we investigated whether periconceptional maternal folic acid use and markers of global DNA methylation potential (S-adenosylmethionine and S-adenosylhomocysteine blood levels) in mothers and children affect methylation of the insulin-like growth factor 2 gene differentially methylation region (IGF2 DMR) in the child. Moreover, we tested whether the methylation of the IGF2 DMR was independently associated with birth weight.
Systematic Testing of Literature Reported Genetic Variation Associated with Coronary Restenosis: Results of the GENDER Study
Jeffrey J. W. Verschuren, Stella Trompet, Iris Postmus, M. Lourdes Sampietro, Bastiaan T. Heijmans, Jeanine J. Houwing-Duistermaat, P. Eline Slagboom, J. Wouter Jukema
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0042401
Abstract: Background Coronary restenosis after percutaneous coronary intervention still remains a significant problem, despite all medical advances. Unraveling the mechanisms leading to restenosis development remains challenging. Many studies have identified genetic markers associated with restenosis, but consistent replication of the reported markers is scarce. The aim of the current study was to analyze the joined effect of previously in literature reported candidate genes for restenosis in the GENetic DEterminants of Restenosis (GENDER) databank. Methodology/Principal Findings Candidate genes were selected using a MEDLINE search including the terms ‘genetic polymorphism’ and ‘coronary restenosis’. The final set included 36 genes. Subsequently, all single nucleotide polymorphisms (SNPs) in the genomic region of these genes were analyzed in GENDER using set-based analysis in PLINK. The GENDER databank contains genotypic data of 2,571,586 SNPs of 295 cases with restenosis and 571 matched controls. The set, including all 36 literature reported genes, was, indeed, significantly associated with restenosis, p = 0.024 in the GENDER study. Subsequent analyses of the individual genes demonstrated that the observed association of the complete set was determined by 6 of the 36 genes. Conclusion Despite overt inconsistencies in literature, with regard to individual candidate gene studies, this is the first study demonstrating that the joint effect of all these genes together, indeed, is associated with restenosis.
Prenatal Famine and Genetic Variation Are Independently and Additively Associated with DNA Methylation at Regulatory Loci within IGF2/H19
Elmar W. Tobi, P. Eline Slagboom, Jenny van Dongen, Dennis Kremer, Aryeh D. Stein, Hein Putter, Bastiaan T. Heijmans, L. H. Lumey
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037933
Abstract: Both the early environment and genetic variation may affect DNA methylation, which is one of the major molecular marks of the epigenome. The combined effect of these factors on a well-defined locus has not been studied to date. We evaluated the association of periconceptional exposure to the Dutch Famine of 1944–45, as an example of an early environmental exposure, and single nucleotide polymorphisms covering the genetic variation (tagging SNPs) with DNA methylation at the imprinted IGF2/H19 region, a model for an epigenetically regulated genomic region. DNA methylation was measured at five differentially methylated regions (DMRs) that regulate the imprinted status of the IGF2/H19 region. Small but consistent differences in DNA methylation were observed comparing 60 individuals with periconceptional famine exposure with unexposed same-sex siblings at all IGF2 DMRs (PBH<0.05 after adjustment for multiple testing), but not at the H19 DMR. IGF2 DMR0 methylation was associated with IGF2 SNP rs2239681 (PBH = 0.027) and INS promoter methylation with INS SNPs, including rs689, which tags the INS VNTR, suggesting a mechanism for the reported effect of the VNTR on INS expression (PBH = 3.4×10?3). Prenatal famine and genetic variation showed similar associations with IGF2/H19 methylation and their contributions were additive. They were small in absolute terms (<3%), but on average 0.5 standard deviations relative to the variation in the population. Our analyses suggest that environmental and genetic factors could have independent and additive similarly sized effects on DNA methylation at the same regulatory site.
Lipoprotein Particle Profiles Mark Familial and Sporadic Human Longevity
Bastiaan T Heijmans ,Marian Beekman,Jeanine J Houwing-Duistermaat,Mark R Cobain,Jonathan Powell,Gerard Jan Blauw,Frans van der Ouderaa,Rudi G. J Westendorp,P. Eline Slagboom
PLOS Medicine , 2006, DOI: 10.1371/journal.pmed.0030495
Abstract: Background Genetic and biochemical studies have indicated an important role for lipid metabolism in human longevity. Ashkenazi Jewish centenarians and their offspring have large low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particles as compared with control individuals. This profile also coincided with a lower prevalence of disease. Here, we investigate whether this observation can be confirmed for familial longevity in an outbred European population and whether it can be extended to sporadic longevity in the general population. Methods and Findings NMR-measured lipoprotein profiles were analyzed in 165 families from the Leiden Longevity Study, consisting of 340 long-lived siblings (females >91 y, males >89 y), 511 of their offspring, and 243 partners of the offspring. Offspring had larger (21.3 versus 21.1 nm; p = 0.020) and fewer (1,470 versus 1,561 nmol/l; p = 0.011) LDL particles than their same-aged partners. This effect was even more prominent in the long-lived siblings (p < 10?3) and could be pinpointed to a reduction specifically in the concentration of small LDL particles. No differences were observed for HDL particle phenotypes. The mean LDL particle sizes in 259 90-y-old singletons from a population-based study were similar to those in the long-lived siblings and thus significantly larger than in partners of the offspring, suggesting that the relevance of this phenotype extends beyond familial longevity. A low concentration of small LDL particles was associated with better overall health among both long-lived siblings (p = 0.003) and 90-y-old singletons (p = 0.007). Conclusions Our study indicates that LDL particle profiles mark both familial and sporadic human longevity already in middle age.
Pathway Analysis Using Genome-Wide Association Study Data for Coronary Restenosis – A Potential Role for the PARVB Gene
Jeffrey J. W. Verschuren, Stella Trompet, M. Lourdes Sampietro, Bastiaan T. Heijmans, Werner Koch, Adnan Kastrati, Jeanine J. Houwing-Duistermaat, P. Eline Slagboom, Paul H. A. Quax, J. Wouter Jukema
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0070676
Abstract: Background Coronary restenosis after percutaneous coronary intervention (PCI) still remains a significant limitation of the procedure. The causative mechanisms of restenosis have not yet been fully identified. The goal of the current study was to perform gene-set analysis of biological pathways related to inflammation, proliferation, vascular function and transcriptional regulation on coronary restenosis to identify novel genes and pathways related to this condition. Methods The GENetic DEterminants of Restenosis (GENDER) databank contains genotypic data of 556,099SNPs of 295 cases with restenosis and 571 matched controls. Fifty-four pathways, related to known restenosis-related processes, were selected. Gene-set analysis was performed using PLINK, GRASS and ALIGATOR software. Pathways with a p<0.01 were fine-mapped and significantly associated SNPs were analyzed in an independent replication cohort. Results Six pathways (cell-extracellular matrix (ECM) interactions pathway, IL2 signaling pathway, IL6 signaling pathway, platelet derived growth factor pathway, vitamin D receptor pathway and the mitochondria pathway) were significantly associated in one or two of the software packages. Two SNPs in the cell-ECM interactions pathway were replicated in an independent restenosis cohort. No replication was obtained for the other pathways. Conclusion With these results we demonstrate a potential role of the cell-ECM interactions pathway in the development of coronary restenosis. These findings contribute to the increasing knowledge of the genetic etiology of restenosis formation and could serve as a hypothesis-generating effort for further functional studies.
Non-Homologous End-Joining Pathway Associated with Occurrence of Myocardial Infarction: Gene Set Analysis of Genome-Wide Association Study Data
Jeffrey J. W. Verschuren, Stella Trompet, Joris Deelen, David J. Stott, Naveed Sattar, Brendan M. Buckley, Ian Ford, Bastiaan T. Heijmans, Henk-Jan Guchelaar, Jeanine J. Houwing-Duistermaat, P. Eline Slagboom, J. Wouter Jukema
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056262
Abstract: Purpose DNA repair deficiencies have been postulated to play a role in the development and progression of cardiovascular disease (CVD). The hypothesis is that DNA damage accumulating with age may induce cell death, which promotes formation of unstable plaques. Defects in DNA repair mechanisms may therefore increase the risk of CVD events. We examined whether the joints effect of common genetic variants in 5 DNA repair pathways may influence the risk of CVD events. Methods The PLINK set-based test was used to examine the association to myocardial infarction (MI) of the DNA repair pathway in GWAS data of 866 subjects of the GENetic DEterminants of Restenosis (GENDER) study and 5,244 subjects of the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER) study. We included the main DNA repair pathways (base excision repair, nucleotide excision repair, mismatch repair, homologous recombination and non-homologous end-joining (NHEJ)) in the analysis. Results The NHEJ pathway was associated with the occurrence of MI in both GENDER (P = 0.0083) and PROSPER (P = 0.014). This association was mainly driven by genetic variation in the MRE11A gene (PGENDER = 0.0001 and PPROSPER = 0.002). The homologous recombination pathway was associated with MI in GENDER only (P = 0.011), for the other pathways no associations were observed. Conclusion This is the first study analyzing the joint effect of common genetic variation in DNA repair pathways and the risk of CVD events, demonstrating an association between the NHEJ pathway and MI in 2 different cohorts.
Markers of Endogenous Desaturase Activity and Risk of Coronary Heart Disease in the CAREMA Cohort Study
Yingchang Lu, Anika Vaarhorst, Audrey H. H. Merry, Martijn E. T. Dollé, Robert Hovenier, Sandra Imholz, Leo J. Schouten, Bastiaan T. Heijmans, Michael Müller, P. Eline Slagboom, Piet A. van den Brandt, Anton P. M. Gorgels, Jolanda M. A. Boer, Edith J. M. Feskens
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041681
Abstract: Background Intakes of n-3 polyunsaturated fatty acids (PUFAs), especially EPA (C20:5n-3) and DHA (C22:6n-3), are known to prevent fatal coronary heart disease (CHD). The effects of n-6 PUFAs including arachidonic acid (C20:4n-6), however, remain unclear. δ-5 and δ-6 desaturases are rate-limiting enzymes for synthesizing long-chain n-3 and n-6 PUFAs. C20:4n-6 to C20:3n-6 and C18:3n-6 to C18:2n-6 ratios are markers of endogenous δ-5 and δ-6 desaturase activities, but have never been studied in relation to incident CHD. Therefore, the aim of this study was to investigate the relation between these ratios as well as genotypes of FADS1 rs174547 and CHD incidence. Methods We applied a case-cohort design within the CAREMA cohort, a large prospective study among the general Dutch population followed up for a median of 12.1 years. Fatty acid profile in plasma cholesteryl esters and FADS1 genotype at baseline were measured in a random subcohort (n = 1323) and incident CHD cases (n = 537). Main outcome measures were hazard ratios (HRs) of incident CHD adjusted for major CHD risk factors. Results The AA genotype of rs174547 was associated with increased plasma levels of C204n-6, C20:5n-3 and C22:6n-3 and increased δ-5 and δ-6 desaturase activities, but not with CHD risk. In multivariable adjusted models, high baseline δ-5 desaturase activity was associated with reduced CHD risk (P for trend = 0.02), especially among those carrying the high desaturase activity genotype (AA): HR (95% CI) = 0.35 (0.15–0.81) for comparing the extreme quintiles. High plasma DHA levels were also associated with reduced CHD risk. Conclusion In this prospective cohort study, we observed a reduced CHD risk with an increased C20:4n-6 to C20:3n-6 ratio, suggesting that δ-5 desaturase activity plays a role in CHD etiology. This should be investigated further in other independent studies.
DNA Methylation of IGF2DMR and H19 Is Associated with Fetal and Infant Growth: The Generation R Study
Marieke I. Bouwland-Both, Nina H. van Mil, Lisette Stolk, Paul H. C. Eilers, Michael M. P. J. Verbiest, Bastiaan T. Heijmans, Henning Tiemeier, Albert Hofman, Eric A. P. Steegers, Vincent W. V. Jaddoe, Régine P. M. Steegers-Theunissen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0081731
Abstract: Changes in epigenetic programming of embryonic growth genes during pregnancy seem to affect fetal growth. Therefore, in a population-based prospective birth cohort in the Netherlands, we examined associations between fetal and infant growth and DNA methylation of IGF2DMR, H19 and MTHFR. For this study, we selected 69 case children born small-for-gestational age (SGA, birth weight <-2SDS) and 471 control children. Fetal growth was assessed with serial ultrasound measurements. Information on birth outcomes was retrieved from medical records. Infant weight was assessed at three and six months. Methylation was assessed in DNA extracted from umbilical cord white blood cells. Analyses were performed using linear mixed models with DNA methylation as dependent variable. The DNA methylation levels of IGF2DMR and H19 in the control group were, median (90% range), 53.6% (44.5–61.6) and 30.0% (25.6–34.2) and in the SGA group 52.0% (43.9–60.9) and 30.5% (23.9–32.9), respectively. The MTHFR region was found to be hypomethylated with limited variability in the control and SGA group, 2.5% (1.4–4.0) and 2.4% (1.5–3.8), respectively. SGA was associated with lower IGF2DMR DNA methylation (β = ?1.07, 95% CI ?1.93; ?0.21, P-value = 0.015), but not with H19 methylation. A weight gain in the first three months after birth was associated with lower IGF2DMR DNA methylation (β = ?0.53, 95% CI ?0.91; ?0.16, P-value = 0.005). Genetic variants in the IGF2/H19 locus were associated with IGF2DMR DNA methylation (P-value<0.05), but not with H19 methylation. Furthermore, our results suggest a possibility of mediation of DNA methylation in the association between the genetic variants and SGA. To conclude, IGF2DMR and H19 DNA methylation is associated with fetal and infant growth.
L’enclos Saint-Césaire à Arles, un chantier controversé
Marc Heijmans
Bulletin du Centre d’études Médiévales d’Auxerre , 2010, DOI: 10.4000/cem.11405
Abstract: Contrairement à la plupart des sites présentés lors de ces journées à Luxeuil, le cas de la fouille de l’enclos Saint-Césaire d’Arles n’en est qu’à ses débuts, et rien ne garantit actuellement que le site sera un jour présenté, pour tout ou partie, au public. Sans vouloir dire que c’est un exemple à ne pas suivre, il montre la lente évolution d’un projet de rénovation où l’importance du patrimoine antique et médiéval n’a été que progressivement prise en compte. Cette contribution présente don...
Optical Scattering Measurements of Laser Induced Damage in the Intraocular Lens
Bastiaan Kruijt, Thomas J. T. P. van den Berg
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0031764
Abstract: This study optically determines whether the amount of light scatter due to laser-induced damage to the intraocular lens (IOL) is significant in relation to normal straylight values in the human eye. Two IOLs with laser-induced damage were extracted from two donor eyes. Each IOL had 15 pits and/or cracks. The surface area of each pit was measured using a microscope. For 6 pits per intraocular lens the point spread function (PSF) in terms of straylight was measured and the total straylight for all 15 pits was estimated. The damage in the IOLs was scored as mild/moderate. The total damaged surface areas, for a 3.5 mm pupil, in the two IOLs were 0.13% (0.0127 mm2) and 0.66% (0.064 mm2), respectively. The angular dependence of the straylight caused by the damage was similar to that of the normal PSF. The total average contribution to straylight was log(s) = ?0.82 and ?0.42, much less than the straylight value of the normal eye. The straylight due to normal levels of laser induced damage of the IOL is much lower than normal straylight values found clinically for the normal eye and may therefore be considered not significant.
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