<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Unhee Lim</style></author><author><style face="normal" font="default" size="100%">Kun Peng</style></author><author><style face="normal" font="default" size="100%">Barry Shane</style></author><author><style face="normal" font="default" size="100%">Patrick J Stover</style></author><author><style face="normal" font="default" size="100%">Augusto A Litonjua</style></author><author><style face="normal" font="default" size="100%">Scott T Weiss</style></author><author><style face="normal" font="default" size="100%">J Michael Gaziano</style></author><author><style face="normal" font="default" size="100%">Robert L Strawderman</style></author><author><style face="normal" font="default" size="100%">Farbod Raiszadeh</style></author><author><style face="normal" font="default" size="100%">Jacob Selhub</style></author><author><style face="normal" font="default" size="100%">Katherine L Tucker</style></author><author><style face="normal" font="default" size="100%">Patricia A Cassano</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Polymorphisms in cytoplasmic serine hydroxymethyltransferase and methylenetetrahydrofolate reductase affect the risk of cardiovascular disease in men</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of Nutrition</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">80 and over</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Cardiovascular Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytoplasm</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Glycine Hydroxymethyltransferase</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Methylenetetrahydrofolate Reductase {(NADPH2)</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism</style></keyword><keyword><style  face="normal" font="default" size="100%">Reference Values</style></keyword><keyword><style  face="normal" font="default" size="100%">Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">{Case-Control} Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">} Middle Aged</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/2005</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16046727</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">8</style></number><volume><style face="normal" font="default" size="100%">135</style></volume><pages><style face="normal" font="default" size="100%">1989–1994</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Genetic variation in folate-regulating enzymes contributes to the risk of cardiovascular disease (CVD). The cytoplasmic serine hydroxymethyltransferase (cSHMT) enzyme is proposed to regulate a key metabolic intersection in folate metabolism. We hypothesized that a variant in cSHMT (cSHMT} 1420C–&gt;T) affects CVD risk, and that the effect depends on a linked step in the metabolic pathway catalyzed by methylenetetrahydrofolate reductase (MTHFR). A nested case-control study of incident CVD was conducted within the all-male Normative Aging Study cohort. Of the incident CVD cases, 507 had DNA samples; 2 controls/case were selected by risk set sampling (matched on age and birth year). A significant gene-gene interaction (P-values} 0.0013, 0.0064) was found between MTHFR and cSHMT, and there was little or no change in the coefficients in covariate-adjusted models. The effect of MTHFR 677C–&gt;T genotype on CVD risk varied by cSHMT 1420C–&gt;T genotype. Among men with cSHMT 1420C–&gt;T TT genotype, the odds ratios (OR) for CVD risk for MTHFR 677C–&gt;T CT and TT genotypes compared with the MTHFR 677C–&gt;T CC genotype were 3.6 (95% CI, 1.7-7.8) and 10.6 (95% CI, 2.5-46.0), respectively. Among men with the cSHMT 1420C–&gt;T CC/CT genotype, the corresponding ORs were 1.0 (95% CI, 0.8-1.2) and 1.3 (95% CI, 0.9-1.8). Plasma total homocysteine concentrations were highest in the subgroup of men with both polymorphisms, MTHFR 677C–&gt;T TT and cSHMT 1420C–&gt; TT, consistent with a higher risk of CVD in this subgroup. A more complete understanding of the molecular mechanism awaits identification of the functional effect of the polymorphism.</style></abstract><notes><style face="normal" font="default" size="100%">{PMID:} 16046727</style></notes></record></records></xml>