16 research outputs found
Fibrinogen beta variants confer protection against coronary artery disease in a Greek case-control study
<p>Abstract</p> <p>Background</p> <p>Although plasma fibrinogen levels are related to cardiovascular risk, data regarding the role of fibrinogen genetic variation in myocardial infarction (MI) or coronary artery disease (CAD) etiology remain inconsistent. The purpose of the present study was to investigate the effect of <it>fibrinogen A (FGA)</it>, <it>fibrinogen B (FGB) </it>and <it>fibrinogen G (FGG) </it>gene SNPs and haplotypes on susceptibility to CAD in a homogeneous Greek population.</p> <p>Methods</p> <p>We genotyped for rs2070022, rs2070016, rs2070006 in <it>FGA </it>gene, the rs7673587, rs1800789, rs1800790, rs1800788, rs1800787, rs4681 and rs4220 in <it>FGB </it>gene and for the rs1118823, rs1800792 and rs2066865 SNPs in <it>FGG </it>gene applying an arrayed primer extension-based genotyping method (APEX-2) in a sample of CAD patients (n = 305) and controls (n = 305). Logistic regression analysis was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs), before and after adjustment for potential confounders.</p> <p>Results</p> <p>None of the <it>FGA </it>and <it>FGG </it>SNPs and <it>FGA, FGB, FGG </it>and <it>FGA-FGG </it>haplotypes was associated with disease occurrence after adjustment. Nevertheless, rs1800787 and rs1800789 SNPs in <it>FGB </it>gene seem to decrease the risk of CAD, even after adjustment for potential confounders (OR = 0.42, 95%CI: 0.19-0.90, p = 0.026 and OR = 0.44, 95%CI:0.21-0.94, p = 0.039, respectively).</p> <p>Conclusions</p> <p><it>FGA </it>and <it>FGG </it>SNPs as well as <it>FGA, FGB, FGG </it>and <it>FGA-FGG </it>haplotypes do not seem to be important contributors to CAD occurrence in our sample. On the contrary, <it>FGB </it>rs1800787 and rs1800789 SNPs seem to confer protection to disease onset lowering the risk by about 50% in homozygotes for the minor alleles.</p
ROS1 Asp2213Asn polymorphism is not associated with coronary artery disease in a Greek case-control study
Background: Rs619203 (Cys2229Ser) and rs529038 (Asp2213Asn) polymorphisms in the ROS1 gene have been studied in relation to myocardial infarction (MI) yielding inconsistent results. We investigated the role of ROS1 rs529038 polymorphism in coronary artery disease (CAD) in Greeks using a case-control study. Methods: Genotyping for rs529038 polymorphism was performed using a multiplex PCR technique in patients with CAD (n=294) and controls (n=311). Logistic regression analysis was used to calculate crude and adjusted odds ratios (ORs). Results: Logistic regression analysis did not show any statistically significant effect of ROS1 polymorphism in the occurrence of CAD (AG vs. AA, OR: 1.08, p=0.635; GG vs. AA, OR: 0.62, p=0.220). Adjustment for confounding factors gave similar results, irrespective of the type of disease (i.e., stable coronary artery disease vs. acute coronary syndrome). Conclusions: Our findings do not support the hypothesis that ROS1 rs529038 polymorphism is an important contributing factor in the etiology of CAD in the Greek population. Clin Chem Lab Med 2009;47:1471–3.Peer Reviewe
Fibrinogen beta variants confer protection against coronary artery disease in a Greek case-control study
Background: Although plasma fibrinogen levels are related to
cardiovascular risk, data regarding the role of fibrinogen genetic
variation in myocardial infarction (MI) or coronary artery disease (CAD)
etiology remain inconsistent. The purpose of the present study was to
investigate the effect of fibrinogen A (FGA), fibrinogen B (FGB) and
fibrinogen G (FGG) gene SNPs and haplotypes on susceptibility to CAD in
a homogeneous Greek population.
Methods: We genotyped for rs2070022, rs2070016, rs2070006 in FGA gene,
the rs7673587, rs1800789, rs1800790, rs1800788, rs1800787, rs4681 and
rs4220 in FGB gene and for the rs1118823, rs1800792 and rs2066865 SNPs
in FGG gene applying an arrayed primer extension-based genotyping method
(APEX-2) in a sample of CAD patients (n = 305) and controls (n = 305).
Logistic regression analysis was used to calculate odds ratios (ORs) and
95% confidence intervals (CIs), before and after adjustment for
potential confounders.
Results: None of the FGA and FGG SNPs and FGA, FGB, FGG and FGA-FGG
haplotypes was associated with disease occurrence after adjustment.
Nevertheless, rs1800787 and rs1800789 SNPs in FGB gene seem to decrease
the risk of CAD, even after adjustment for potential confounders (OR =
0.42, 95% CI: 0.19-0.90, p = 0.026 and OR = 0.44, 95% CI: 0.21-0.94, p
= 0.039, respectively).
Conclusions: FGA and FGG SNPs as well as FGA, FGB, FGG and FGA-FGG
haplotypes do not seem to be important contributors to CAD occurrence in
our sample. On the contrary, FGB rs1800787 and rs1800789 SNPs seem to
confer protection to disease onset lowering the risk by about 50% in
homozygotes for the minor alleles
Association of meal and snack patterns with micronutrient intakes among Greek children and adolescents: data from the Hellenic National Nutrition and Health Survey
Background The present study aimed to examine how different meal and
snack patterns are associated with micronutrient intakes and diet
quality among a nationally representative sample of Greek children and
adolescents aged 1-19 years from the cross-sectional Hellenic National
Nutrition and Health Survey (n = 598). Methods Meal and snack patterns
were derived using 24-h dietary recalls. Mean adequacy ratio (MAR) was
used as an overall measure of diet quality. Multiple linear regression
adjusted for covariates was conducted to examine associations between
eating patterns, nutrient intakes and MAR. Results Four most frequently
reported eating schemes were identified including breakfast (B), lunch
(L), dinner (D) and two snacks (S) (20.9%); B, L, D and 1S (16.2%); B,
L, D and 3S (10.8%); and B, L and D (7.9%). Based on these schemes,
the daily consumption of all main meals from the majority of the sample
was highlighted. In children and adolescents aged 4-19 years, increasing
snack frequency was positively associated with intakes of vitamin D,
vitamin K, riboflavin, niacin, pantothenic acid, folate, magnesium,
copper and selenium. An inverse association was recorded for vitamin E,
vitamin B-6, calcium and iron. Among children aged 1-3 years, only
niacin and copper were significantly associated with number of snacks,
with the group of ‘B-L-D-2S’ presenting the highest intake. As for the
overall diet quality, among all participants, there was no significant
association of MAR with the type of meal and snack pattern, and thus the
snack frequency. Conclusions Snacking behaviour is a common practice
among children and adolescents. Modifying current snack foods with
nutrient-rich choices could lead to an improvement of their diet’s
nutritional quality
Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture
<p>Approaches exploiting trait distribution extremes may be used to identify loci associated with common traits, but it is unknown whether these loci are generalizable to the broader population. In a genome-wide search for loci associated with the upper versus the lower 5th percentiles of body mass index, height and waist-to-hip ratio, as well as clinical classes of obesity, including up to 263,407 individuals of European ancestry, we identified 4 new loci (IGFBP4, H6PD, RSRC1 and PPP2R2A) influencing height detected in the distribution tails and 7 new loci (HNF4G, RPTOR, GNAT2, MRPS33P4, ADCY9, HS6ST3 and ZZZ3) for clinical classes of obesity. Further, we find a large overlap in genetic structure and the distribution of variants between traits based on extremes and the general population and little etiological heterogeneity between obesity subgroups.</p>
Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture
Approaches exploiting trait distribution extremes may be used to identify loci associated with common traits, but it is unknown whether these loci are generalizable to the broader population. In a genome-wide search for loci associated with the upper versus the lower 5th percentiles of body mass index, height and waist-to-hip ratio, as well as clinical classes of obesity, including up to 263,407 individuals of European ancestry, we identified 4 new loci (IGFBP4, H6PD, RSRC1 and PPP2R2A) influencing height detected in the distribution tails and 7 new loci (HNF4G, RPTOR, GNAT2, MRPS33P4, ADCY9, HS6ST3 and ZZZ3) for clinical classes of obesity. Further, we find a large overlap in genetic structure and the distribution of variants between traits based on extremes and the general population and little etiological heterogeneity between obesity subgroups