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Activated immune-inflammatory pathways are associated with long-standing depressive symptoms: Evidence from gene-set enrichment analyses in the Young Finns Study.

https://arctichealth.org/en/permalink/ahliterature275217
Source
J Psychiatr Res. 2015 Dec;71:120-5
Publication Type
Article
Date
Dec-2015
Author
Marko Elovainio
Tuukka Taipale
Ilkka Seppälä
Nina Mononen
Emma Raitoharju
Markus Jokela
Laura Pulkki-Råback
Thomas Illig
Melanie Waldenberger
Christian Hakulinen
Taina Hintsa
Mika Kivimäki
Mika Kähönen
Liisa Keltikangas-Järvinen
Olli Raitakari
Terho Lehtimäki
Source
J Psychiatr Res. 2015 Dec;71:120-5
Date
Dec-2015
Language
English
Publication Type
Article
Keywords
Adult
Depressive Disorder - epidemiology - immunology
Female
Finland - epidemiology
Gene Expression Profiling
Humans
Male
Prospective Studies
Psychiatric Status Rating Scales
Severity of Illness Index
Abstract
We used genome wide expression (GWE) data of circulating blood cells and pathway analysis to investigate the inflammatory and other molecular pathways that may be associated with long-standing depressive symptoms. Participants were 607 women and 316 men (mean age 42 years) from the Young Finns Study who participated in three consecutive study phases in 2001, 2007 and 2012. Using Gene-set enrichment analyses (GSEA) we focused our analyses to pathways (available in MSigDB database) that are likely to affect immunological and inflammatory processes. GSEA were performed for blood cell GWE data in 2012. Depressive symptoms were assessed using a modified 21-item Beck Depression Inventory in each of the three study phases. Participants who scored in the top quartile of depressive symptoms in each of the three measurement points (n = 191) differed from other participants (n = 732) in several gene-set pathways related to inflammatory processes or immune-inflammatory signaling including interleukin (IL-1) pathway, and pathways related to various immuno-inflammatory processes, such as toll-like, the NEF protein, the nuclear factor kB, the kinase AKT and the mature B cell antigen receptor pathway (false discovery rates, FDRs
PubMed ID
26473696 View in PubMed
Less detail

Adult-type hypolactasia is not a predisposing factor for the early functional and structural changes of atherosclerosis: the Cardiovascular Risk in Young Finns Study.

https://arctichealth.org/en/permalink/ahliterature159355
Source
Clin Sci (Lond). 2008 Nov;115(9):265-71
Publication Type
Article
Date
Nov-2008
Author
Terho Lehtimäki
Nina Hutri-Kähönen
Mika Kähönen
Jukka Hemminki
Vera Mikkilä
Marika Laaksonen
Leena Räsänen
Nina Mononen
Markus Juonala
Jukka Marniemi
Jorma Viikari
Olli Raitakari
Author Affiliation
Laboratory of Atherosclerosis Genetics, Department of Clinical Chemistry, Tampere University Hospital and the Medical School at the University of Tampere, 33014 Tampere, Finland. terho.lehtimaki@uta.fi
Source
Clin Sci (Lond). 2008 Nov;115(9):265-71
Date
Nov-2008
Language
English
Publication Type
Article
Keywords
Adult
Atherosclerosis - epidemiology - etiology - genetics - physiopathology
Brachial Artery - physiopathology - ultrasonography
Carotid Arteries - pathology - ultrasonography
Dairy Products - statistics & numerical data
Diet - statistics & numerical data
Epidemiologic Methods
Female
Finland - epidemiology
Genetic Predisposition to Disease
Genotype
Humans
Lactase - deficiency
Lactase-Phlorizin Hydrolase - genetics
Lactose Intolerance - complications - epidemiology - genetics - pathology
Male
Polymorphism, Genetic
Tunica Intima - pathology - ultrasonography
Tunica Media - pathology - ultrasonography
Vasodilation
Abstract
Individuals suffering from ATH (adult-type hypolactasia), defined by the LCT (gene encoding lactase-phlorizin hydrolase) C/C(-13910) genotype (rs4988235), use less milk and dairy products and may have higher plasma HDL (high-density lipoprotein) and lower triacylglycerol (triglyceride) concentrations than their counterparts without ATH. To investigate the effects of ATH status on the early markers of atherosclerosis, we examined its association with CIMT (carotid intima-media thickness), CAC (carotid artery compliance) and brachial artery FMD (flow-mediated dilation) in a young population-based cohort of otherwise healthy individuals. As part of the Cardiovascular Risk in Young Finns Study, we performed CIMT, CAC and FMD analyses, LCT C/T(-13910) genotyping and risk factor determination in 2109 young subjects 24-39 years of age (45% males) at the time of the examination. The consumption of both milk and dairy products was lowest and the consumption of alcohol highest in subjects with the C/C(-13910) genotype (P
PubMed ID
18194137 View in PubMed
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Association of apolipoprotein E promoter polymorphisms with bone structural traits is modified by dietary saturated fat intake - the Cardiovascular Risk in Young Finns study.

https://arctichealth.org/en/permalink/ahliterature137625
Source
Bone. 2011 May 1;48(5):1058-65
Publication Type
Article
Date
May-1-2011
Author
Sanna Tolonen
Vera Mikkilä
Marika Laaksonen
Harri Sievänen
Nina Mononen
Jussi Hernesniemi
Kimmo Vehkalahti
Jorma Viikari
Olli Raitakari
Mika Kähönen
Terho Lehtimäki
Author Affiliation
Department of Food and Environmental Sciences, University of Helsinki, Finland.
Source
Bone. 2011 May 1;48(5):1058-65
Date
May-1-2011
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Apolipoproteins E - genetics
Bone and Bones - anatomy & histology - radiography
Cardiovascular Diseases - blood - genetics
Child
Child, Preschool
Cholesterol - blood
Dietary Fats - pharmacology
Fatty Acids - pharmacology
Feeding Behavior - drug effects
Female
Finland
Gene Frequency - genetics
Heterozygote
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Promoter Regions, Genetic
Radius - anatomy & histology - radiography
Risk factors
Tibia - anatomy & histology - radiography
Abstract
Association of apolipoprotein E (APOE) e4 allele with peripheral quantitative computed tomography (pQCT) bone traits at the distal and shaft sites of the radius and tibia was evaluated in the Young Finns Cohort (n=1777). We also analyzed the interactions of the APOE promoter polymorphisms (-219G/T rs405509 and +113G/C rs440446) and bone traits within the APOE e3/e3 genotype (n=1025 and n=1013, respectively), and investigated the gene-environment interactions on bone traits with longitudinal saturated fatty acids (SAFA) intake. Differences between the e4 allele carriers and noncarriers were modest and mostly nonsignificant. Within the APOE promoter -219G/T polymorphism, cortical strength index (CSI) and compressive bone strength index (BSI) at the distal radius (linear, P=0.003 and P=0.05, respectively) and tibia (linear, P=0.01 and P=0.03, respectively), and CSI at the tibial shaft (linear, P=0.04) decreased towards the -219T/T genotype in women. In men, total cross-sectional areas at the radial site and stress-strain index (SSI) at the radial shaft (linear, P=0.03 and P=0.04 and P=0.05, respectively) increased, and conversely cortical bone density and CSI at the radial shaft (linear, P=0.005 and P=0.05, respectively) and CSI at the tibial shaft (linear, P=0.03) decreased towards the -219T/T genotype. In the highest SAFA tertile, women with the -219T/T genotype had the smallest total area and SSI at the radial shaft (P=0.01 and P=0.02, respectively). Subjects with the APOE +113C/C genotype shared similar bone traits as subjects with the APOE -219T/T genotype. In conclusion, APOE genotypes -219T/T and +113C/C could be genetic markers for cortical bone strength. Furthermore, high longitudinal SAFA intake seems to be more detrimental to bone in women with the -219T/T and +133C/C genotypes than others.
PubMed ID
21266206 View in PubMed
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Blood pathway analyses reveal differences between prediabetic subjects with or without dyslipidaemia. The Cardiovascular Risk in Young Finns Study.

https://arctichealth.org/en/permalink/ahliterature292119
Source
Diabetes Metab Res Rev. 2017 10; 33(7):
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
10-2017
Author
Jaakko Laaksonen
Tuukka Taipale
Ilkka Seppälä
Emma Raitoharju
Nina Mononen
Leo-Pekka Lyytikäinen
Melanie Waldenberger
Thomas Illig
Nina Hutri-Kähönen
Tapani Rönnemaa
Markus Juonala
Jorma Viikari
Mika Kähönen
Olli Raitakari
Terho Lehtimäki
Author Affiliation
Department of Clinical Chemistry, Fimlab Laboratories and Finnish Cardiovascular Research Center - Tampere, Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland.
Source
Diabetes Metab Res Rev. 2017 10; 33(7):
Date
10-2017
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adult
Blood glucose
Cardiovascular Diseases - etiology - genetics
Cholesterol - biosynthesis
Dyslipidemias - blood - complications - genetics
Female
Finland
Gene Expression
Gene Expression Profiling
Humans
Insulin Resistance
Male
Middle Aged
Prediabetic State - blood - complications - genetics
Signal Transduction - genetics
Up-Regulation
Waist Circumference
Abstract
Prediabetes often occurs together with dyslipidaemia, which is paradoxically treated with statins predisposing to type 2 diabetes mellitus. We examined peripheral blood pathway profiles in prediabetic subjects with (PRD ) and without dyslipidaemia (PR0 ) and compared these to nonprediabetic controls without dyslipidaemia (C0 ).
The participants were from the Cardiovascular Risk in Young Finns Study, including 1240 subjects aged 34 to 49 years. Genome-wide expression data of peripheral blood and gene set enrichment analysis were used to investigate the differentially expressed genes and enriched pathways between different subtypes of prediabetes.
Pathways for cholesterol synthesis, interleukin-12-mediated signalling events, and downstream signalling in naïve CD8+ T-cells were upregulated in the PR0 group in comparison with controls (C0 ). The upregulation of these pathways was independent of waist circumference, blood pressure, smoking status, and insulin. Adjustment for CRP left the CD8+ T-cell signalling and interleukin-12-mediated signalling event pathway upregulated. The cholesterol synthesis pathway was also upregulated when all prediabetic subjects (PR0 and PRD ) were compared with the nonprediabetic control group. No pathways were upregulated or downregulated when the PRD group was compared with the C0 group. Five genes in the PR0 group and 1 in the PRD group were significantly differentially expressed in comparison with the C0 group.
Blood cell gene expression profiles differ significantly between prediabetic subjects with and without dyslipidaemia. Whether this classification may be used in detection of prediabetic individuals at a high risk of cardiovascular complications remains to be examined.
PubMed ID
28609607 View in PubMed
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Catechol-O-methyltransferase val108/158met genotype, major depressive disorder and response to selective serotonin reuptake inhibitors in major depressive disorder.

https://arctichealth.org/en/permalink/ahliterature146093
Source
Psychiatry Res. 2010 Mar 30;176(1):85-7
Publication Type
Article
Date
Mar-30-2010
Author
Ari Illi
Eija Setälä-Soikkeli
Olli Kampman
Merja Viikki
Timo Nuolivirta
Outi Poutanen
Heini Huhtala
Nina Mononen
Terho Lehtimäki
Esa Leinonen
Author Affiliation
University of Tampere, Medical School, Tampere, Finland. ari.illi@uta.fi
Source
Psychiatry Res. 2010 Mar 30;176(1):85-7
Date
Mar-30-2010
Language
English
Publication Type
Article
Keywords
Catechol O-Methyltransferase - genetics
Depressive Disorder, Major - drug therapy - genetics
Finland
Gene Frequency
Genome-Wide Association Study
Genotype
Humans
Methionine - genetics
Pharmacogenetics
Polymorphism, Single Nucleotide
Serotonin Uptake Inhibitors - therapeutic use
Valine - genetics
Abstract
The functional val108/158met polymorphism of the COMT gene (rs4680) was evaluated in major depressive disorder (MDD), and in the treatment response to antidepressants in MDD. We could not demonstrate any significant difference in the distribution of this COMT single-nucleotide polymorphism (SNP) in the treatment response to selective serotonin reuptake inhibitors or between patients with MDD and control subjects.
PubMed ID
20071037 View in PubMed
Less detail

Genetic profiling using genome-wide significant coronary artery disease risk variants does not improve the prediction of subclinical atherosclerosis: the Cardiovascular Risk in Young Finns Study, the Bogalusa Heart Study and the Health 2000 Survey--a meta-analysis of three independent studies.

https://arctichealth.org/en/permalink/ahliterature127437
Source
PLoS One. 2012;7(1):e28931
Publication Type
Article
Date
2012
Author
Jussi A Hernesniemi
Ilkka Seppälä
Leo-Pekka Lyytikäinen
Nina Mononen
Niku Oksala
Nina Hutri-Kähönen
Markus Juonala
Leena Taittonen
Erin N Smith
Nicholas J Schork
Wei Chen
Sathanur R Srinivasan
Gerald S Berenson
Sarah S Murray
Tomi Laitinen
Antti Jula
Johannes Kettunen
Samuli Ripatti
Reijo Laaksonen
Jorma Viikari
Mika Kähönen
Olli T Raitakari
Terho Lehtimäki
Author Affiliation
Department of Clinical Chemistry, University of Tampere, Medical School, and Tampere University Hospital, Tampere, Finland. jussi.hernesniemi@uta.fi
Source
PLoS One. 2012;7(1):e28931
Date
2012
Language
English
Publication Type
Article
Keywords
Adult
Carotid Intima-Media Thickness
Coronary Artery Disease - epidemiology - genetics - physiopathology
Data Collection
Female
Finland - epidemiology
Genetic Predisposition to Disease - genetics
Genome-Wide Association Study
Health
Humans
Louisiana - epidemiology
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Risk factors
Abstract
Genome-wide association studies (GWASs) have identified a large number of variants (SNPs) associating with an increased risk of coronary artery disease (CAD). Recently, the CARDIoGRAM consortium published a GWAS based on the largest study population so far. They successfully replicated twelve already known associations and discovered thirteen new SNPs associating with CAD. We examined whether the genetic profiling of these variants improves prediction of subclinical atherosclerosis--i.e., carotid intima-media thickness (CIMT) and carotid artery elasticity (CAE)--beyond classical risk factors.
We genotyped 24 variants found in a population of European ancestry and measured CIMT and CAE in 2001 and 2007 from 2,081, and 2,015 subjects (aged 30-45 years in 2007) respectively, participating in the Cardiovascular Risk in Young Finns Study (YFS). The Bogalusa Heart Study (BHS; n?=?1179) was used as a replication cohort (mean age of 37.5). For additional replication, a sub-sample of 5 SNPs was genotyped for 1,291 individuals aged 46-76 years participating in the Health 2000 population survey. We tested the impact of genetic risk score (GRS(24SNP/CAD)) calculated as a weighted (by allelic odds ratios for CAD) sum of CAD risk alleles from the studied 24 variants on CIMT, CAE, the incidence of carotid atherosclerosis and the progression of CIMT and CAE during a 6-year follow-up.
CIMT or CAE did not significantly associate with GRS(24SNP/CAD) before or after adjusting for classical CAD risk factors (p>0.05 for all) in YFS or in the BHS. CIMT and CAE associated with only one SNP each in the YFS. The findings were not replicated in the replication cohorts. In the meta-analysis CIMT or CAE did not associate with any of the SNPs.
Genetic profiling, by using known CAD risk variants, should not improve risk stratification for subclinical atherosclerosis beyond conventional risk factors among healthy young adults.
Notes
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PubMed ID
22295058 View in PubMed
Less detail

Genetic variants and their interactions in the prediction of increased pre-clinical carotid atherosclerosis: the cardiovascular risk in young Finns study.

https://arctichealth.org/en/permalink/ahliterature140110
Source
PLoS Genet. 2010 Sep;6(9):e1001146
Publication Type
Article
Date
Sep-2010
Author
Sebastian Okser
Terho Lehtimäki
Laura L Elo
Nina Mononen
Nina Peltonen
Mika Kähönen
Markus Juonala
Yue-Mei Fan
Jussi A Hernesniemi
Tomi Laitinen
Leo-Pekka Lyytikäinen
Riikka Rontu
Carita Eklund
Nina Hutri-Kähönen
Leena Taittonen
Mikko Hurme
Jorma S A Viikari
Olli T Raitakari
Tero Aittokallio
Author Affiliation
Biomathematics Research Group, Department of Mathematics, University of Turku, Turku, Finland.
Source
PLoS Genet. 2010 Sep;6(9):e1001146
Date
Sep-2010
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Carotid Artery Diseases - genetics - pathology - ultrasonography
Child
Child, Preschool
Disease Progression
Epistasis, Genetic
Finland
Follow-Up Studies
Genetic Predisposition to Disease
Humans
Middle Aged
Polymorphism, Single Nucleotide - genetics
Risk factors
Tunica Intima - pathology - ultrasonography
Tunica Media - pathology - ultrasonography
Young Adult
Abstract
The relative contribution of genetic risk factors to the progression of subclinical atherosclerosis is poorly understood. It is likely that multiple variants are implicated in the development of atherosclerosis, but the subtle genotypic and phenotypic differences are beyond the reach of the conventional case-control designs and the statistical significance testing procedures being used in most association studies. Our objective here was to investigate whether an alternative approach--in which common disorders are treated as quantitative phenotypes that are continuously distributed over a population--can reveal predictive insights into the early atherosclerosis, as assessed using ultrasound imaging-based quantitative measurement of carotid artery intima-media thickness (IMT). Using our population-based follow-up study of atherosclerosis precursors as a basis for sampling subjects with gradually increasing IMT levels, we searched for such subsets of genetic variants and their interactions that are the most predictive of the various risk classes, rather than using exclusively those variants meeting a stringent level of statistical significance. The area under the receiver operating characteristic curve (AUC) was used to evaluate the predictive value of the variants, and cross-validation was used to assess how well the predictive models will generalize to other subsets of subjects. By means of our predictive modeling framework with machine learning-based SNP selection, we could improve the prediction of the extreme classes of atherosclerosis risk and progression over a 6-year period (average AUC 0.844 and 0.761), compared to that of using conventional cardiovascular risk factors alone (average AUC 0.741 and 0.629), or when combined with the statistically significant variants (average AUC 0.762 and 0.651). The predictive accuracy remained relatively high in an independent validation set of subjects (average decrease of 0.043). These results demonstrate that the modeling framework can utilize the "gray zone" of genetic variation in the classification of subjects with different degrees of risk of developing atherosclerosis.
Notes
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PubMed ID
20941391 View in PubMed
Less detail

Germ-line alterations in MSR1 gene and prostate cancer risk.

https://arctichealth.org/en/permalink/ahliterature182868
Source
Clin Cancer Res. 2003 Nov 1;9(14):5252-6
Publication Type
Article
Date
Nov-1-2003
Author
Eija H Seppälä
Tarja Ikonen
Ville Autio
Annika Rökman
Nina Mononen
Mika P Matikainen
Teuvo L J Tammela
Johanna Schleutker
Author Affiliation
Laboratory of Cancer Genetics, Institute of Medical Technology, University of Tampere, Finland. eija.seppala@uta.fi
Source
Clin Cancer Res. 2003 Nov 1;9(14):5252-6
Date
Nov-1-2003
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Case-Control Studies
Chromosomes, Human, Pair 8 - genetics
Cohort Studies
Family
Finland - epidemiology
Germ-Line Mutation - genetics
Humans
Male
Middle Aged
Polymerase Chain Reaction
Polymorphism, Single-Stranded Conformational
Prostatic Neoplasms - genetics
Receptors, Immunologic - genetics
Receptors, Scavenger
Risk factors
Scavenger Receptors, Class A
Abstract
The MSR1 gene maps to 8p22-23, a novel susceptibility locus for hereditary prostate cancer (HPC). Mutations in MSR1 have been reported to associate with prostate cancer (PRCA) risk. Here we report a follow-up study from Finland to evaluate the association between PRCA and MSR1 gene.
The youngest affected patient from each of 120 HPC families was initially used for the screening of MSR1 mutations by single-strand conformational polymorphism analysis. Selected variants of MSR1 gene were then screened in 537 unselected PRCA cases and in 480 controls.
Among 120 HPC families, five MSR1 sequence variants were identified. The carrier frequencies of the R293X, P275A, and -14743A>G variants were compared between the probands with HPC, unselected PRCA cases, and healthy male blood donors. No significant differences were observed. The odds ratios for R293X, P275A, and -14743A>G mutations were also calculated to estimate the PRCA risk. No significantly elevated or lowered risks for PRCA among these three variants were detected. However, the mean age at diagnosis of the R293X mutation carriers among HPC probands was significantly lower compared with noncarriers (55.4 versus 65.4 years; t test, P = 0.04). The same trend was observed among unselected PRCA cases (65.7 versus 68.7 years; t test, P = 0.37).
Our results do not support a major role for the MSR1 gene in the causation of hereditary or unselected PRCAs but suggest a possible modifying role in cancer predisposition.
PubMed ID
14614006 View in PubMed
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Germline alterations of the RNASEL gene, a candidate HPC1 gene at 1q25, in patients and families with prostate cancer.

https://arctichealth.org/en/permalink/ahliterature190658
Source
Am J Hum Genet. 2002 May;70(5):1299-304
Publication Type
Article
Date
May-2002
Author
Annika Rökman
Tarja Ikonen
Eija H Seppälä
Nina Nupponen
Ville Autio
Nina Mononen
Joan Bailey-Wilson
Jeffrey Trent
John Carpten
Mika P Matikainen
Pasi A Koivisto
Teuvo L J Tammela
Olli-P Kallioniemi
Johanna Schleutker
Author Affiliation
Laboratory of Cancer Genetics, Institute of Medical Technology, Temepere University, and Tempere University Hospital, Tempere, Finland. annika.rokman@uta.fi
Source
Am J Hum Genet. 2002 May;70(5):1299-304
Date
May-2002
Language
English
Publication Type
Article
Keywords
Age of Onset
Chromosomes, Human, Pair 1 - genetics
DNA Mutational Analysis
Endoribonucleases - chemistry - genetics
Female
Finland
Gene Frequency
Germ-Line Mutation - genetics
Humans
Male
Mutation, Missense - genetics
Pedigree
Polymorphism, Single-Stranded Conformational
Prostatic Neoplasms - enzymology - epidemiology - genetics - pathology
Abstract
The RNASEL gene (2',5'-oligoisoadenylate-synthetase dependent) encodes a ribonuclease that mediates the antiviral and apoptotic activities of interferons. The RNASEL gene maps to the hereditary-prostate-cancer (HPC)-predisposition locus at 1q24-q25 (HPC1) and was recently shown to harbor truncating mutations in two families with linkage to HPC1. Here, we screened for RNASEL germline mutations in 66 Finnish patients with HPC, and we determined the frequency of the changes in the index patients from 116 families with HPC, in 492 patients with unselected prostate cancer (PRCA), in 223 patients with benign prostatic hyperplasia (BPH), and in 566 controls. A truncating mutation, E265X, was found in 5 (4.3%) of the 116 patients from families with HPC. This was significantly higher (odds ratio [OR] =4.56; P=.04) than the frequency of E265X in controls (1.8%). The highest mutation frequency (9.5%) was found in patients from families with four or more affected members. Possible segregation was detected only in a single family. However, the median age at disease onset for E265X carriers was 11 years less than that for noncarriers in the same families. In addition, of the four missense variants found, R462Q showed an association with HPC (OR=1.96; P=.07). None of the variants showed any differences between controls and either patients with BPH or patients with PRCA. We conclude that, although RNASEL mutations do not explain disease segregation in Finnish families with HPC, the variants are enriched in families with HPC that include more than two affected members and may also be associated with the age at disease onset. This suggests a possible modifying role in cancer predisposition. The impact that the RNASEL sequence variants have on PRCA burden at the population level seems small but deserves further study.
Notes
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Erratum In: Am J Hum Genet. 2004 Dec;75(6):1158
Erratum In: Am J Hum Genet 2002 Jul;71(1):215
PubMed ID
11941539 View in PubMed
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IL-18 gene polymorphism, cardiovascular mortality and coronary artery disease.

https://arctichealth.org/en/permalink/ahliterature141308
Source
Eur J Clin Invest. 2010 Nov;40(11):994-1001
Publication Type
Article
Date
Nov-2010
Author
Jussi A Hernesniemi
Kaisa Anttila
Tuomo Nieminen
Mika Kähönen
Nina Mononen
Kjell Nikus
Väinö Turjanmaa
Jari Viik
Rami Lehtinen
Terho Lehtimäki
Author Affiliation
Laboratory of Atherosclerosis Genetics, Department of Clinical Chemistry, Tampere University Hospital, Centre for Laboratory Medicine, Tampere, Finland Medical School, University of Tampere, Tampere, Finland. jussi.hernesniemi@uta.fi
Source
Eur J Clin Invest. 2010 Nov;40(11):994-1001
Date
Nov-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Atherosclerosis - genetics - mortality
Chi-Square Distribution
Cohort Studies
Coronary Angiography
Coronary Artery Disease - genetics - mortality
European Continental Ancestry Group - genetics
Female
Finland
Genetic Predisposition to Disease
Haplotypes
Humans
Interleukin-18 - genetics
Male
Middle Aged
Polymorphism, Genetic
Risk factors
Sex Factors
Abstract
Interleukin 18(IL-18) is a pro-atherosclerotic cytokine. Elevated IL-18 levels and the genetic variation of the IL-18 have been previously linked with acute coronary events and cardiovascular mortality among patients with coronary artery disease (CAD). We studied the possible association between the IL-18 gene polymorphism and cardiovascular mortality during follow-up among Finnish patients who had undergone a clinical exercise stress test, in addition to the possible effect on the expression of angiography-verified CAD.
A total of 2152 patients of the Finnish Cardiovascular Study (cohort study) were followed up for 6·3years and cardiovascular mortality was recorded. Angiography was performed on 461 patients. Genotyping of five common single nucleotide polymorphisms (SNPs) of the IL-18 gene was performed using the 5'nuclease assay for allelic discrimination with the ABI Prism 7900HT Sequence Detection System.
Among the study population, IL-18 gene polymorphism did not associate with cardiovascular mortality. According to adjusted binary regression analysis, the male carriers of one major haplotype (the only ones carrying the t allele of the +127 C/t SNP) had a lower occurrence rate for significant CAD defined as > 50% stenosis in at least one of the main branches of the coronary arteries (OR 0·495, 95% CI 0·862-0·284, P=0·041). No associations were observed among women. The sex-by-genotype interaction was significant (P=0·033).
The IL-18 gene was not found to associate significantly with mortality. Among patients who had coronary angiography, one major haplotype of the IL-18 gene has a gender-dependent different impact on the expression of CAD.
PubMed ID
20735470 View in PubMed
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