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[Analysis of polymorphism of the D11S2008 locus of the catalase gene in patients with hypertension and ischemic heart disease in non-insulin-dependent diabetes mellitus in the Muscovite population].

https://arctichealth.org/en/permalink/ahliterature198800
Source
Genetika. 2000 Mar;36(3):423-6
Publication Type
Article
Date
Mar-2000
Author
D A Chistiakov
R I Turakulov
L N Shcherbacheva
G G Mamaeva
M I Galabolkin
V V Nosikov
Author Affiliation
State Research Institute of Genetics, Moscow, Russia. dchistiakov@hotmail.com
Source
Genetika. 2000 Mar;36(3):423-6
Date
Mar-2000
Language
Russian
Publication Type
Article
Keywords
Base Sequence
Catalase - genetics
Chromosome Mapping
DNA Primers
Diabetes Mellitus, Type 2 - complications - enzymology - genetics
Genetic Predisposition to Disease
Genotype
Humans
Hypertension - complications - genetics - metabolism
Moscow
Myocardial Ischemia - complications - enzymology - genetics
Polymerase Chain Reaction
Polymorphism, Genetic
Abstract
The allele and genotype frequency distributions of the D11S2008 tetranucleotide microsatellite linked with the catalase (CAT) gene were compared between patients with insulin-dependent diabetes mellitus (IDDM) with (N = 72) and without (N = 82) coronary heart disease (CHD), and between IDDM patients with normal arterial tension (N = 82) and with arterial hypertension (N = 42). In total, eight alleles were found. The alleles varied in length from 120 to 148 bp and included from 15 to 22 tetranucleotide repeats. The groups did not differ in D11S2008 allele and genotype frequencies; the only exception was that the frequency of genotype 18/19 in patients with CHD (31.9%) was significantly higher than in the controls (18.3%). Thus, the D11S2008 polymorphic locus located in proximity to the catalase gene proved to be weakly associated with CHD, but not associated with arterial hypertension, in IDDM patients. Genotype 18/19 was associated with a higher risk of CHD.
PubMed ID
10779920 View in PubMed
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Association between coronary heart disease and the C3F-gene in essential hypertension.

https://arctichealth.org/en/permalink/ahliterature56010
Source
Circulation. 1978 Oct;58(4):622-5
Publication Type
Article
Date
Oct-1978
Author
B O Kristensen
G B Petersen
Source
Circulation. 1978 Oct;58(4):622-5
Date
Oct-1978
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Alleles
Complement C3 - genetics
Coronary Disease - complications - genetics
Denmark
Female
Humans
Hypertension - complications - genetics
Male
Middle Aged
Risk
Sex Factors
Abstract
The occurrence of the C3F allele was investigated in the following three groups: 69 consecutive referred patients with untreated essential hypertension, including borderline hypertension; 70 patients with established and treated essential hypertension, already attending the same outpatient clinic, and 62 age- and sex-matched normotensive healthy subjects without clinical signs of atherosclerosis or familial predisposition to hypertension. In the three groups the C3F allele was found in 38.2%, 29% and 20%, respectively. Among the treated hypertensive patients with C3F gene, 40% had coronary heart disease (CHD) compared to 6.1% among the C3F negative (P less than 0.005), and the relative risk of CHD among the treated hypertensive patients with this allele was found to be 10.2 (P less than 0.002). The C3F gene was present in 72.7% of the treated patients with CHD. In the untreated patients the occurrence of CHD was low, and no differences between C3F positive and negative patients could be demonstrated. No association of the C3F allele with familial predisposition to hypertension was found. This study provides further evidence of a positive association of the C3F allele with atherosclerosis, and it is concluded that this allele in a hypertensive patient might accelerate the atherosclerotic process, with subsequent premature development of vascular complications.
PubMed ID
688571 View in PubMed
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Beta(2)-adrenergic receptor gene variation and hypertension in subjects with type 2 diabetes.

https://arctichealth.org/en/permalink/ahliterature47718
Source
Hypertension. 2001 May;37(5):1303-8
Publication Type
Article
Date
May-2001
Author
K. Bengtsson
M. Orho-Melander
O. Melander
U. Lindblad
J. Ranstam
L. Råstam
L. Groop
Author Affiliation
Department of Endocrinology, Malmö University Hospital, Lund University, Malmö, Sweden. kristina.a.bengtsson@vgregion.se
Source
Hypertension. 2001 May;37(5):1303-8
Date
May-2001
Language
English
Publication Type
Article
Keywords
Aged
Analysis of Variance
Arginine - genetics
Case-Control Studies
Diabetes Mellitus, Type 2 - complications - genetics
Female
Genotype
Glutamic Acid - genetics
Glutamine - genetics
Glycine - genetics
Humans
Hypertension - complications - genetics
Male
Middle Aged
Polymorphism, Genetic
Receptors, Adrenergic, beta-2 - genetics
Research Support, Non-U.S. Gov't
Variation (Genetics)
Abstract
The aim of this study was to investigate whether polymorphisms in the beta(2)-adrenergic receptor gene (5'LC-Arg19Cys, Arg16Gly, Gln27Glu) are associated with hypertension in patients with or without type 2 diabetes and with the blood pressure levels in normotensive sib pairs. The association study included 291 hypertensive patients without type 2 diabetes, 124 hypertensive patients with type 2 diabetes, and 265 healthy control subjects from SWEDEN: In addition, normotensive sib pairs that were discordant for the Arg16Gly (72 pairs) and Gln27Glu (40 pairs) polymorphisms were identified in type 2 diabetes families from FINLAND: Genotyping was performed using polymerase chain reaction-restriction fragment-length polymorphism analysis. Homozygous carriers of the Arg16 allele had a significantly increased odds ratio (OR) for hypertension in patients with type 2 diabetes (OR 2.14; 95% confidence interval [CI], 1.05 to 4.33), particularly among lean (body mass index
PubMed ID
11358945 View in PubMed
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Dynamic convergence and divergence of renal genomic and biological pathways in protection from Dahl salt-sensitive hypertension.

https://arctichealth.org/en/permalink/ahliterature98608
Source
Physiol Genomics. 2010 Mar 3;41(1):63-70
Publication Type
Article
Date
Mar-3-2010
Author
Limin Lu
Peigang Li
Chun Yang
Terry Kurth
Michael Misale
Meredith Skelton
Carol Moreno
Richard J Roman
Andrew S Greene
Howard J Jacob
Jozef Lazar
Mingyu Liang
Allen W Cowley
Author Affiliation
Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Source
Physiol Genomics. 2010 Mar 3;41(1):63-70
Date
Mar-3-2010
Language
English
Publication Type
Article
Keywords
Albuminuria - complications - genetics
Animals
Animals, Congenic
Chromosomes, Mammalian - genetics
Gene Expression Profiling
Gene Expression Regulation
Genome - genetics
Hypertension - complications - genetics - prevention & control
Inbreeding
Kidney - metabolism - pathology
Male
Phenotype
Rats
Rats, Inbred BN
Rats, Inbred Dahl
Reproducibility of Results
Signal Transduction - genetics
Thiobarbituric Acid Reactive Substances - metabolism
Abstract
Chromosome 13 consomic and congenic rat strains were analyzed to investigate the pattern of genomic pathway utilization involved in protection against salt-sensitive hypertension and renal injury. Introgression of the entire Brown-Norway chromosome 13 (consomic SS-13(BN)) or nonoverlapping segments of this chromosome (congenic strains, 16 Mbp in D13Rat151-D13Rat197 or 14 Mbp in D13Rat111-D13Got22) into the genome of the Dahl salt-sensitive rat attenuated salt-induced hypertension and proteinuria. mRNA abundance profiles in the renal cortex and the renal medulla from rats receiving 0.4% or 8% NaCl diets revealed two important features of pathway recruitment in these rat strains. First, the two congenic strains shared alterations in several pathways compared with Dahl salt-sensitive rats, despite the fact that the genomic segments introgressed in the two congenic strains did not overlap. Second, even though the genomic segment introgressed in each congenic strain was a part of the chromosome introgressed in the consomic strain, pathways altered in each congenic strain were not simply a subset of those altered in the consomic. Supporting the relevance of the mRNA data, differential expression of oxidative stress-related genes among the four strains of rats was associated with differences in urinary excretion of lipid peroxidation products. The findings suggest that different genetic alterations might converge to influence shared pathways in protection from hypertension, and that, depending on the genomic context, the same genetic alteration might diverge to affect different pathways.
PubMed ID
20009007 View in PubMed
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Effects of chromosome 17 on features of the metabolic syndrome in the Lyon hypertensive rat.

https://arctichealth.org/en/permalink/ahliterature86664
Source
Physiol Genomics. 2008 Apr 22;33(2):212-7
Publication Type
Article
Date
Apr-22-2008
Author
Gilibert S.
Kwitek A E
Hubner N.
Tschannen M.
Jacob H J
Sassard J.
Bataillard A.
Author Affiliation
Département de Physiologie et Pharmacologie Clinique, Institut des Sciences Pharmaceutiques et Biologiques, Université Lyon 1, Lyon, France.
Source
Physiol Genomics. 2008 Apr 22;33(2):212-7
Date
Apr-22-2008
Language
English
Publication Type
Article
Keywords
Animals
Blood pressure
Body Weight
Cholesterol - blood
Chromosomes, Mammalian - genetics
Hypertension - complications - genetics - physiopathology
Metabolic Syndrome X - complications - genetics - physiopathology
Phenotype
Polymorphism, Single Nucleotide - genetics
Rats
Rats, Inbred Strains
Time Factors
Triglycerides - blood
Abstract
The metabolic syndrome (involving obesity, hypertension, dyslipidemia, insulin resistance, and a proinflammatory/prethrombotic state) is a major risk factor for cardiovascular disease. Its incidence continues to rise, in part because of the epidemic increase in obesity. The Lyon hypertensive (LH) rat is a model for hypertension and several other features of the metabolic syndrome, having high body weight, plasma cholesterol, and triglycerides, increased insulin-to-glucose ratio, and salt-sensitive hypertension. Previous genetic studies in LH/Mav rats and a normotensive control (LN/Mav) identified quantitative trait loci (QTLs) on rat chromosome (RNO)17 for multiple features of the metabolic syndrome. To further evaluate the role of RNO17 in the LH rat, we generated a consomic strain (LH-17(BN)) by substituting LH RNO17 with that of the sequenced Brown Norway (BN/NHsdMcwi) rat. Male LH and BN rats and LH-17(BN) rats were characterized for blood pressure and metabolic and morphological parameters. Similar to the protective effect of LN alleles, the LH-17(BN) rat also showed decreased body weight, triglycerides, and blood pressure; however, there was no significant difference in cholesterol or insulin-to-glucose ratio. Therefore, the substitution of the LH chromosome 17 is sufficient to recapitulate some, but not all, of the traits previously mapped to this chromosome. This could be due to the lack of a susceptible LH genome background or due to the introgression of chromosome 17 from another strain. Regardless, this study provides a single-chromosome genetic model for further dissection of blood pressure and morphological and metabolic traits on this chromosome.
PubMed ID
18285521 View in PubMed
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Genome-wide scan for loci of adolescent obesity and their relationship with blood pressure.

https://arctichealth.org/en/permalink/ahliterature130335
Source
J Clin Endocrinol Metab. 2012 Jan;97(1):E145-50
Publication Type
Article
Date
Jan-2012
Author
Melkaye G Melka
Manon Bernard
Amel Mahboubi
Michal Abrahamowicz
Andrew D Paterson
Catriona Syme
Anbarasu Lourdusamy
Gunter Schumann
Gabriel T Leonard
Michel Perron
Louis Richer
Suzanne Veillette
Daniel Gaudet
Tomas Paus
Zdenka Pausova
Author Affiliation
The Hospital for Sick Children, Toronto, Canada.
Source
J Clin Endocrinol Metab. 2012 Jan;97(1):E145-50
Date
Jan-2012
Language
English
Publication Type
Article
Keywords
Adolescent
Age of Onset
Blood Pressure - genetics - physiology
Body mass index
Canada - epidemiology
Child
Chromosome Mapping
Female
Genetic Loci - genetics - physiology
Genetic Predisposition to Disease
Genome-Wide Association Study
Humans
Hypertension - complications - genetics
Male
Obesity - complications - epidemiology - genetics - physiopathology
Quebec - epidemiology
Validation Studies as Topic
Abstract
Hypertension, typically considered a disorder of adulthood, is now emerging in adolescence. This is mainly due to the growing prevalence of obesity and the fact that excess body fat increases blood pressure (BP).
The objective of the study was to investigate whether genome-wide identified gene loci of obesity are associated with elevated BP in adolescence.
This was a genotype-phenotype association study.
The study was conducted in a French-Canadian founder population.
Participants included 598 adolescents, aged 12-18 yr.
Testing associations between 530,011 single-nucleotide polymorphisms (SNP; Human610W-Quad BeadChip) and obesity measures and between identified SNP and BP.
Total fat mass (TFM) was assessed with bioelectrical impedance, and body mass index (BMI) was determined with anthropometry. BP was measured beat by beat during an hour-long protocol.
The genome-wide association studies of TFM and BMI revealed two novel and several previously identified loci of obesity. The former were PAX5 (rs16933812, TFM: P = 9.3 × 10(-9)) and MRPS22 (rs7638110, BMI: P = 4.6 × 10(-8)), and the top ones among the latter (P
PubMed ID
22013104 View in PubMed
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Higher risk for renal failure in first-degree relatives of white patients with end-stage renal disease: a population-based study.

https://arctichealth.org/en/permalink/ahliterature203908
Source
Am J Kidney Dis. 1998 Nov;32(5):794-801
Publication Type
Article
Date
Nov-1998
Author
D F O'Dea
S W Murphy
D. Hefferton
P S Parfrey
Author Affiliation
Division of Nephrology, The Health Sciences Center, Memorial University of Newfoundland, St John's, Canada.
Source
Am J Kidney Dis. 1998 Nov;32(5):794-801
Date
Nov-1998
Language
English
Publication Type
Article
Keywords
Case-Control Studies
Cause of Death
Confidence Intervals
Diabetes Complications
Diabetes Mellitus - genetics
European Continental Ancestry Group
Female
Glomerulonephritis - complications
Humans
Hypertension - complications - genetics
Incidence
Kidney Diseases - complications - genetics
Kidney Failure, Chronic - etiology - genetics
Male
Middle Aged
Newfoundland and Labrador
Odds Ratio
Polycystic Kidney, Autosomal Dominant - complications
Population Surveillance
Registries
Renal Dialysis
Risk factors
Spouses
Abstract
To explore the possibility that hereditary factors increase the risk for end-stage renal disease (ESRD), 669 patients with ESRD in the province of Newfoundland, Canada from 1987 to 1993 were studied. Detailed family histories were obtained from 584 (87%) consecutive probands and 499 spousal control subjects. Diseases with a Mendelian pattern of inheritance accounted for 8.4% of the cases; 4.5% of the cases were caused by autosomal dominant polycystic kidney disease (ADPKD). Glomerulonephritis was the original cause of renal failure in 25% of the probands, diabetes mellitus (DM) in 20%, unknown in 14%, interstitial kidney disease in 11%, other disease in 12%, multifactorial in 4%, and hypertension in 5%. In the group without a Mendelian pattern of inheritance, 28% of the probands had a first-, second-, or third-degree relative with renal failure associated with death or dialysis versus 15% of the controls. Compared with 0.4% of the control group, 1.2% of the first-degree relatives of probands developed renal failure (odds ratio [OR]=3.0; 95% confidence interval [CI], 1.7 to 5.2). No difference was observed when risks were compared for second-degree relatives, but a highly significant increased risk was observed for third-degree relatives (OR=2.1; 95% CI, 1.2 to 3.4). The highest rates of affected first-degree relatives occurred in probands with hypertensive renal failure (2.3%), DM (1.6%), and interstitial kidney disease (1.6%). The annual provincial incidence of ESRD, registered with the Canadian Organ Replacement Registry (CORR) from 1981 to 1993 was 79 per million, excluding the 8% of patients with Mendelian inherited disease. The similar rate of ESRD in first-degree relatives of probands without Mendelian inherited disease was 297 per million. We conclude that not only is the contribution of Mendelian inherited diseases to ESRD high, but there is also an increased risk for renal failure in first-degree relatives of probands without a Mendelian inherited renal disease in a white population.
PubMed ID
9820449 View in PubMed
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Homozygosity for the EPHX2 K55R polymorphism increases the long-term risk of ischemic stroke in men: a study in Swedes.

https://arctichealth.org/en/permalink/ahliterature98389
Source
Pharmacogenet Genomics. 2010 Feb;20(2):94-103
Publication Type
Article
Date
Feb-2010
Author
Cristiano Fava
Martina Montagnana
Elisa Danese
Peter Almgren
Bo Hedblad
Gunnar Engström
Göran Berglund
Pietro Minuz
Olle Melander
Author Affiliation
Department of Clinical Sciences, Lund University, University Hospital of Malmö, Sweden. cristiano.fava@med.lu.se
Source
Pharmacogenet Genomics. 2010 Feb;20(2):94-103
Date
Feb-2010
Language
English
Publication Type
Article
Keywords
Amino Acid Substitution - genetics
Blood Pressure - physiology
Demography
Endpoint Determination
Epoxide Hydrolases - genetics
Female
Genetic Predisposition to Disease
Homozygote
Humans
Hypertension - complications - genetics - physiopathology
Incidence
Ischemia - complications - epidemiology - genetics - physiopathology
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Sex Characteristics
Stroke - epidemiology - etiology - genetics - physiopathology
Sweden - epidemiology
Abstract
OBJECTIVES: The soluble epoxide hydrolase (gene name EPHX2) is responsible for metabolism of 8,9 11,12 and 14,15-epoxyeicosatrienoic acids, vasodilator and anti-inflammatory substances. There are several functional polymorphisms in the EPHX2 gene: two of them, the K55R and R287Q, showing an altered metabolic activity in vitro, were associated with coronary heart disease and ischemic stroke in previous studies. The aim of this study was to evaluate the effect of four polymorphisms in the EPHX2 gene on blood pressure levels, hypertension prevalence, and risk of incident cardiovascular events in a large sample of middle-aged Swedes. METHODS: The incidence of cardiovascular events (coronary events, n = 274; ischemic stroke, n = 197) was monitored over 10 years of follow-up. RESULTS: In the whole population, all polymorphisms had no effect on the studied parameters but a positive interaction between male sex and three SNPs including the K55R was evident: male, but not female, EPHX2 R55R homozygotes had significantly higher crude and adjusted systolic blood pressure and higher hypertension prevalence with respect to K-carriers. Kaplan-Meier curves showed higher incidence of ischemic strokes in male R55R homozygotes with respect to K-carriers (P = 0.015 by log-rank test). After adjustment for major cardiovascular risk factors, the hazard ratio for incident ischemic stroke in male R55R homozygotes remained significantly higher (hazard ratio: 4.8; 95% confidence interval: 1.2-19.9). CONCLUSION: The functional K55R polymorphism of the EPHX2 gene confers a higher risk of hypertension prevalence and increases the risk of incident ischemic stroke in male homozygotes. Additional studies are needed to confirm these data and to elucidate the interaction between sex and the EPHX2 K55R polymorphism.
PubMed ID
20065888 View in PubMed
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Localization of a gene for peripheral arterial occlusive disease to chromosome 1p31.

https://arctichealth.org/en/permalink/ahliterature47591
Source
Am J Hum Genet. 2002 Mar;70(3):586-92
Publication Type
Article
Date
Mar-2002
Author
Gudmundur Gudmundsson
Stefan E Matthiasson
Haukur Arason
Halldor Johannsson
Freyr Runarsson
Hjördis Bjarnason
Katrin Helgadottir
Steinthora Thorisdottir
Gudrun Ingadottir
Klaus Lindpaintner
Jesus Sainz
Vilmundur Gudnason
Michael L Frigge
Augustine Kong
Jeffrey R Gulcher
Kari Stefansson
Author Affiliation
deCODE Genetics, Reykjavik, Iceland.
Source
Am J Hum Genet. 2002 Mar;70(3):586-92
Date
Mar-2002
Language
English
Publication Type
Article
Keywords
Arterial Occlusive Diseases - complications - genetics
Chromosome Mapping
Chromosomes, Human, Pair 1 - genetics
Diabetes Complications
Diabetes Mellitus - genetics
Female
Humans
Hyperlipidemia - complications - genetics
Hypertension - complications - genetics
Iceland
Lod Score
Male
Microsatellite Repeats - genetics
Pedigree
Risk factors
Smoking - adverse effects
Abstract
Peripheral arterial occlusive disease (PAOD) results from atherosclerosis of large and medium peripheral arteries, as well as the aorta, and has many risk factors, including smoking, diabetes, hypertension, and hyperlipidemia. PAOD often coexists with coronary artery disease and cerebrovascular disease. Cross-matching a population-based list of Icelandic patients with PAOD who had undergone angiography and/or revascularization procedures with a genealogy database of the entire Icelandic nation defined 116 extended families containing 272 patients. A genomewide scan with microsatellite markers revealed significant linkage to chromosome 1p31 with an allele-sharing LOD score of 3.93 (P=1.04 x 10(-5)). We designate this locus as "PAOD1." Subtracting 35 patients with a history of stroke increased the LOD score to 4.93. This suggests that, although PAOD and other vascular diseases share risk factors, genetic factors specific to subtypes of vascular disease may exist.
PubMed ID
11833003 View in PubMed
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18 records – page 1 of 2.