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Article ; Online: Epigenetic histone acetylation modifiers in vascular remodelling: new targets for therapy in cardiovascular disease.

Pons, Douwe / de Vries, Florentine R / van den Elsen, Peter J / Heijmans, Bastiaan T / Quax, Paul H A / Jukema, J Wouter

European heart journal

2009 Volume 30, Issue 3, Page(s) 266–277

Abstract: Significant progress has been made in the clinical management of a variety of cardiovascular diseases. Nevertheless, the therapeutic efficacy of the current treatment modalities for atherosclerosis and restenosis is not fully sufficient in a large ... ...

Abstract	Significant progress has been made in the clinical management of a variety of cardiovascular diseases. Nevertheless, the therapeutic efficacy of the current treatment modalities for atherosclerosis and restenosis is not fully sufficient in a large proportion of patients. One of the major contributing factors is the clinical and biological heterogeneity of these still life-threatening diseases, which involve processes that we do not fully understand at the moment. Over the past decades, it has become increasingly clear that part of the gene-environmental interactions relevant for complex diseases is regulated by epigenetic mechanisms such as histone acetylation and DNA methylation. Epigenetic processes modulate gene expression patterns without modifying the actual DNA sequence and have profound effects on the cellular repertoire of expressed genes. They contribute to the expression of genes that play a key role in extracellular matrix formation, inflammation, and proliferation, processes involved in cardiovascular pathologies such as atherosclerosis and restenosis. Therefore, in this review, we argue that epigenetic regulators involved in histone acetylating and deacetylating activities contribute to the pathogenesis of atherosclerosis and restenosis. Furthermore, as alterations in chromatin structure are reversible, these epigenetic modifications are amendable to pharmacological intervention, which may prove to be an effective treatment modality for the management of cardiovascular diseases.
MeSH term(s)	Acetylation ; Atherosclerosis/drug therapy ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Cell Proliferation ; Epigenesis, Genetic ; Extracellular Matrix/metabolism ; Histone Acetyltransferases/physiology ; Histone Deacetylases/physiology ; Humans ; Muscle, Smooth, Vascular/pathology
Chemical Substances	Histone Acetyltransferases (EC 2.3.1.48) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2009-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603098-1
ISSN	1522-9645 ; 0195-668X
ISSN (online)	1522-9645
ISSN	0195-668X
DOI	10.1093/eurheartj/ehn603
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Article ; Online: Metabolic Background Determines the Importance of NOS3 Polymorphisms in Restenosis after Percutaneous Coronary Intervention

Douwe Pons / Pascalle S. Monraats / Aeilko H. Zwinderman / Moniek P. M. de Maat / Pieter A. F. M. Doevendans / Robbert J. de Winter / René A. Tio / Johannes Waltenberger / J. Wouter Jukema

Disease Markers, Vol 26, Iss 2, Pp 75-

A Study in Patients with and without the Metabolic Syndrome

2009 Volume 83

Abstract: Variation in the NOS3 gene has been related to the development of restenosis. The Glu298Asp polymorphism has previously been investigated for its effect on NO levels and the development of restenosis. However, the variability of findings gave rise to the ...

Abstract	Variation in the NOS3 gene has been related to the development of restenosis. The Glu298Asp polymorphism has previously been investigated for its effect on NO levels and the development of restenosis. However, the variability of findings gave rise to the hypothesis that the functional significance of this polymorphism may only become manifest under conditions of endothelial dysfunction. Since patients with the metabolic syndrome are known to have endothelial dysfunction, we aimed to investigate if the significance of NOS3 polymorphisms may depend on the presence of the metabolic syndrome.
Keywords	Medicine (General) ; R5-920
Language	English
Publishing date	2009-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
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Article ; Online: The 5352 A allele of the pro-inflammatory caspase-1 gene predicts late-acquired stent malapposition in STEMI patients treated with sirolimus stents.

Bergheanu, Sandrin C / Pons, Douwe / van der Hoeven, Bas L / Liem, Su-San / Siegerink, Bob / Schalij, Martin J / van der Bom, Johanna G / Jukema, J Wouter

Heart and vessels

2010 Volume 26, Issue 3, Page(s) 235–241

Abstract: Late-acquired stent malapposition (LASM) is a common finding after sirolimus-eluting stent (SES) implantation and may be the cause for late stent thrombosis. Inflammation may play a pivotal role in LASM just as it plays in stent restenosis. We have ... ...

Abstract	Late-acquired stent malapposition (LASM) is a common finding after sirolimus-eluting stent (SES) implantation and may be the cause for late stent thrombosis. Inflammation may play a pivotal role in LASM just as it plays in stent restenosis. We have therefore investigated seven polymorphisms involved in inflammatory processes, related in previous reports to restenosis, on the risk of LASM in SES patients. Patients with ST-elevation myocardial infarction who underwent SES implantation and had intravascular ultrasonography (IVUS) data available for both immediate post-intervention and 9-month follow-up were included in the present study. In total, 104 patients from the MISSION! Intervention Study were genotyped for the caspase-1 5352 G/A, eotaxin 1382 A/G, CD14 260 A/G, colony stimulating factor 2 1943 C/T, IL10 -1117 C/T, IL10 4251 C/T, and the tumor necrosis factor alpha 1211 C/T polymorphisms. LASM occurred in 26/104 (25%) of patients. We found a significantly higher risk for LASM in patients carrying the caspase-1 (CASP1) 5352 A allele (RR = 2.32; 95% CI 1.22-4.42). In addition, mean neointimal growth was significantly lower in patients carrying this LASM risk allele (1.6 vs. 4.1%, p = 0.014). The other six polymorphisms related to inflammation were not significantly related to the risk of LASM. In conclusion, carriers of the 5352 A allele in the caspase-1 gene are at increased risk of developing LASM after SES implantation. If this is confirmed in larger studies, then screening for this polymorphism in patients undergoing percutaneous coronary interventions could eventually help cardiologists to better select between commercially available stents.
MeSH term(s)	Aged ; Angioplasty, Balloon, Coronary/adverse effects ; Angioplasty, Balloon, Coronary/instrumentation ; Cardiovascular Agents/administration & dosage ; Caspase 1/genetics ; Chi-Square Distribution ; Drug-Eluting Stents ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Humans ; Inflammation/diagnostic imaging ; Inflammation/enzymology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation Mediators ; Male ; Middle Aged ; Myocardial Infarction/diagnostic imaging ; Myocardial Infarction/enzymology ; Myocardial Infarction/genetics ; Myocardial Infarction/therapy ; Netherlands ; Prospective Studies ; Risk Assessment ; Risk Factors ; Sirolimus/administration & dosage ; Time Factors ; Treatment Outcome ; Ultrasonography, Interventional
Chemical Substances	Cardiovascular Agents ; Inflammation Mediators ; Caspase 1 (EC 3.4.22.36) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2010-10-30
Publishing country	Japan
Document type	Journal Article ; Randomized Controlled Trial
ZDB-ID	89678-0
ISSN	1615-2573 ; 0910-8327 ; 0935-736X
ISSN (online)	1615-2573
ISSN	0910-8327 ; 0935-736X
DOI	10.1007/s00380-010-0046-8
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Article ; Online: Toll-like receptor 4 gene polymorphisms show no association with the risk of clinical or angiographic restenosis after percutaneous coronary intervention.

Beijk, Marcel A M / Boekholdt, S Matthijs / Rittersma, Saskia Z H / Pons, Douwe / Zwinderman, Aeilko H / Doevendans, Pieter A F / Tio, Rene A / Tijssen, Jan G P / Jukema, J Wouter / de Winter, Robbert J

Pharmacogenetics and genomics

2010 Volume 20, Issue 9, Page(s) 544–552

Abstract: Objective: Restenosis after percutaneous coronary intervention (PCI) remains an issue even in the drug-eluting stent era. Genetic polymorphisms may provide insight in the pathogenesis of restenosis and may help in the stratification of patients at risk ... ...

Abstract	Objective: Restenosis after percutaneous coronary intervention (PCI) remains an issue even in the drug-eluting stent era. Genetic polymorphisms may provide insight in the pathogenesis of restenosis and may help in the stratification of patients at risk for restenosis. The aim of this study was to examine whether polymorphisms at the toll-like receptor 4 (TLR4) locus, that are associated with impaired innate immune system and with an increased risk of cardiovascular events, were associated with clinical and/or angiographic restenosis after PCI. Methods: The GENetic Determinants of Restenosis (GENDER) project was a prospective, multicenter study that enrolled 3146 consecutive patients after successful PCI. Frequencies of the TLR4 896A/G (Asp299Gly; rs4986790) and 1196C/T (Thr399Ile; rs4986791) polymorphisms and haplotypes were assessed. Patients were followed up for 1 year and in a subgroup of 406 patients angiographic follow-up was obtained. Results: We included a total of 2682 patients that underwent successful PCI. There was no association between genotypes and the risk of target vessel revascularization at 1-year or late luminal loss at 6-months angiographic follow-up (P=0.53 and 0.44, respectively). Absence of association with target lesion revascularization and late luminal loss was replicated in the GEnetic risk factors for In-Stent Hyperplasia study Amsterdam (GEISHA) cohort study of 674 patients and in a subgroup of 550 patients with angiographic follow-up available (P=0.26, and 0.86, respectively). Moreover, in both the studies, no significant differences between haplotypes A/C and G/T were observed for target vessel revascularization at late luminal loss. Conclusion: Although inflammation has been implicated in the pathophysiology of restenosis, the 896A/G and 1196C/T polymorphisms or haplotypes based on these polymorphisms at the TLR4 locus are not associated with an increased risk of target vessel revascularization or angiographic restenosis after PCI. These polymorphisms are not useful for pre-PCI identification of patients at risk for restenosis.
MeSH term(s)	Angioplasty, Balloon, Coronary/adverse effects ; Coronary Angiography ; Coronary Restenosis/etiology ; Coronary Restenosis/genetics ; Female ; Follow-Up Studies ; Gene Frequency/genetics ; Genetic Predisposition to Disease ; Haplotypes/genetics ; Humans ; Linkage Disequilibrium/genetics ; Male ; Middle Aged ; Neovascularization, Physiologic ; Polymorphism, Single Nucleotide/genetics ; Risk Factors ; Toll-Like Receptor 4/genetics ; Treatment Outcome
Chemical Substances	TLR4 protein, human ; Toll-Like Receptor 4
Language	English
Publishing date	2010-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2175826-8
ISSN	1744-6880 ; 0960-314X ; 1744-6872
ISSN (online)	1744-6880
ISSN	0960-314X ; 1744-6872
DOI	10.1097/FPC.0b013e32833d7b29
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Article ; Online: Myocardial infarction occurs with a similar 24 h pattern in the 4G/5G versions of plasminogen activator inhibitor-1.

Bergheanu, Sandrin C / Pons, Douwe / Jukema, J Wouter / van der Hoeven, Bas L / Liem, Su-San / Vandenbroucke, Jan P / Rosendaal, Frits R / le Cessie, Saskia / Schalij, Martin J / van der Bom, Johanna G

Chronobiology international

2009 Volume 26, Issue 4, Page(s) 637–652

Abstract: PAI-1 expression is regulated by a 4G/5G promoter polymorphism. The 4G allele is associated with greater circadian variation of PAI-1 levels. We hypothesized that the 24 h variation of cardiac risk is more pronounced among persons with the 4G4G genotype ... ...

Abstract	PAI-1 expression is regulated by a 4G/5G promoter polymorphism. The 4G allele is associated with greater circadian variation of PAI-1 levels. We hypothesized that the 24 h variation of cardiac risk is more pronounced among persons with the 4G4G genotype than among ones with 4G5G and 5G5G genotypes. We assessed the time of onset of symptoms in 623 consecutive patients with acute myocardial infarction (AMI) enrolled in the MISSION! Study between February 1, 2004, and October 29, 2006. All of the patients were genotyped for the PAI-1 4G/5G polymorphism. We quantified the amplitude of the 24 h variation of AMI with a generalized linear model with Poisson distribution. A morning peak, between 06:00-11:59 h (n = 197; 32% of all cases), in the onset of symptoms of AMI was observed. The group composed of patients with the 4G4G genotype did not have a more pronounced morning peak than the groups composed of other genotypes; the 24 h variation was 38% (95% confidence interval 12-70%) in the group of 4G4G patients and 34% (14-58%) and 56% (20-100%) in the 4G5G and 5G5G groups of patients, respectively. Our findings show that 24 h variation of cardiac risk is not more pronounced among the 4G4G genotype of PAI-1.
MeSH term(s)	Circadian Rhythm/genetics ; Circadian Rhythm/physiology ; Cohort Studies ; Female ; Genotype ; Humans ; Incidence ; Male ; Middle Aged ; Myocardial Infarction/genetics ; Myocardial Infarction/physiopathology ; Plasminogen Activator Inhibitor 1/genetics ; Polymorphism, Genetic ; Retrospective Studies
Chemical Substances	Plasminogen Activator Inhibitor 1
Language	English
Publishing date	2009-05
Publishing country	England
Document type	Journal Article
ZDB-ID	998996-1
ISSN	1525-6073 ; 0742-0528
ISSN (online)	1525-6073
ISSN	0742-0528
DOI	10.1080/07420520902925993
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Article ; Online: Efficacy and safety of haloperidol prophylaxis for delirium prevention in older medical and surgical at-risk patients acutely admitted to hospital through the emergency department: study protocol of a multicenter, randomised, double-blind, placebo-controlled clinical trial.

Schrijver, Edmée J M / de Vries, Oscar J / Verburg, Astrid / de Graaf, Karola / Bet, Pierre M / van de Ven, Peter M / Kamper, Ad M / Diepeveen, Sabine Ha / Anten, Sander / Siegel, Andrea / Kuipéri, Esther / Lagaay, Anne M / van Marum, Rob J / van Strien, Astrid M / Boelaarts, Leo / Pons, Douwe / Kramer, Mark H H / Nanayakkara, Prabath W B

BMC geriatrics

2014 Volume 14, Page(s) 96

Abstract: Background: Delirium is associated with substantial morbidity and mortality rates in elderly hospitalised patients, and a growing problem due to increase in life expectancy. Implementation of standardised non-pharmacological delirium prevention ... ...

Abstract	Background: Delirium is associated with substantial morbidity and mortality rates in elderly hospitalised patients, and a growing problem due to increase in life expectancy. Implementation of standardised non-pharmacological delirium prevention strategies is challenging and adherence remains low. Pharmacological delirium prevention with haloperidol, currently the drug of choice for delirium, seems promising. However, the generalisability of randomised controlled trial results is questionable since studies have only been performed in selected postoperative hip-surgery and intensive care unit patient populations. We therefore present the design of the multicenter, randomised, double-blind, placebo-controlled clinical trial on early pharmacological intervention to prevent delirium: haloperidol prophylaxis in older emergency department patients (The HARPOON study). Methods/design: In six Dutch hospitals, at-risk patients aged 70 years or older acutely admitted through the emergency department for general medicine and surgical specialties are randomised (n = 390) for treatment with prophylactic haloperidol 1 mg or placebo twice daily for a maximum of seven consecutive days. Primary outcome measure is the incidence of in-hospital delirium within seven days of start of the study intervention, diagnosed with the Confusion Assessment Method, and the Diagnostic and Statistical Manual of Mental Disorders, fourth edition criteria for delirium. Secondary outcome measures include delirium severity and duration assessed with the Delirium Rating Scale Revised 98; number of delirium-free days; adverse events; hospital length-of-stay; all-cause mortality; new institutionalisation; (Instrumental) Activities of Daily Living assessed with the Katz Index of ADL, and Lawton IADL scale; cognitive function assessed with the Six-item Cognitive Impairment Test, and the Dutch short form Informant Questionnaire on Cognitive Decline in the Elderly. Patients will be contacted by telephone three and six months post-discharge to collect data on cognitive- and physical function, home residency, all-cause hospital admissions, and all-cause mortality. Discussion: The HARPOON study will provide relevant information on the efficacy and safety of prophylactic haloperidol treatment for in-hospital delirium and its effects on relevant clinical outcomes in elderly at-risk medical and surgical patients. Trial registration: EudraCT Number: 201100476215; ClinicalTrials.gov Identifier: NCT01530308; Dutch Clinical Trial Registry: NTR3207.
MeSH term(s)	Aged ; Aged, 80 and over ; Antipsychotic Agents/administration & dosage ; Antipsychotic Agents/adverse effects ; Basal Ganglia Diseases/chemically induced ; Delirium/diagnosis ; Delirium/prevention & control ; Double-Blind Method ; Emergency Service, Hospital/trends ; Female ; Follow-Up Studies ; Haloperidol/administration & dosage ; Haloperidol/adverse effects ; Humans ; Male ; Patient Admission/trends ; Risk Factors ; Surgery Department, Hospital/trends ; Treatment Outcome
Chemical Substances	Antipsychotic Agents ; Haloperidol (J6292F8L3D)
Language	English
Publishing date	2014-08-28
Publishing country	England
Document type	Journal Article ; Multicenter Study ; Randomized Controlled Trial
ZDB-ID	2059865-8
ISSN	1471-2318 ; 1471-2318
ISSN (online)	1471-2318
ISSN	1471-2318
DOI	10.1186/1471-2318-14-96
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Article ; Online: Factor VII Activating Protease Polymorphism (G534E) Is Associated with Increased Risk for Stroke and Mortality.

Trompet, Stella / Pons, Douwe / Kanse, Sandip M / de Craen, Anton J M / Ikram, M Arfan / Verschuren, Jeffrey J W / Zwinderman, Aeilko H / Doevendans, Pieter A F M / Tio, René A / de Winter, Robbert J / Slagboom, P Eline / Westendorp, Rudi G J / Jukema, J Wouter

Stroke research and treatment

2011 Volume 2011, Page(s) 424759

Abstract: Introduction. The FSAP-Marburg I polymorphism (1704G > A), which reduces FSAP activity, is associated with late complications of carotid stenosis in humans. Therefore, this study examines the influence of the Marburg I polymorphism and the closely linked ...

Abstract	Introduction. The FSAP-Marburg I polymorphism (1704G > A), which reduces FSAP activity, is associated with late complications of carotid stenosis in humans. Therefore, this study examines the influence of the Marburg I polymorphism and the closely linked Marburg II polymorphism (1280G > C) on various cardiovascular outcomes in two large independent study populations. Methods. The two Marburg polymorphisms in the HABP2 gene encoding FSAP were genotyped in a large population of elderly patients at risk for vascular disease (the PROSPER-study, n = 5804) and in a study population treated with a percutaneous coronary intervention (the GENDER-study, n = 3104). Results. In the PROSPER study, the Marburg I polymorphism was associated with an increased risk of clinical stroke (HR: 1.60, 95% CI: 1.13-2.28) and all-cause mortality (HR: 1.33, 95% CI: 1.04-1.71). In the GENDER study carriers of this variant seemed at lower risk of developing restenosis (HR: 0.59, 95% CI: 0.34-1.01). The Marburg II polymorphism showed similar but weaker results. Conclusion. The increase in stroke risk in Marburg I carriers could be due to differential effects on smooth muscle cells and on matrix metalloproteinases, thereby influencing plaque stability. The possible protective effect on restenosis could be the result of reduced activation of zymogens, which are involved in hemostasis and matrix remodeling.
Language	English
Publishing date	2011-06-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573724-7
ISSN	2042-0056 ; 2090-8105
ISSN (online)	2042-0056
ISSN	2090-8105
DOI	10.4061/2011/424759
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Article: Metabolic background determines the importance of NOS3 polymorphisms in restenosis after percutaneous coronary intervention: A study in patients with and without the metabolic syndrome.

Pons, Douwe / Monraats, Pascalle S / Zwinderman, Aeilko H / de Maat, Moniek P M / Doevendans, Pieter A F M / de Winter, Robbert J / Tio, René A / Waltenberger, Johannes / Jukema, J Wouter

Disease markers

2009 Volume 26, Issue 2, Page(s) 75–83

Abstract	Variation in the NOS3 gene has been related to the development of restenosis. The Glu298Asp polymorphism has previously been investigated for its effect on NO levels and the development of restenosis. However, the variability of findings gave rise to the hypothesis that the functional significance of this polymorphism may only become manifest under conditions of endothelial dysfunction. Since patients with the metabolic syndrome are known to have endothelial dysfunction, we aimed to investigate if the significance of NOS3 polymorphisms may depend on the presence of the metabolic syndrome. We examined the impact of the -949 A/G, the -716 C/T and the Glu298Asp polymorphisms in the NOS3 gene on the risk of clinical restenosis in a previously described subpopulation of the GENDER-study, a multicenter prospective study design that enrolled consecutive patients after successful PCI. This subpopulation consisted of 901 patients of whom sufficient data were available to establish absence or presence of the metabolic syndrome. Of these patients, 448 had the metabolic syndrome. Clinical restenosis, defined as target vessel revascularization (TVR), was the primary endpoint. We demonstrated that the minor -949G, -716T and 298Asp alleles were associated with a significantly increased risk of TVR in patients with the metabolic syndrome (HR: 1.58 [95%CI: 1.04-2.40], HR: 1.95 [95%CI: 1.02-3.70] and HR: 1.67 [95%CI: 1.09-2.54], respectively). In the group without the metabolic syndrome we observed no association between the three polymorphisms and TVR.
MeSH term(s)	Angioplasty, Balloon, Coronary ; Coronary Angiography ; Coronary Restenosis/diagnostic imaging ; Coronary Restenosis/genetics ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Metabolic Syndrome/diagnostic imaging ; Metabolic Syndrome/genetics ; Middle Aged ; Nitric Oxide Synthase Type III/genetics ; Polymorphism, Genetic/genetics ; Prospective Studies ; Risk Factors
Chemical Substances	NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2009-04-30
Publishing country	United States
Document type	Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
ZDB-ID	604951-5
ISSN	1875-8630 ; 0278-0240
ISSN (online)	1875-8630
ISSN	0278-0240
DOI	10.3233/DMA-2009-0609
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Article: Platelet receptor P2RY12 haplotypes predict restenosis after percutaneous coronary interventions

Rudež, Goran / Pons, Douwe / Leebeek, Frank / Monraats, Pascalle / Schrevel, Marlies / Zwinderman, Aeilko / de Winter, Robbert / Tio, René / Doevendans, Pieter / Jukema, Wouter / de Maat, Moniek

Human mutation. 2008 Mar., v. 29, no. 3

2008

Abstract: The platelet receptor P2Y12 (gene symbol P2RY12) is involved in several processes that contribute to restenosis after percutaneous coronary interventions (PCI). Therefore, common variation in the P2Y12 gene may serve as a useful marker for risk ... ...

Abstract	The platelet receptor P2Y12 (gene symbol P2RY12) is involved in several processes that contribute to restenosis after percutaneous coronary interventions (PCI). Therefore, common variation in the P2Y12 gene may serve as a useful marker for risk stratification. We studied whether common variation in the platelet receptor P2Y12 gene affects the risk of restenosis after PCI. Comprehensive coverage of common variation in the P2Y12 gene was obtained by genotyping five haplotype-tagging SNPs (ht-SNPs) in 2,062 PCI-treated patients who received a stent and participated in the GENetic DEterminants of Restenosis (GENDER) Study. Haplotypes were inferred and their association with target vessel revascularization (TVR) was studied. Seven P2Y12 haplotypes were identified with an allelic frequency above 5% (designated here H1 to H7) of which two (H5 and H7) were associated with a higher risk of TVR (hazard ratios [HR]=1.4, 95% confidence interval [CI]=1.0-2.0; and HR=1.6, 95% CI=1.2-2.0, respectively) than the reference P2Y12 haplotype (H1), which contains the common alleles of all five P2Y12 ht-SNPs. Our study shows that common variation in the P2Y12 gene predicts restenosis in PCI-treated patients. Hum Mutat 29(3), 375-380, 2008.
Language	English
Dates of publication	2008-03
Size	p. 375-380.
Publishing place	Wiley Subscription Services, Inc., A Wiley Company
Document type	Article
ZDB-ID	1126646-6
ISSN	1098-1004 ; 1059-7794
ISSN (online)	1098-1004
ISSN	1059-7794
DOI	10.1002/humu.20641
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Platelet receptor P2RY12 haplotypes predict restenosis after percutaneous coronary interventions.

Rudez, Goran / Pons, Douwe / Leebeek, Frank / Monraats, Pascalle / Schrevel, Marlies / Zwinderman, Aeilko / de Winter, Robbert / Tio, René / Doevendans, Pieter / Jukema, Wouter / de Maat, Moniek

Human mutation

2008 Volume 29, Issue 3, Page(s) 375–380

Abstract	The platelet receptor P2Y12 (gene symbol P2RY12) is involved in several processes that contribute to restenosis after percutaneous coronary interventions (PCI). Therefore, common variation in the P2Y12 gene may serve as a useful marker for risk stratification. We studied whether common variation in the platelet receptor P2Y12 gene affects the risk of restenosis after PCI. Comprehensive coverage of common variation in the P2Y12 gene was obtained by genotyping five haplotype-tagging SNPs (ht-SNPs) in 2,062 PCI-treated patients who received a stent and participated in the GENetic DEterminants of Restenosis (GENDER) Study. Haplotypes were inferred and their association with target vessel revascularization (TVR) was studied. Seven P2Y12 haplotypes were identified with an allelic frequency above 5% (designated here H1 to H7) of which two (H5 and H7) were associated with a higher risk of TVR (hazard ratios [HR]=1.4, 95% confidence interval [CI]=1.0-2.0; and HR=1.6, 95% CI=1.2-2.0, respectively) than the reference P2Y12 haplotype (H1), which contains the common alleles of all five P2Y12 ht-SNPs. Our study shows that common variation in the P2Y12 gene predicts restenosis in PCI-treated patients.
MeSH term(s)	Aged ; Alleles ; Angioplasty, Balloon, Coronary ; Blood Platelets/metabolism ; Coronary Disease/blood ; Coronary Disease/genetics ; Coronary Disease/therapy ; Coronary Restenosis/blood ; Coronary Restenosis/etiology ; Coronary Restenosis/genetics ; Female ; Follow-Up Studies ; Gene Frequency ; Haplotypes ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Receptors, Purinergic P2/genetics ; Receptors, Purinergic P2Y12 ; Risk Factors ; Stents
Chemical Substances	P2RY12 protein, human ; Receptors, Purinergic P2 ; Receptors, Purinergic P2Y12
Language	English
Publishing date	2008-03
Publishing country	United States
Document type	Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
ZDB-ID	1126646-6
ISSN	1098-1004 ; 1059-7794
ISSN (online)	1098-1004
ISSN	1059-7794
DOI	10.1002/humu.20641
Database	MEDical Literature Analysis and Retrieval System OnLINE

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