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  1. Article ; Online: Association of glutathione-S-transferase omega haplotypes with susceptibility to chronic obstructive pulmonary disease.

    Yanbaeva, Dilyara G / Wouters, Emiel F M / Dentener, Mieke A / Spruit, Martijn A / Reynaert, Niki L

    Free radical research

    2009  Volume 43, Issue 8, Page(s) 738–743

    Abstract: Cigarette smoking is the main risk factor for developing the inflammatory lung disease chronic obstructive pulmonary disease (COPD). Differences in susceptibility among smokers have been attributed to a genetic predisposition. A recent publication on the ...

    Abstract Cigarette smoking is the main risk factor for developing the inflammatory lung disease chronic obstructive pulmonary disease (COPD). Differences in susceptibility among smokers have been attributed to a genetic predisposition. A recent publication on the Framingham Heart Study found a strong association of the Asn142Asp SNP in Glutatthione-S-transferase Omega (GSTO) 2 with forced expiratory volume in the first second (FEV(1)) and forced vital capacity (FVC). FEV(1) is the main parameter reflecting the degree of airflow limitation in patients with COPD. Therefore the present study was undertaken to investigate whether the Asn142Asp polymorphism in GSTO2 occurs more frequently in patients with COPD than healthy subjects and to replicate the finding that it strongly correlates with FEV(1). Furthermore, the Ala140Asp substitution in GSTO1 was examined. Genotyping was carried out in 195 healthy controls and 355 patients with COPD. The results demonstrate that the Asn142Asp polymorphism in GSTO2 and the GSTO1140Asp/GSTO2142Asp haplotype were associated with increased risk of COPD. However, single-marker and haplotype-based analyses failed to reveal an association between lung function parameters and investigated non-synonymous coding SNPs in the GSTO genes. In conclusion, GSTO2 is a candidate gene for COPD, but is not associated with FEV(1).
    MeSH term(s) Aged ; Case-Control Studies ; Female ; Forced Expiratory Volume/genetics ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genotype ; Glutathione Transferase/genetics ; Haplotypes/genetics ; Humans ; Male ; Middle Aged ; Mutation, Missense ; Netherlands ; Point Mutation ; Polymorphism, Single Nucleotide ; Pulmonary Disease, Chronic Obstructive/epidemiology ; Pulmonary Disease, Chronic Obstructive/etiology ; Pulmonary Disease, Chronic Obstructive/genetics ; Smoking/adverse effects ; Vital Capacity/genetics
    Chemical Substances GSTO1 protein, human (EC 2.5.1.18) ; GSTO2 protein, human (EC 2.5.1.18) ; Glutathione Transferase (EC 2.5.1.18)
    Language English
    Publishing date 2009-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1194130-3
    ISSN 1029-2470 ; 1071-5762
    ISSN (online) 1029-2470
    ISSN 1071-5762
    DOI 10.1080/10715760903038440
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2236: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: Systemic effects of smoking.

    Yanbaeva, Dilyara G / Dentener, Mieke A / Creutzberg, Eva C / Wesseling, Geertjan / Wouters, Emiel F M

    Chest

    2007  Volume 131, Issue 5, Page(s) 1557–1566

    Abstract: Smoking is one of the major lifestyle factors influencing the health of human beings. Life-long cigarette smokers have a higher prevalence of common diseases such as atherosclerosis and COPD with significant systemic impact. The present review evaluates ... ...

    Abstract Smoking is one of the major lifestyle factors influencing the health of human beings. Life-long cigarette smokers have a higher prevalence of common diseases such as atherosclerosis and COPD with significant systemic impact. The present review evaluates current knowledge concerning possible pathways through which cigarette smoking can affect human health, with special focus on extrapulmonary effects. Long-term smoke exposure can result in systemic oxidants-antioxidants imbalance as reflected by increased products of lipid peroxidation and depleted levels of antioxidants like vitamins A and C in plasma of smokers. A low-grade systemic inflammatory response is evident in smokers as confirmed by numerous population-based studies: elevated levels of C-reactive protein (CRP), fibrinogen, and interleukin-6, as well as increased counts of WBC have been reported. Furthermore, rheologic, coagulation and endothelial function markers like hematocrit, blood and/or plasma viscosity, fibrin d-dimer, circulating adhesion molecules (intracellular adhesion molecule-1, selectins), tissue plasminogen activator antigen, and plasminogen activator inhibitor type I are altered in chronic cigarette smokers. Although most of smoking-induced changes are reversible after quitting, some inflammatory mediators like CRP are still significantly raised in ex-smokers up to 10 to 20 years after quitting, suggesting ongoing low-grade inflammatory response persisting in former smokers. New longitudinal epidemiologic and genetic studies are required to evaluate the role of smoking itself and possible gene/environment interplay in initiation and development of smoking-induced common diseases affecting humans.
    MeSH term(s) Atherosclerosis/etiology ; Atherosclerosis/physiopathology ; Blood Coagulation Disorders/etiology ; Blood Coagulation Disorders/physiopathology ; Chronic Disease ; Endothelium, Vascular/physiopathology ; Environment ; Genetic Predisposition to Disease ; Hemostasis/physiology ; Humans ; Inflammation/etiology ; Inflammation/physiopathology ; Oxidative Stress/physiology ; Smoking/adverse effects ; Smoking/genetics
    Language English
    Publishing date 2007-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1378/chest.06-2179
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui III Zs.45: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 349: Show issues

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  3. Article: Systemic inflammation in COPD: is genetic susceptibility a key factor?

    Yanbaeva, Dilyara G / Dentener, Mieke A / Creutzberg, Eva C / Wouters, Emiel F M

    COPD

    2006  Volume 3, Issue 1, Page(s) 51–61

    Abstract: COPD is a multicomponent disease characterized by abnormal inflammatory response of the lungs to noxious particles that is accompanied by systemic effects like weight loss, muscle wasting, reduced functional capacity and impaired health status. A ... ...

    Abstract COPD is a multicomponent disease characterized by abnormal inflammatory response of the lungs to noxious particles that is accompanied by systemic effects like weight loss, muscle wasting, reduced functional capacity and impaired health status. A persistent low-grade systemic inflammatory response reflected by enhanced levels of acute phase proteins like C-reactive protein (CRP) and pro-inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, is present in part of the COPD population. The production of inflammatory proteins is partly genetically determined. Several studies have shown that polymorphisms within genes coding for these inflammatory mediators may modulate systemic inflammatory responses. Among all of these genes, the TNF family (TNF-alpha, lymphotoxin (LT)-alph and their receptors TNF-R55 and TNF-R75), interleukin (IL)-6 and CRP gene polymorphisms are the most prominent candidates. However, large carefully designed studies in well-characterized COPD cohorts are required to unravel the exact role of genetic background in the systemic component of this disease.
    MeSH term(s) C-Reactive Protein/genetics ; C-Reactive Protein/physiology ; Genetic Predisposition to Disease ; Humans ; Inflammation/genetics ; Interleukin-6/analysis ; Interleukin-6/genetics ; Lymphotoxin-alpha/genetics ; Polymorphism, Genetic ; Pulmonary Disease, Chronic Obstructive/genetics ; Receptors, Tumor Necrosis Factor/genetics ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/physiology
    Chemical Substances Interleukin-6 ; Lymphotoxin-alpha ; Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha ; C-Reactive Protein (9007-41-4)
    Language English
    Publishing date 2006-12-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2171107-0
    ISSN 1541-2555
    ISSN 1541-2555
    DOI 10.1080/15412550500493436
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5990: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: IL6 and CRP haplotypes are associated with COPD risk and systemic inflammation: a case-control study.

    Yanbaeva, Dilyara G / Dentener, Mieke A / Spruit, Martijn A / Houwing-Duistermaat, Jeanine J / Kotz, Daniel / Passos, Valéria Lima / Wouters, Emiel F M

    BMC medical genetics

    2009  Volume 10, Page(s) 23

    Abstract: Background: Elevated circulating levels of C-reactive protein (CRP), interleukin (IL)-6 and fibrinogen (FG) have been repeatedly associated with many adverse outcomes in patients with chronic obstructive pulmonary disease (COPD). To date, it remains ... ...

    Abstract Background: Elevated circulating levels of C-reactive protein (CRP), interleukin (IL)-6 and fibrinogen (FG) have been repeatedly associated with many adverse outcomes in patients with chronic obstructive pulmonary disease (COPD). To date, it remains unclear whether and to what extent systemic inflammation is primary or secondary in the pathogenesis of COPD. The aim of this study was to examine the association between haplotypes of CRP, IL6 and FGB genes, systemic inflammation, COPD risk and COPD-related phenotypes (respiratory impairment, exercise capacity and body composition).
    Methods: Eighteen SNPs in three genes, representing optimal haplotype-tagging sets, were genotyped in 355 COPD patients and 195 healthy smokers. Plasma levels of CRP, IL-6 and FG were measured in the total study group. Differences in haplotype distributions were tested using the global and haplotype-specific statistics.
    Results: Raised plasma levels of CRP, IL-6 and fibrinogen were demonstrated in COPD patients. However, COPD population was very heterogeneous: about 40% of patients had no evidence of systemic inflammation (CRP < 3 mg/uL or no inflammatory markers in their top quartile). Global test for haplotype effect indicated association of CRP gene and CRP plasma levels (P = 0.0004) and IL6 gene and COPD (P = 0.003). Subsequent analysis has shown that IL6 haplotype H2, associated with an increased COPD risk (p = 0.004, OR = 4.82; 1.64 to 4.18), was also associated with very low CRP levels (p = 0.0005). None of the genes were associated with COPD-related phenotypes.
    Conclusion: Our findings suggest that common genetic variation in CRP and IL6 genes may contribute to heterogeneity of COPD population associated with systemic inflammation.
    MeSH term(s) Adult ; Aged ; C-Reactive Protein/genetics ; Case-Control Studies ; Female ; Fibrinogen/genetics ; Genome-Wide Association Study ; Genotype ; Haplotypes ; Humans ; Inflammation/blood ; Inflammation/genetics ; Inflammation Mediators/blood ; Interleukin-6/genetics ; Male ; Middle Aged ; Phenotype ; Polymorphism, Single Nucleotide ; Pulmonary Disease, Chronic Obstructive/blood ; Pulmonary Disease, Chronic Obstructive/genetics
    Chemical Substances Inflammation Mediators ; Interleukin-6 ; Fibrinogen (9001-32-5) ; C-Reactive Protein (9007-41-4)
    Language English
    Publishing date 2009-03-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1471-2350
    ISSN (online) 1471-2350
    DOI 10.1186/1471-2350-10-23
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: IL6 and CRP haplotypes are associated with COPD risk and systemic inflammation

    Passos Valéria / Kotz Daniel / Houwing-Duistermaat Jeanine J / Spruit Martijn A / Dentener Mieke A / Yanbaeva Dilyara G / Wouters Emiel FM

    BMC Medical Genetics, Vol 10, Iss 1, p

    a case-control study

    2009  Volume 23

    Abstract: Abstract Background Elevated circulating levels of C-reactive protein (CRP), interleukin (IL)-6 and fibrinogen (FG) have been repeatedly associated with many adverse outcomes in patients with chronic obstructive pulmonary disease (COPD). To date, it ... ...

    Abstract Abstract Background Elevated circulating levels of C-reactive protein (CRP), interleukin (IL)-6 and fibrinogen (FG) have been repeatedly associated with many adverse outcomes in patients with chronic obstructive pulmonary disease (COPD). To date, it remains unclear whether and to what extent systemic inflammation is primary or secondary in the pathogenesis of COPD. The aim of this study was to examine the association between haplotypes of CRP , IL6 and FGB genes, systemic inflammation, COPD risk and COPD-related phenotypes (respiratory impairment, exercise capacity and body composition). Methods Eighteen SNPs in three genes, representing optimal haplotype-tagging sets, were genotyped in 355 COPD patients and 195 healthy smokers. Plasma levels of CRP, IL-6 and FG were measured in the total study group. Differences in haplotype distributions were tested using the global and haplotype-specific statistics. Results Raised plasma levels of CRP, IL-6 and fibrinogen were demonstrated in COPD patients. However, COPD population was very heterogeneous: about 40% of patients had no evidence of systemic inflammation (CRP < 3 mg/uL or no inflammatory markers in their top quartile). Global test for haplotype effect indicated association of CRP gene and CRP plasma levels (P = 0.0004) and IL6 gene and COPD (P = 0.003). Subsequent analysis has shown that IL6 haplotype H2, associated with an increased COPD risk (p = 0.004, OR = 4.82; 1.64 to 4.18), was also associated with very low CRP levels (p = 0.0005). None of the genes were associated with COPD-related phenotypes. Conclusion Our findings suggest that common genetic variation in CRP and IL6 genes may contribute to heterogeneity of COPD population associated with systemic inflammation.
    Keywords Internal medicine ; RC31-1245 ; Genetics ; QH426-470
    Subject code 616
    Language English
    Publishing date 2009-03-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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