Titre : |
Analysis and evaluation of environmental tobacco smoke exposure as a risk factor for chronic cough |
Type de document : |
texte imprimé |
Auteurs : |
Beatrix Groneberg-Kloft, Auteur ; Wojciech Feleszko, Auteur ; Quoc Thai Dinh, Auteur ; Anke van Mark, Auteur |
Editeur : |
BioMed Central |
Année de publication : |
2007 |
Collection : |
Cough, ISSN 1745-9974 num. 3 |
Importance : |
6 p. |
Présentation : |
tab., graph. |
Langues : |
Anglais (eng) |
Catégories : |
[TABAC] étude [TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive [TABAC] tabagisme:tabagisme actif [TABAC] tabagisme:tabagisme passif
|
Index. décimale : |
TA 7.4.2.2 chez l'adulte |
Résumé : |
Exposure to environmental tobacco smoke (ETS) and active tobacco smoking has been shown to increase symptoms of bronchial asthma such as bronchoconstriction but effects on other respiratory symptoms remain poorly assessed. Current levels of exposure to tobacco smoke may also be responsible for the development of chronic cough in both children and adults. The present study analyses the effects of tobacco smoke exposure as potential causes of chronic cough. A panel of PubMed-based searches was performed relating the symptom of cough to various forms of tobacco smoke exposure. It was found that especially prenatal and postnatal exposures to ETS have an important influence on children's respiratory health including the symptom of cough. These effects may be prevented if children and pregnant women are protected from exposure to ETS. Whereas the total number of studies adressing the relationship between cough and ETS exposure is relatively small, the present study demonstrated that there is a critical amout of data pointing to a causative role of environmental ETS exposure for the respiratory symptom of cough. Since research efforts have only targeted this effect to a minor extent, future epidemiological and experimental studies are needed to further unravel the relation between ETS and cough. |
En ligne : |
https://coughjournal.biomedcentral.com/articles/10.1186/1745-9974-3-6 |
Format de la ressource électronique : |
HTML |
Permalink : |
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Titre : |
Association of genetic variations in the CSF2 and CSF3 genes with lung function in smoking-induced COPD |
Type de document : |
texte imprimé |
Auteurs : |
J-Q. He, Auteur ; K. Shumansky, Auteur ; J.E. Connett, Auteur ; N.R. Anthonisen, Auteur |
Editeur : |
European Respiratory Society (ERS) |
Année de publication : |
2008 |
Collection : |
European Respiratory Journal num. 32 |
Importance : |
p. 25-34 |
Présentation : |
tab., graph. |
Langues : |
Anglais (eng) |
Catégories : |
[TABAC] étude [TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive [TABAC] tabagisme:risque:facteur associé:génétique
|
Index. décimale : |
TA 3.2.2.4 Pathologies respiratoires (sauf 3.2.2.1, 3.2.2.2, 3.2.2.3) |
Résumé : |
Granulocyte-macrophage colony-stimulating factor (CSF), also known as CSF2, and granulocyte CSF, also known as CSF3, are important survival and proliferation factors for neutrophils and macrophages. The objective of the present study was to determine whether single nucleotide polymorphisms (SNPs) of CSF2 and CSF3 are associated with lung function in smoking-induced chronic obstructive pulmonary disease. In total, five SNPs of CSF2 and CSF3 were studied in 587 non-Hispanic white subjects with the fastest (n = 281) or the slowest (n = 306) decline of lung function selected from among continuous smokers in the National Heart, Lung, and Blood Institute Lung Health Study (LHS). These SNPs were also studied in 1,074 non-Hispanic white subjects with the lowest (n = 536) or the highest (n = 538) baseline lung function at the beginning of the LHS. An increase in the number of CSF3 -1719T alleles was significantly associated with protection against low lung function (odds ratio 0.73, 95% confidence interval 0.56-0.95), and was still significant after adjustment for multiple comparisons. There was also a significant association of a CSF3 haplotype with baseline levels of forced expiratory volume in one second. No association was found for CSF2 SNPs and lung function, nor was there evidence of epistasis. In conclusion, genetic variation in colony-stimulating factor 3 is associated with cross-sectionally measured lung function in smokers. |
En ligne : |
https://erj.ersjournals.com/content/32/1/25.long |
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(1998)
Réservation
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Documents numériques
La BPCO nous concerne tous !Adobe Acrobat PDF | | |
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(15/05/2009)
Exemplaires (1)
|
TA 002231 | TA 6.7 VER B | Article/Périodique | Bibliothèque FARES | Tabac | Consultation sur place Exclu du prêt |
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(15/01/2012)
Exemplaires (1)
|
TA 004644 | TA 6.2 MAU C | Article/Périodique | Bibliothèque FARES | Tabac | Consultation sur place Exclu du prêt |
Aucun avis, veuillez vous identifier pour ajouter le vôtre !
Titre : |
Cigarette smoke enhances {beta}-defensin 2 expression in rat airways via nuclear factor-{kappa}B activation |
Type de document : |
texte imprimé |
Auteurs : |
L. Chen, Auteur ; P.P. Sun, Auteur ; T. Wang, Auteur ; X. Wang, Auteur |
Editeur : |
European Respiratory Society (ERS) |
Année de publication : |
2010 |
Collection : |
European Respiratory Journal num. 36 |
Importance : |
p.638-645 |
Présentation : |
graph., ill. |
Langues : |
Anglais (eng) |
Catégories : |
[TABAC] chimie du tabac:fumée [TABAC] étude [TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive
|
Index. décimale : |
TA 3.2.2.1 Expérimentation |
Résumé : |
β-defensin 2 (BD-2), an antimicrobial peptide, participates in airway defence. Cigarette smoke (CS) is a major risk factor for the development of chronic obstructive pulmonary disease. This study mainly aims to investigate the effect of CS on rat BD-2 (rBD-2) expression in rat airways. Rats were exposed to CS and treated with caffeic acid phenethyl ester (CAPE), a nuclear factor (NF)-κB inhibitor, or astragaloside IV (AS-IV), an active ingredient of Astragalus mongholicus. Besides the analysis of bronchoalveolar lavage fluid (BALF) and histological changes after CS exposure, rBD-2 expression was investigated with immunohistochemistry, reverse transcription PCR and ELISA. Total glutathione and nitric oxide (NO) levels in rat lungs were also detected. CS exposure markedly increased rBD-2 immunoreactivity, as well as rBD-2 mRNA and protein levels in rat airways, which were inhibited by CAPE treatment. Moreover, associated airway inflammation induced by CS was demonstrated by histological changes, increased cell counts and pro-inflammatory cytokines in BALF, and NF-κB activation and high levels of total glutathione and NO, which were all reversed by AS-IV in a dose-dependent fashion. In conclusion, CS exposure induces rBD-2 expression in rat airways via a NF-κB-dependent pathway, and AS-IV attenuates CS-induced airway inflammation due to its anti-inflammatory and antioxidant properties, at least partly through NF-κB inactivation. |
En ligne : |
https://erj.ersjournals.com/content/36/3/638.long |
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Titre : |
Cigarette smoke induces CXCL8 production by human neutrophils via activation of TLR9 receptor |
Type de document : |
texte imprimé |
Auteurs : |
E. Mortaz, Auteur ; I.M. Adcock, Auteur ; K. Ito, Auteur ; A.D. Kraneveld, Auteur |
Editeur : |
European Respiratory Society (ERS) |
Année de publication : |
2010 |
Collection : |
European Respiratory Journal num. 36 |
Importance : |
p. 1143-1154 |
Présentation : |
graph. |
Langues : |
Anglais (eng) |
Catégories : |
[TABAC] chimie du tabac:fumée [TABAC] étude [TABAC] tabagisme:effet du tabac:effet sur l'immunité [TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive
|
Index. décimale : |
TA 3.2.2.4 Pathologies respiratoires (sauf 3.2.2.1, 3.2.2.2, 3.2.2.3) |
Résumé : |
Chronic obstructive pulmonary disease (COPD) is a major health problem and cigarette smoke is the main risk factor for the development of COPD. The characteristic changes in airway morphology, inflammatory cell infiltration and mediator expression in COPD may result from direct effects of cigarette smoke on airway cells. Toll-like receptors (TLRs) are key elements in pathogen recognition by the host immune system. Although TLRs have been intensely studied in innate immunity and infection, their critical role in noninfectious challenges has only recently emerged. Here we investigate whether cigarette smoke induces TLR9 signalling in human neutrophils. Human neutrophils were isolated from buffy coat and exposed to cigarette smoke extract. The production of CXC chemokine ligand (CXCL)8 was measured as a functional readout and the role of TLR9 signalling was investigated. Cigarette smoke extract induced CXCL8 release via TLR9 activation in neutrophils, which was confirmed in TLR9 stably transfected human embryonic kidney 293 cells. Moreover, cigarette smoke extract upregulated the expression of TLR9 and the upregulated expression was suppressed by N-acetylcysteine. TLR9 mediates cigarette smoke-induced release of CXCL8 and this may contribute to the accumulation of neutrophils and inflammation within the airways of smokers. |
En ligne : |
https://erj.ersjournals.com/content/36/5/1143 |
Permalink : |
http://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8071 |
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Exemplaires (1)
|
TA 005622 | TA 3.2.2.4 MOR C | Article/Périodique | Bibliothèque FARES | Tabac | Consultation sur place Exclu du prêt |
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Titre : |
Clinical utility of varenicline for smokers with medical and psychiatric comorbidity |
Type de document : |
texte imprimé |
Auteurs : |
Jon O. Ebbert, Auteur ; Kirk D Wyatt, Auteur ; Michael V. Burke, Auteur ; J. Taylor Hays, Auteur ; Ali Zirakzadeh, Auteur |
Editeur : |
Dove Medical Press |
Année de publication : |
2009 |
Collection : |
International journal of Chronic Obstructive Pulmonary Disease, ISSN 1178-2005 num. 4 |
Importance : |
p. 421-430 |
Présentation : |
tab. |
Langues : |
Anglais (eng) |
Catégories : |
[DIVERS] discipline médicale, paramédicale et scientifique:médecine:médecine spécialisée:psychiatrie [TABAC] sevrage tabagique:méthode de sevrage:méthode individuelle:approche pharmacologique:varénicline [TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive
|
Index. décimale : |
TA 6.2.3.2 Autres produits |
Résumé : |
Chronic obstructive pulmonary disease (COPD) is a costly and deadly disease afflicting an estimated 210 million people and accounting for 5% of all global deaths. Exposure to cigarette smoke is the greatest risk factor for COPD in the developed world. Smoking cessation improves respiratory symptoms and lung function and reduces mortality among patients with COPD. Cigarette smokers with COPD and other co-morbid conditions such as cardiovascular disease and psychiatric illnesses should receive comprehensive tobacco treatment interventions incorporating efficacious pharmacotherapies. Varenicline, an alpha(4)beta(2) nicotinic acetylcholine receptor partial agonist, is the newest and most effective drug currently available to promote smoking cessation. In conjunction with behavioral interventions and clinical monitoring for potential side effects, varenicline offers great hope for reducing smoking-attributable death and disability. |
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Documents numériques
Clinical utility of varenicline for smokers with medical and psychiatric comorbidityAdobe Acrobat PDF | | |
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(10/09/2014)
Exemplaires (1)
|
TA 005321 | TA 3.2.2.4 LAN D | Article/Périodique | Bibliothèque FARES | Tabac | Consultation sur place Exclu du prêt |
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(01/04/1998)
Exemplaires (1)
|
TA 000172 | 0.1 VAN M | Article/Périodique | Bibliothèque FARES | Tabac | Consultation sur place Exclu du prêt |
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Exemplaires (1)
|
TA 000981 | TA 6.3.5 NYS E | Mémoire/Thèse | Bibliothèque FARES | Tabac | Consultation sur place Exclu du prêt |
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(juin 2017)
Titre : |
Fumer à tout prix |
Titre original : |
"je t'en supplie maman, arrête de fumer !" |
Type de document : |
texte imprimé |
Auteurs : |
Marianne Wéry (1962 - ...), Auteur |
Editeur : |
Saint-Denis [France] : Edilivre |
Année de publication : |
juin 2017 |
Importance : |
165 p. |
Présentation : |
ill. |
ISBN/ISSN/EAN : |
978-2-414-07397-9 |
Prix : |
20 € |
Langues : |
Français (fre) |
Catégories : |
[TABAC] prévention:témoignage [TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive
|
Index. décimale : |
TA 0.5 Témoignage |
Résumé : |
Résumé de l'auteur :
Un véritable hymne à l’amour d’une fille non-fumeuse à sa maman fumeuse. La BPCO, maladie respiratoire, n’est pas guérissable. Elle est mortelle, sauf si le patient arrête de fumer.
« Je suis anéantie. On vient de m’annoncer que maman est à l’entrée du couloir de la mort, que la porte est entrouverte mais qu’elle a la possibilité de la refermer. Elle décide pourtant d’enclencher le processus, elle sait que dès qu’elle aura fait un pas dans ce couloir, plus ou moins long, elle ne pourra plus revenir en arrière. Et la tête haute, droite comme un “i”, elle en franchit le seuil ! Que me reste-t-il à faire, si ce n’est encaisser, tenter de comprendre ou pas ? Mais surtout continuer à l’aimer avec force et le lui montrer chaque jour davantage. » |
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(2018)
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Titre : |
Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space |
Type de document : |
texte imprimé |
Auteurs : |
P. Glader, Auteur ; B. Eldh, Auteur ; S. Bozinovski, Auteur ; K. Andelid, Auteur |
Editeur : |
European Respiratory Society (ERS) |
Année de publication : |
2008 |
Collection : |
European Respiratory Journal num. 32 |
Importance : |
p.644-650 |
Présentation : |
tab., ill. |
Langues : |
Anglais (eng) |
Catégories : |
[TABAC] chimie du tabac:fumée [TABAC] étude [TABAC] tabagisme:effet du tabac [TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive
|
Index. décimale : |
TA 3.2.2.4 Pathologies respiratoires (sauf 3.2.2.1, 3.2.2.2, 3.2.2.3) |
Résumé : |
Clinical studies have indicated increased gelatinase activity in the airways of patients suffering from chronic obstructive pulmonary disease caused by tobacco smoke. The present study aimed to determine whether acute exposure to tobacco smoke per se causes a substantial and lasting impact on gelatinases and their inhibitors in the peripheral airways of atopic and nonatopic human subjects.
Bronchoscopy with bronchoalveolar lavage (BAL) was performed on occasional smokers with and without atopy before and after smoking 10 cigarettes over a 48-h period. Samples from a group of never-smokers not exposed to tobacco smoke served as controls. Gelatinase identity and activity were measured using zymography, and gelatinase activity assay and concentrations of matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of MMP (TIMP)-1 and TIMP-2 were measured using ELISA.
The results revealed no pronounced changes in identity, net activity or concentration of the gelatinases or changes in concentrations of TIMP-1 and TIMP-2 in BAL fluid before and after acute exposure to tobacco smoke.
In conclusion, the present experimental study indicates that acute exposure to tobacco smoke does not cause any substantial impact on gelatinases or their inhibitors in the peripheral airways, irrespective of atopy status, a finding that is compatible with the fact that it takes many years of tobacco smoking to establish chronic obstructive pulmonary disease. |
En ligne : |
https://erj.ersjournals.com/content/32/3/644 |
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