e-learning
resources
Copenhagen 2005
Tuesday 20.09.2005
Mechanisms of inflammatory reactions in asthma, COPD and models of allergic airway disease
Login
Search all ERS
e-learning
resources
Disease Areas
Airways Diseases
Interstitial Lung Diseases
Respiratory Critical Care
Respiratory Infections
Paediatric Respiratory Diseases
Pulmonary Vascular Diseases
Sleep and Breathing Disorders
Thoracic Oncology
Events
International Congress
Courses
Webinars
Conferences
Research Seminars
Journal Clubs
Publications
Breathe
Monograph
ERJ
ERJ Open Research
ERR
European Lung White Book
Handbook Series
Guidelines
All ERS guidelines
e-learning
CME Online
Case reports
Short Videos
SpirXpert
Procedure Videos
CME tests
Reference Database of Respiratory Sounds
Radiology Image Challenge
Brief tobacco interventions
EU Projects
VALUE-Dx
ERN-LUNG
ECRAID
UNITE4TB
Disease Areas
Events
Publications
Guidelines
e-learning
EU Projects
Login
Search
Deficiency of tenascin C attenuates airway hyperresponsiveness in an experimental model of bronchial asthma
H. Nakahara, E. C. Gabazza, Y. Nishii, H. Fujimoto, H. Kobayashi, C. N. D‘Alessandro-Gabazza, H. Yasui, O. Taguchi (Tsu, Japan)
Source:
Annual Congress 2005 - Mechanisms of inflammatory reactions in asthma, COPD and models of allergic airway disease
Session:
Mechanisms of inflammatory reactions in asthma, COPD and models of allergic airway disease
Session type:
Thematic Poster Session
Number:
3743
Disease area:
Airway diseases
Rating:
You must
login
to grade this presentation.
Share or cite this content
Citations should be made in the following way:
H. Nakahara, E. C. Gabazza, Y. Nishii, H. Fujimoto, H. Kobayashi, C. N. D‘Alessandro-Gabazza, H. Yasui, O. Taguchi (Tsu, Japan). Deficiency of tenascin C attenuates airway hyperresponsiveness in an experimental model of bronchial asthma. Eur Respir J 2005; 26: Suppl. 49, 3743
You must
login
to share this Presentation/Article on Twitter, Facebook, LinkedIn or by email.
Member's Comments
No comment yet.
You must
Login
to comment this presentation.
Related content which might interest you:
Late Breaking Abstract - Implications of treatable traits and treatment choices on exacerbation risk in moderate-severe asthma
Management of Severe Asthma in Pediatric Patients by an Interdisciplinary Team in a Public Hospital Setting.
Respiratory sequelae of preterm birth across the life span
Related content which might interest you:
Activated protein C inhibits bronchial inflammation and hyperresponsiveness in a mouse model of asthma
Source: Eur Respir J 2002; 20: Suppl. 38, 618s
Year: 2002
MMP-9 deficiency reduces airway inflammation and hyperresponsiveness in a mouse model of asthma
Source: Eur Respir J 2001; 18: Suppl. 33, 20s
Year: 2001
Estrogen prevents airway hyperresponsiveness in a murine model of allergic asthma
Source: Eur Respir J 2006; 28: Suppl. 50, 433s
Year: 2006
Airway remedeling in a mouse model of chronic asthma: relation between the degree of airway remodeling and airway hyperresponsiveness
Source: Eur Respir J 2004; 24: Suppl. 48, 38s
Year: 2004
Osteopontin deficiency protects from airway remodelling and hyperresponsiveness in chronic asthma
Source: Annual Congress 2009 - Novel mechanisms in the pathogenesis of asthma
Year: 2009
Effect of neutrophil elastase inhibitor on airway inflammation and airway hyperresponsiveness in a murine model of asthma
Source: Annual Congress 2009 - Animal models of airways inflammation
Year: 2009
Estrogen prevents airway inflammation and hyperresponsiveness in a murine model of acute allergic asthma
Source: Eur Respir J 2007; 30: Suppl. 51, 360s
Year: 2007
Effects of N-acetylcysteine on airway inflammation, airway hyperresponsiveness and abnormal lung function in chronic ozone-induced COPD model
Source: Annual Congress 2012 - Animal models of asthma and COPD and late-breaking abstracts on RCT in asthma and COPD
Year: 2012
Budesonide prevents but does not reverse sustained airway hyperresponsiveness in mice
Source: Eur Respir J 2008; 32: 970-978
Year: 2008
Osteopontin exacerbates airway hyperresponsiveness and lung remodeling in chronic asthma
Source: Annual Congress 2008 - Basic science in asthma and COPD
Year: 2008
Effects of OVA-induced allergic airway inflammation and remodeling in mice in three distinct asthma models
Source: Annual Congress 2010 - Animal models of asthma and lung inflammation
Year: 2010
Obesity enhances allergen-induced airway inflammation in a murine model of asthma
Source: International Congress 2019 – Modelling and monitoring of airway diseases
Year: 2019
Mechanisms of bronchial hyperresponsiveness in asthma
Source: Annual Congress 2009 - PG13 Asthma: pathology and treatment
Year: 2009
Deficiency of MMP-19 promotes allergen-induced eosinophil burden and airway responsiveness in mice
Source: Annual Congress 2007 - Regulation of allergic airway inflammation in animal models of asthma
Year: 2007
Effect of bronchial neutrophilia on airway remodeling in asthma
Source: International Congress 2019 – Cellular responses and cell therapy in lung injury and repair
Year: 2019
Correlation between bronchial hyperresponsiveness and bronchial inflammation in asthmatic patients
Source: Eur Respir J 2002; 20: Suppl. 38, 49s
Year: 2002
Airway hyperresponsiveness in asthma: lessons from in vitro model systems and animal models
Source: Eur Respir J 2008; 32: 487-502
Year: 2008
Monitoring asthma in children: lung function, bronchial hyperresponsiveness and inflammation
Source: International Congress 2014 – Monitoring asthma in children: results of the ERS Task Force
Year: 2014
Galectn-3 : marker of airway inflammation in bronchial asthma
Source: International Congress 2018 – Studying novel biomarkers in asthma and COPD
Year: 2018
Experimental specific immunotherapy with timpol decreases allergic sensitization and airway inflammation in murine model of bronchial asthma
Source: Annual Congress 2010 - Animal models of asthma and lung inflammation
Year: 2010
We use cookies on our website to give you the most relevant experience by remembering your preferences and repeat visits. By clicking "Accept", you consent to the use of the cookies.
Accept