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Asthmatic Individuals (asthmatic + individual)
Selected AbstractsCorrelates of smoking among adolescents with asthmaJOURNAL OF CLINICAL NURSING, Issue 5-6 2010Su-Er Guo Aims and objective., This study examined the correlates of smoking among asthmatic adolescents to gain a better understanding of who is at particular risk. Background., Smoking is especially harmful to individuals with asthma. However, smoking is surprisingly prevalent among asthmatic individuals, with prevalence rates similar to or higher than those of the general adult or adolescent populations. Despite this notable finding, there has been little research about factors (i.e. biophysical, psychosocial and behavioural) influencing asthmatic adolescents' tobacco use patterns. Design., A Canadian provincial cross-sectional survey. Method., The study about adolescents' tobacco use and health status was conducted in secondary schools in 2004, 608 asthmatic adolescents participated. Demographic factors, biophysical (body mass index and physical health), psychosocial factors (parents' and peers' smoking, environmental tobacco smoke exposure and depression) and behavioural factors (marijuana use, alcohol use and exercise frequency) were explored. Multinomial logistic regression analyses were conducted to identify risk factors associated with tobacco use. Results and conclusions., Of the 608 asthmatic adolescents, 17·4% currently smoked and 12·0% formerly smoked. Girls, compared with boys, were more likely to smoke (OR: 3·34, 95% CI: 1·62,6·96) after adjusting for differences in the other demographic, biophysical, psychosocial and behavioural factors. Asthmatic girls who had relatively higher body mass index, were in the higher school grades, used marijuana or alcohol, had minor to severe depressive symptoms, had environmental tobacco smoke exposure in their homes and had friends who smoked or were currently more likely to smoke. The former smokers had similar risk factors including higher body mass index, environmental tobacco smoke exposure at home, friends who smoked and marijuana use. Relevance to clinical practice., Despite their health condition, asthmatic adolescents continue currently or formerly to smoke. Gender appropriate prevention and cessation interventions for asthmatic adolescents may need to address important psychosocial and environmental factors that increase the risk of these adolescents initiating and maintaining tobacco use. [source] Further studies on the clinical ef,cacy of Solanum xanthocarpum and Solanum trilobatum in bronchial asthmaPHYTOTHERAPY RESEARCH, Issue 10 2004S. Govindan Abstract The clinical ef,cacy of two herbs S. xanthocarpum and S. trilobatum in a dose of 300 mg tds for 3 days was investigated in mild to moderate bronchial asthma. Their effect was compared with standard bronchodilator drugs, salbutamol (4 mg) and deriphylline (200 mg). The respiratory function was assessed by measuring the peak expiratory ,ow rate (PEFR) using a mini peak ,ow meter. In addition, improvement in lung function was assessed by physical examination (rhonchi and crepitation) and other symptoms such as cough, breathlessness and sputum. S. xanthocarpum and S. trilobatum produced a progressive improvement in the ventilatory function of asthmatic individuals over 3 days. The scores for rhonchi, cough, breathlessness and sputum were decreased by these drug treatments. The improvement in PEFR and the reduction in other symptom scores clearly indicate a bronchodilator effect, a decrease of oedema and secretions in the airway lumen. The response to these herbs can be considered to be equivalent to that of deriphylline but less than salbutamol. No untoward effects were reported during the study. The present study further con,rms the traditional use of these herbs in bronchial asthma. Copyright © 2004 John Wiley & Sons, Ltd. [source] T cells and eosinophils in bronchial smooth muscle cell death in asthmaCLINICAL & EXPERIMENTAL ALLERGY, Issue 6 2009K. Solarewicz-Madejek Summary Background Bronchial smooth muscle cells (SMC) proliferate, express adhesion molecules, secrete cytokines and thus efficiently contribute to the pathogenesis of asthma. Objective The aim of the study was to investigate whether, and by which mechanism, T cells and eosinophils can cause death of airway SMC. Methods The T cell- and eosinophil-induced cell death was analysed in primary human bronchial SMC cultures as well as in bronchial biopsy specimens from non-asthmatic and asthmatic individuals. Results Bronchial SMC death showed characteristic morphological features of apoptosis in 3,6 days cultures with inflammatory cytokines (IFN-,, TNF-,), soluble death ligands [sFasL, TNF-related apoptosis-inducing ligand (TRAIL)] and activated T-helper type 1 (Th1) and Th2 cell supernatants. The recombinant eosinophil cationic protein induced SMC necrosis within 1 h. Resting SMC expressed the death receptors TNFR1, TNFR2, Fas, TRAILR1, TRAILR2 and membrane FasL as a death-inducing ligand. IFN-, and TNF-, up-regulated TNFR1, TNFR2, Fas and membrane FasL on SMC. TNF-, up-regulated TRAILR1 and TRAILR2; sFasL up-regulated TNFR2. The intracellular caspase-3 activation in SMC was significantly increased by IFN-,, sFasL, TRAIL, Th1 and Th2 cell supernatants. Increased expression of TRAIL in asthmatics, but not in non-asthmatic individuals was demonstrated in situ. The apoptosis receptors TRAILR1 and TRAILR2 were expressed in SMC and epithelial cells both in healthy and asthmatic biopsies. Prominent apoptosis of SMC was observed in fatal asthma, but not intermittent asthma biopses. Conclusion The demonstration of bronchial SMC death both by apoptosis and necrosis indicates the essential role of T cells and eosinophils in the bronchial tissue injury particularly in the severe asthma. [source] Association of angiotensin I-converting enzyme gene polymorphisms with aspirin intolerance in asthmaticsCLINICAL & EXPERIMENTAL ALLERGY, Issue 11 2008T-H. Kim Summary Background Aspirin-intolerant asthma (AIA) refers to the development of bronchoconstriction in asthmatic individuals following the ingestion of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs). Angiotensin I-converting enzyme (ACE), a membrane-bound peptidase present in the lung, plays a pivotal role in the metabolism of the endogenous peptides involved in the pathogenesis of asthma. Methods We screened a Korean asthma cohort (581 asthmatics including 81 aspirin-intolerant asthmatics and 231 aspirin-tolerant asthmatics, and 181 normal controls) for four single nucleotide polymorphisms (SNPs; ,262 A>T and ,115 T>C in the 5,-flanking region and +5467 T>C [Pro450Pro] and+11860 A>G [Thr776Thr] in the coding region) and one ins/del (+21288 CT) in the ACE gene. Results None of the SNPs or haplotypes showed any association with the development of asthma, but they were significantly associated with the risk of AIA. Logistic regression indicated that the frequency of the rare alleles of ,262 A>T and ,115 T>C was higher in subjects with AIA than in subjects with aspirin-tolerant asthma (ATA) (P=0.003,0.01, P corr=0.015,0.05). Subjects homozygous for the rare alleles of ,262 A>T and ,115 T>C showed a greater decline in forced expiratory volume in 1 s (FEV1) after aspirin provocation than those homozygous for the common alleles (P<0.05). A luciferase reporter assay indicated that ACE promoters containing the rare ,262 A>T allele possessed lower activity than did those containing the common allele (P=0.009). In addition, ACE promoters bearing the rare ,115 T>C allele had no luciferase activity. DNA,protein binding assays revealed a band containing the ACE promoter region (including ,262 A) and a protein complex. Conclusion The ,262 A>T polymorphism in the promoter of the ACE gene is associated with AIA, and the rare allele of ,262 A>T may confer aspirin hypersensitivity via the down-regulation of ACE expression. [source] Modulation of the epithelial inflammatory response to rhinovirus in an atopic environmentCLINICAL & EXPERIMENTAL ALLERGY, Issue 3 2008M. Xatzipsalti Summary Background Immune responses to rhinovirus (RV) as well as direct effects of RV on respiratory epithelium may contribute to the induction of asthma exacerbations. Objective To evaluate the effect of the environment resulting from an atopic immune response on RV-induced epithelial inflammation, replication and cytotoxicity. Methods Peripheral blood mononuclear cells (PBMC) from atopic asthmatic subjects and matched controls (12 pairs) were isolated and stimulated by RVs. Human bronchial epithelial (BEAS-2B) cells were infected with RV in the presence of conditioned media from RV-stimulated PBMC cultures. IL-6, IL-8, RANTES and TGF-,1 levels were measured by ELISA, RV-induced cytotoxicity by a colorimetric method and RV titres on Ohio-HeLa cells. Results RV-induced epithelial production of IL-6, IL-8 and RANTES was significantly lower, while TGF-,1 was higher when cells were exposed to conditioned media from atopic asthmatic subjects compared with those from normal controls. Exposure to the ,atopic' environment also resulted in elevated RV titres and increased RV-induced cytotoxicity. Conclusions Under the influence of an atopic environment, the epithelial inflammatory response to RV is down-regulated, associated with increased viral proliferation and augmented cell damage, while TGF is up-regulated. These changes may help explain the propensity of atopic asthmatic individuals to develop lower airway symptoms after respiratory infections and indicate a mechanism through which viral infections may promote airway remodelling. [source] | ||||||||||