bluuebunny/crossref_metadata_2025_split huggingface dataset:
Climate, traffic-related air pollutants and allergic rhinitis prevalence in middle-school children in Taiwan
Authors: Lee Y-L. , Shaw C-K. , Su H-J. , Lai J-S. , Ko Y-C. , Huang S-L. , Sung F-C. , Guo Y.L. 
Published: September 2008

The prevalence of allergic rhinitis, a common respiratory disorder, may be rapidly increasing. Epidemiological studies, however, indicate little about its association with climatic factors and air pollution. The relationship between traffic-related air pollutants and allergic rhinitis in middle-school students was therefore investigated.In a nationwide survey of middle-school students in Taiwan conducted in 1995/1996, the lifetime prevalence of physician-diagnosed allergic rhinitis and typical symptoms of allergic rhinitis were compared with air-monitoring station data on temperature, relative humidity, sulphur dioxide (SO2), nitrogen oxides (NOx), ozone (O3), carbon monoxide (CO) and particulate matter with a 50% cut-off aerodynamic diameter of 10 µm (PM10).A total of 331,686 nonsmoking children attended schools located within 2 km of 55 stations. Mean (range) annual exposures were: CO 853 (381–1,610) parts per billion (ppb), NOx 35.1 (10.2–72.4) ppb, SO27.57 (0.88–21.2) ppb, PM1069.2 (40.1–116.2) µg·m−3, O321.3 (12.4–34.1) ppb, temperature 22.9 (19.6–25.1)°C, and relative humidity 76.2 (64.8–86.2)%. The prevalence of physician-diagnosed allergic rhinitis was 28.6 and 19.5% in males and females, respectively, with prevalence of questionnaire-determined allergic rhinitis 42.4 and 34.0%. After adjustment for age, parental education and history of atopic eczema, physician-diagnosed allergic rhinitis was found to be associated with higher nonsummer (September–May) warmth and traffic-related air pollutants, including CO, NOx and O3. Questionnaire-determined allergic rhinitis correlated only with traffic-related air pollutants.Nonsummer warmth and traffic-related air pollution, probably mediated through exposure to common allergens such as dust mites, are possible risk factors for allergic rhinitis in middle-school-aged children.
Pseudomonas aeruginosaadherence to human basement membrane collagenin vitro
Authors: Tsang K.W. , Shum D.K. , Chan S. , Ng P. , Mak J. , Leung R. , Shum I.H. , Ooi G.C. , Tipoe G.L. , Lam W.K. 
Published: September 2008

The mechanisms forPseudomonas aeruginosacolonisation in the airways of patients with bronchiectasis and cystic fibrosis are poorly understood.P. aeruginosacould evade mucociliary clearance by adhering to the basement membrane at areas denuded of intact respiratory epithelium.The authors have developed anin vitromodel to studyP. aeruginosaadherence tohuman basement membrane type-IV collagen by using scanning electron microscopy.P. aeruginosaadherence density was determined as the number ofP. aeruginosaper 20microscope fields (2,000×) to log inocular size after incubation at 37°C for 45 min.The presence of phytohaemagglutinin (PHA)-E, which binds specifically to d-galactose-β1–4-d-N-acetylglucosamine, significantly reducedP. aeruginosaadherence density compared with control. The presence of heparin and calcium also significantly reducedP. aeruginosaadherence density.P. aeruginosaadherence was not affected by the presence of proline, trans-hydroxyproline, glycine, galactose,N-acetylneuraminic acid,N-acetylglucosamine orArachis hypogea.Pseudomonas aeruginosaadherence probably actsviarecognition of the d-galactose-β1–4-d-N-acetylglucosamine sequence on type-IV collagen and this process could be inhibited by heparin and calcium. As persistentPseudomonas aeruginosacolonisation is detrimental to patients with cystic fibrosis and bronchiectasis and there is currently no effective treatment for its eradication, these results could lead to novel therapy for persistentPseudomonas aeruginosainfection.
Respiratory symptoms in children and exposure to pesticides
Authors: Salameh P.R. , Baldi I. , Brochard P. , Raherison C. , Abi Saleh B. , Salamon R. 
Published: September 2008

In Lebanon, childhood asthma is an important disease and pesticides are commonly used. The objective of this study was to evaluate whether exposure to pesticides has chronic effects on the respiratory health of Lebanese children.A cross­sectional study was performed on children from a randomly selected sample of Lebanese public schools. Exposure to pesticides was evaluated by a standardised questionnaire and a residential exposure score, and respiratory symptoms were assessed by using the American Thoracic Society standardised questionnaire.A chronic respiratory disease was reported in 407 (12.4%) out of 3,291 children. The baseline difference in mean age was small but statistically significant. Any exposure to pesticides, including residential, para­occupational and domestic, was associated with respiratory disease and chronic respiratory symptoms (chronic phlegm, chronic wheezing, ever wheezing), except for chronic cough.Exposure to pesticides was associated with chronic respiratory symptoms and disease among Lebanese children.
Variation of CD8+ T‐lymphocytes around the bronchial internal perimeter in chronic bronchitis
Authors: Gamble E. , Burns W. , Zhu J. , Ansari T. , De Rose V. , Kips J. , Barnes N.C. , Jeffery P.K. 
Published: September 2008

The variation of CD8+ cells has been determined around the internal perimeter of intrapulmonary bronchi in smokers with chronic bronchitis (CB), and the amount of tissue required to confidently estimate the true mean has been calculated.Lung specimens were obtained from 10 smokers with CB. Paraffin sections of intrapulmonary bronchi were immunostained and CD8+ cells counted in the epithelium and subepithelium in up to 10 sequential 1‐mm segments around the internal perimeter of each airway.The percentage of counts falling between ±20% of the final mean was 43.0% for epithelium and 40.9% for subepithelium. In 90% of subjects, the cumulative mean was stable after examination of subepithelial tissue associated with 5 mm of reticular basement membrane.There is considerable variation in the counts of CD8+ cells between adjacent 1‐mm airway mucosal segments in chronic bronchitis. In order to achieve a representative count and to maximise statistical power to detect differences between study populations, subepithelial tissue including a minimum of 5 mm of reticular basement membrane length should be examined.
Combined bronchoalveolar lavage and transbronchial lung biopsy: safety and yield in ventilated patients
Authors: Bulpa P.A. , Dive A.M. , Mertens L. , Delos M.A. , Jamart J. , Evrard P.A. , Gonzalez M.R. , lnstallé E.J. 
Published: September 2008

The aim of this study was to evaluate the safety and diagnostic yield of bedside bronchoalveolar lavage (BAL) combined with fibrescopic transbronchial lung biopsy (TBLB) in determining the aetiology of pulmonary infiltrates in mechanically ventilated patients.The records of 38 mechanically ventilated patients who underwent BAL/TBLB to investigate unexplained pulmonary infiltrates were retrospectively reviewed. Patients were divided into two groups: immunocompetent (group 1: n=22; group 1a: n=11, late acute respiratory distress syndrome (ARDS); group 1b: n=11, no ARDS) and immunocompromised (group 2, n=16).The procedure allowed a diagnosis in 28 patients (74%), inducing therapeutic modification in 24 (63%) and confirmation of clinical diagnosis in four (11%). In groups 1a, 1b and 2, diagnosis was obtained in 11 out of 11 (fibroproliferation), seven out of 11 and 10 out of 16 patients, and therapy changed in 11 out of 11 (administration of steroids), six out of 11 and seven out of 16 patients, respectively. Pneumothorax occurred in nine patients (four of group 1a), bleeding in four (<35 mL), and transient hypotension in two. No fatalities were procedure-related.Combined bronchoalveolar lavage/transbronchial lung biopsy is of diagnostic and therapeutic value in mechanically ventilated patients with unexplained pulmonary infiltrates, excluding those with late acute respiratory distress syndrome. Although complications are to be expected, the benefits of the procedure appear to exceed the risks in patients in whom a histological diagnosis is deemed necessary.
The role of mean inspiratory effort on daytime sleepiness
Authors: Pelin Z. , Karadeniz D. , Öztürk L. , Gözükirmizi E. , Kaynak H. 
Published: September 2008

This study has investigated the role of average maximum inspiratory effort in excessive daytime sleepiness in patients with obstructive sleep apnoea syndrome (OSAS) and upper airway resistance syndrome (UARS).Fifteen patients diagnosed with UARS and 32 patients with OSAS, with >5.5 h total sleep time (TST) during 8 h of nocturnal polygraphic recordings, were included in the study. Demographical data, polysomnographical data and data about daytime sleepiness, including Epworth sleepiness scale (ESS) and multiple sleep latency test (MSLT), were evaluated. In order to compute the average maximum inspiratory effort from oesophageal pressure (Poes) measurements, maximumPoeswas obtained from 20 representative obstructive respiratory events (obstructive apnoeas, hypopnoeas or flow limitations) for each sleep stage in both supine and side positions. FromPoesmeasurements during sleep, the increase inPoes(ΔPoes) during respiratory events was also calculated.The average maximumPoes, ΔPoes, respiratory disturbance index (RDI) and arousal index were significantly correlated with ESS in OSAS patients. In patients with UARS, the only significant correlation was obtained between average maximumPoesand ESS. The MSLT score did not show any significant correlation with arousal index, number of stage variations, RDI, averagePoes, ΔPoes, minimum oxygen saturation (Sa,O2) and percentage of TST with anSa,O2<90% in both UARS and OSAS patients. The results of multiple regression analysis showed that average maximumPoescorrelates best with the variance in ESS for OSAS patients.In conclusion, the data from this study indicate the possible important role of average inspiratory effort in determining subjective sleepiness in both obstructive sleep apnoea syndrome and upper airway resistance syndrome patients.
Pulmonary disease caused byM. malmoensein HIV negative patients: 5‐yr follow-up of patients receiving standardised treatment
Authors:   The Research Committee of the British Thoracic Society
Published: September 2008

The literature concerning the management of pulmonary disease caused byMycobacterium malmoenseconsists of retrospective reports on small series of patients. A recent multicentre trial conducted by the British Thoracic Society provided an opportunity to prospectively document the clinical features and response to treatment of this relatively rare but challenging disease in a substantial number of patients.When two positive cultures were confirmed by the Mycobacterium Reference Units for England, Wales, Scotland or Scandinavia, the coordinating physician invited the patient's physician to enrol the patient, who was then treated on a random basis with either rifampicin plus ethambutol or rifampicin, ethambutol and isoniazid for 2 yrs. Clinical, bacteriological and radiological progress were monitored at set intervals for 5 yrs.In over 5 yrs a total of 106 patients were recruited to the study. The mean age was 58 yrs, range 24–89 yrs. A total of 58% were male and just over half previously or at the time of the study had other lung diseases. Sputum was positive on direct smear in 58%. Cavitation was seen on the chest radiographs of 74%, the majority having cavities of ≥2 cm in diameter. Less than half of the patients showed bilateral disease, 26% having involvement of more than three lung zones. Disease was confined to the upper zone(s) in 30%. Other lung diseases were evident in 52%. Although clinical response was judged satisfactory at most reviews (90%), one in three patients died within 5 yrs and <5% were thought to have died primarily because ofM. malmoense. There were three failures of treatment and eight relapses after the end of treatment. There was no correlation between failure of treatment/relapse andin vitroresistance. A total of 63 (59%) of patients were alive at 5 yrs, of whom 44 (42% of the total entry) were known to be cured.Pulmonary disease caused byMycobacterium malmoenseis a serious condition that is associated with high morbidity and mortality. The results of standard susceptibility tests do not correlate with the bacteriological response of the disease to chemotherapy. Rifampicin and ethambutol, with or without isoniazid, cured only 42% of patients but were better tolerated than previously described, more complex regimens of equal or lesser efficacy. There is a need for more effective regimens that will reduce mortality and failure of treatment/relapse rates, but, in addition, attention should be directed at improving management of comorbid conditions and improving the general health of the patient.
A role of GM-CSF in the accumulation of neutrophils in the airways caused by IL-17 and TNF‐α
Authors: Laan M. , Prause O. , Miyamoto M. , Sjöstrand M. , Hytönen A.M. , Kaneko T. , Lötvall J. , Lindén A. 
Published: September 2008

The T‐cell cytokine interleukin (IL)-17 selectively accumulates neutrophils in murine airwaysin vivoand may thus constitute a link between activation of T‐lymphocytes and accumulation of neutrophils. In this study, the authors evaluated the role of granulocyte macrophage-colony stimulating factor (GM-CSF) in accumulation of neutrophils in the airways caused by IL-17 and tumour necrosis factor (TNF)‐α.In vitro, human (h) IL-17 concentration-dependently stimulated the release of GM-CSF protein (enzyme-linked immunosorbent assay) in human bronchial epithelial cells (16HBE). IL-17 also time-dependently stimulated the release of GM-CSF protein in venous endothelial (human umbilical vein endothelial cells) cellsin vitro. Co-stimulation with IL-17 plus the pro-inflammatory cytokine TNF‐α potentiated the release of GM-CSF protein in 16HBE cells. hIL-17 also enhanced the expression of GM-CSF messenger ribonucleic acid in 16HBE cells (reverse transcriptase polymerase chain reaction), with a similar order of magnitude as TNF‐α. Conditioned cell medium from bronchial epithelial cells co-stimulated with hIL-17 plus TNF‐α prolonged survival (trypan blue exclusion) of human neutrophilsin vitroand this effect was blocked by an anti-GM-CSF antibody.In vivo, local co-stimulation with mouse IL-17 plus TNF‐α caused an additive potentiation of the accumulation of neutrophils in bronchoalveolar lavage fluid from mouse airways and this effect was blocked by an anti‐GM-CSF antibody given systemically.In conclusion, granulocyte macrophage-colony stimulating factor is involved in the accumulation of neutrophils in the airways caused by interleukin-17 and tumour necrosis factor‐α, probablyviaeffects on both recruitment and survival of neutrophils.
Bronchial asthma causing symptoms suggestive of angina pectoris
Authors: Kiss D. , Veegh W. , Schragel D. , Bachl C. , Stöllberger C. , Sertl K. 
Published: September 2008

Many patients undergoing pharmacological stress echocardiography for assessing symptoms suggestive of coronary artery disease are found to have a normal test. This study was performed to evaluate whether asthma symptoms simulate angina pectoris.A total 41 consecutive patients who had a negative pharmacological stress echocardiography and had been evaluated for angina pectoris were studied. Patients with previously known coronary artery disease or obstructive lung disease were excluded. Lung function testing was performed and the authors proceeded either with the administration of a bronchodilator or with methacholine challenge testing. A questionnaire was applied to assess the symptoms dyspnoea, chest tightness and substernal burning at the end of the challenge test. In addition, patients were asked if they were experiencing those symptoms that made them seek medical attention. From the 41 patients tested, 26 patients showed a significant bronchial hyperreactivity (mean±sd provocative concentration causing a 20% fall in the forced expiratory volume in one second 5.93±4.50 mg·mL−1). A total of 20 patients confirmed having those symptoms that led to cardiac evaluation.It was concluded that symptoms suggestive of angina pectoris might represent bronchial asthma. This should be considered in the differential diagnosis of angina pectoris.
Inhaled corticosteroids and growth of airway function in asthmatic children
Authors: Merkus P.J.F.M. , van Pelt W. , van Houwelingen J.C. , van Essen-Zandvliet L.E.M. , Duiverman E.J. , Kerrebijn K.F. , Quanjer P.H. 
Published: September 2008

Airway inflammation and remodelling play an important role in the pathophysiology of asthma. Remodelling may affect childhood lung function, and this process may be reversed by anti-inflammatory treatment. The current study assessed longitudinally whether asthma affects growth of airway function relative to airspaces, and if so whether this is redressed by inhaled corticosteroids (ICS).Every 4 months for up to 3 yrs, lung function was assessed in 54 asthmatic children (initial age 7–16 yrs), who inhaled 0.2 mg salbutamolt.i.d.and 0.2 mg budesonidet.i.d.(β2‐agonist (BA)+ICS), or placebo (PL)t.i.d. (BA+PL) in a randomised, double-blind design. Measurements were carried out before and after maximal bronchodilation. Airway growth was assessed from the change of forced expiratory volume in one second and of maximal expiratory flows (at 60% and 40% of total lung capacity (TLC) remaining in the lung) relative to TLC, as measures of more central, intermediate and more peripheral airways. Growth patterns were compared with the longitudinal findings in 376 healthy children.Airway patency after maximal bronchodilation in patients on BA+PL remained reduced compared to healthy subjects, whereas in patients on BA+ICS a marked improvement was observed to subnormal. No differences between patients and controls could be demonstrated for growth patterns of central and intermediate airway function. Compliance with BA+ICS was 75% of the prescribed dose, resulting in significant, sustained improvement of symptoms and postbronchodilator calibre of central and intermediate airways to subnormal within 2 months, but postbronchodilator small airway patency remained reduced, though improved compared to patients on BA+PL.Anti-inflammatory treatment of asthmatic children is associated with normal functional development of central and intermediate airways. The persistently reduced postbronchodilator patency of peripheral airways may reflect remodelling, or insufficient anti-inflammatory treatment.
Effect of saliva contamination on induced sputum cell counts, IL‐8 and eosinophil cationic protein levels
Authors: Simpson J.L. , Timmins N.L. , Fakes K. , Talbot P.I. , Gibson P.G. 
Published: September 2008

Excessive salivary contamination of induced sputum samples prevents the satisfactory examination of lower airway inflammation. The effects of salivary contamination on different sputum fluid phase measures and the levels of salivary contamination preventing analysis are not defined. The present study sought to examine this by investigating the effect of increasing salivary contamination on induced sputum samples.Sputum and saliva samples from subjects with asthma and healthy controls were collected, and treated with dithiothreitol (DTT). Saliva was then added to aliquots of dispersed sputum in increasing proportions (0% to 100%). The effect of increasing saliva contamination was assessed on sputum total cell count, viability, differential cell count and fluid phase levels of interleukin (IL)‐8, eosinophil cationic protein (ECP) and total protein.The addition of saliva to induced sputum reduced total cell counts and absolute cell counts but did not change the differential cell count. Levels of fluid phase ECP and IL‐8 were significantly reduced with increased salivary contamination. There was a progressive reduction in ECP and IL‐8, which reached significance at 70% and 80% saliva contamination, respectively. IL‐8 levels corrected for total protein showed no change with increasing saliva concentrations.Induced sputum differential cell counts expressed as the proportion of nonsquamous cells are robust measures that are not influenced by salivary contamination. Studies reporting total and absolute cell counts and fluid phase mediator levels require control for squamous contamination.
Prenatal nicotine exposure increases connective tissue expression in foetal monkey pulmonary vessels
Authors: Sekhon H.S. , Proskocil B.J. , Clark J.A. , Spindel E.R. 
Published: September 2008

Among the many deleterious effects of maternal smoking during pregnancy on foetal development, is a higher incidence of persistent pulmonary hypertension. The recent identification of nicotinic acetylcholine receptors (nAChR) on cells of the pulmonary vessel walls suggests that maternal smoking during pregnancy may produce morphological alterations in foetal pulmonary vasculature.Timed­pregnant rhesus monkeys were treated with nicotine (1 mg·kg−1·day−1) delivered by subcutaneous osmotic mini­pumps from days 26–134 of gestation (term: 165 days). Lung sections from 134‐day foetal monkeys were used for morphometric analysis,in situhybridisation and immunohistochemical staining.Following nicotine treatment, total wall and tunica adventitia thickness of airway associated vessels (AAV) increased significantly. Nicotine exposure significantly increased collagen I and III mRNA and protein in tunica adventitia in all AAV but not in tunica media. By contrast, levels of elastin protein were significantly decreased. α7 nAChR were detected in AAV fibroblasts that expressed collagen mRNA. Choline acetyltransferase, the enzyme which synthesises acetylcholine, the ligand for α7 nAChR was also detected in endothelium and fibroblasts.These findings suggest that with smoking during pregnancy, nicotine is transported across the placenta and directly interacts with nicotinic acetylcholine receptors in pulmonary vessels to alter connective tissue expression and therefore produce vascular structural alterations.
Effect of inhaled steroids on lung function in young children: a cohort study
Authors: Devulapalli C.S. , Haaland G. , Pettersen M. , Carlsen K.H. , Lødrup Carlsen K.C. 
Published: September 2008

The objectives of the present study were to determine the use of inhaled corticosteroids (ICS) for treating recurrent bronchial obstruction (rBO) in young children up to 2 yrs of age and to assess possible modifying effects of ICS on lung function in young children with rBO. From an observational, noninterventional birth cohort of 3,754 newborn children (3,697 with complete questionnaire data by 2 yrs of age), 306 children with documented rBO by age 2 yrs (cases) were identified along with 306 matched controls.Two tidal flow/volume measurements were taken, one at presentation of disease (children were steroid naïve) and one at 2 yrs of age (mean age 11.2 and 25.6 months, respectively), from: 21 cases who subsequently received ICS (ICS+); 33 who did not (ICS−); and in 15 controls. The mean±sd duration of ICS treatment was 10.3±6.5 months. The main outcomes were treatment with ICS and baseline ratio of time to peak expiratory flow/total expiratory time (tPTEF/tE).From the entire cohort, 77 children (2.1%) and 21% of children with rBO had received ICS by 2 yrs of age. BaselinetPTEF/tEwas significantly lower at the first visit only in ICS+ as compared to ICS− subjects, as well as in ICS+ and ICS- as compared to controls. The mean difference in baselinetPTEF/tEfrom first to second visit was borderline statistically significant in the ICS+ group only and correlated significantly with duration of ICS treatment.The present observational cohort study demonstrated that one-fifth of young children with recurrent bronchial obstruction had received inhaled corticosteroids. Early inhaled corticosteroid treatment improved lung function by age 2 yrs, mostly in those with the longest duration of treatment.