bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transforming growth factor‐β induces collagen synthesis without inducing IL‐8 production in mesothelial cells
Authors: Lee Y.C.G. , Lane K.B. , Zoia O. , Thompson P.J. , Light R.W. , Blackwell T.S. 
Published: July 2003

Conventional pleurodesing agents often provoke acute pleural inflammation followed by fibrosis. The inflammation frequently causes pain and fever. Transforming growth factor (TGF)‐β is a pro-fibrotic but anti-inflammatory cytokine. Intrapleural TGF‐β2administration produces effective pleurodesis in animals, but its effects on mesothelial cells are unknown. The authors hypothesised that, unlike conventional pleurodesing agents, TGF‐β2can induce collagen synthesis without stimulating pleural inflammation.In thein vitrostudies, TGF‐β2, talc and doxycycline were administered to rabbit mesothelial cells for 24 h. These agents were also injected intrapleurally in rabbits and the induced pleural fluids collected at 24 h. TGF‐β2was as potent as talc and doxycycline in upregulating mesothelial cell collagen expression.Talc and doxycycline both induced significant increases in interleukin (IL)‐8 production from mesothelial cellsin vitroand in rabbit pleural fluidsin vivo. TGF‐β2, however, did not stimulate mesothelial cell IL‐8 releasein vitroand induced a dose-dependent suppression of pleural fluid IL‐8. Pleural fluid IL‐8 levels correlated significantly with leukocyte and lactate dehydrogenase concentrations in the fluids.In summary, transforming growth factor‐β was a potent inducer of mesothelial cell collagen synthesis. Unlike talc and tetracycline, which provoked pleural inflammation, transforming growth factor‐β2suppressed pleural inflammationin vivo. Transforming growth factor‐β2can produce effective pleural fibrosis without necessitating acute pleural inflammation.
Cytokine production of RSV/PHA‐stimulated tonsillar mononuclear cells: influences of age and atopy
Authors: Ichinohe S. , Hussain I.R. , Johnston S.L. 
Published: July 2003

Links between immune responses to respiratory syncytial virus (RSV), age and atopic sensitisation are poorly understood.This study investigated the induction of target organ type‐1, type‐2 and pro-inflammatory cytokine responses to RSV and/or phytohaemagglutinin (PHA) in tonsillar mononuclear cells from children, in relation to age and atopic status.In comparison with the control medium, RSV induced production of the type‐1 cytokines interferon (IFN)‐γ and interleukin (IL)‐18, the pro-inflammatory cytokines IL‐6, ‐8 and RANTES (regulated on activation, normal T‐cell expressed and secreted), but not any of the type‐2 cytokines IL‐4, ‐5, ‐10 and ‐13. Induction of IL‐6, ‐8 and RANTES, but not IFN‐γ or IL‐18, were shown to be dependent on virus replication. PHA induced all except IL‐12, ‐13, and ‐15. Induction of IFN‐γ, IL‐6, ‐8, and RANTES was significantly increased in atopic children. Induction of both IFN‐γ andIL‐4 increased in parallel in relation to age, with no change in the IFN‐γ:IL‐4 ratio.These data are compatible with the hypothesis that immature type‐1 immunity during early childhood plays a role in both respiratory syncytial virus bronchiolitis and in its relationship with atopy.
Estimation of lung growth using computed tomography
Authors: de Jong P.A. , Nakano Y. , Lequin M.H. , Merkus P.J. , Tiddens H.A. , Hogg J.C. , Coxson H.O. 
Published: July 2003

Anatomical studies suggest that normal lungs grow by rapid alveolar addition until about 2 yrs of age followed by a gradual increase in alveolar dimensions.The aim of this study was to examine the hypothesis that normal lung growth can be monitored by computed tomography (CT). Therefore, the gas volume per gram of lung tissue was estimated from measurements of lung density obtained from CT scans performed on children throughout the growth period.CT scans were performed on 17 males and 18 females, ranging in age from 15 days–17.6 yrs. CT-measured lung weight was correlated with predictedpost mortemvalues and CT measured gas volume with predicted values of functional residual capacity. The median value for lung expansion was 1.86 mL·g−1at 15 days, decreased to 0.79 mL·g−1by 2 yrs and then increased steadily to 5.07 mL·g−1at 17 yrs.Computed tomography scans can be used to estimate lung weight, gas volume and expansion of normal lungs during the growth period. The increase in the lung expansion after the age of 2 yrs suggests progressive alveolar expansion with increasing lung volume.
Zardaverine and aerosolised iloprost in a model of acute respiratoryfailure
Authors: Schermuly R.T. , Leuchte H. , Ghofrani H.A. , Weissmann N. , Rose F. , Kohstall M. , Olschewski H. , Schudt C. , Grimminger F. , Seeger W. , Walmrath D. 
Published: July 2003

In this study, the impact of aerosolised prostacyclin (PGI2) and iloprost in the absence or presence of subthreshold intravascular doses of the dual-selective phosphodiesterase-3/4 inhibitor zardaverine was investigated in an experimental model of acute respiratory failure.In perfused rabbit lungs, continuous infusion of the thromboxane‐A2‐mimetic U46619 provoked pulmonary hypertension, accompanied by progressive lung oedema formation and severe ventilation-perfusion mismatch with predominance of shunt flow (increasing from ∼2 to 58%, as assessed by the multiple inert gas elimination technique). Aerosolisation of PGI2(in total 1.05 µg·kg−1) for 15 min caused a decrease in pulmonary artery pressure (Ppa) and a limitation of maximum shunt flow to ∼37%. When nebulised PGI2was combined with subthreshold intravascular zardaverine, which did not affect pulmonary haemodynamicsper se, the duration of the PGI2effect was increased. Aerosolisation of 3 µg·kg−1PGI2resulted in a transient decrease inPpa and a reduction in shunt flow. In the presence of subthreshold zardaverine, the effects of this PGI2dose were only marginally increased. Aerosolisation of iloprost (in total 0.7 µg·kg−1) for 15 min caused a more sustained decrease inPpa, some enhanced reduction of oedema formation as compared with PGI2and a decrease in shunt flow to ∼32%. Most impressively, when combined with subthreshold zardaverine, iloprost suppressed oedema formation to <15% and shunt flow to ∼8%.In conclusion, combined use of aerosolised iloprost and subthreshold systemic phosphodiesterase-3/4 inhibitor may result in selective intrapulmonary vasodilation, a reduction in oedema formation and an improvement in ventilation-perfusion matching in acute respiratory failure.
Peripheral deposition of α1‐protease inhibitor using commercial inhalation devices
Authors: Brand P. , Beckmann H. , Maas Enriquez M. , Meyer T. , Müllinger B. , Sommerer K. , Weber N. , Weuthen T. , Scheuch G. 
Published: July 2003

Patients with hereditary α1‐proteinase inhibitor (α1‐PI) deficiency are at risk of developing lung emphysema. To prevent the development of this disease, α1‐PI replacement therapyviainhalation may be a more convenient and effective therapy than the intravenous administration of the drug.In order to optimise this treatment approach, lung deposition of inhaled radiolabelled α1‐PI (Prolastin®) was studied using four different commercial inhalation devices (PARI‐LC Star®, HaloLite®, and AKITA® system in combination with LC Star® and Sidestream®) in six patients with α1‐PI deficiency and mild-to-severe chronic obstructive pulmonary disease.The time required to deposit 50 mg of the Prolastin® (5% solution) in the lung periphery was used as a measure for the efficiency of delivery. The time was calculated from measurements of total and peripheral lung deposition of the radiolabelled α1‐PI. This time was shortest for the AKITA® system (18–24 min) and significantly higher for the PARI‐LC Star® (44 min) and the HaloLite® (100 min).The higher efficiency of drug delivery using the AKITA® system is due to the fact that this device controls breathing patterns, which are optimised for each patient individually.
Neutrophil airway influx by platelet-activating factor in asthma: role of adhesion molecules and LTB4expression
Authors: Gabrijelcic J. , Acuña A. , Profita M. , Paternò A. , Chung K.F. , Vignola A.M. , Rodríguez-Roisin R. 
Published: July 2003

Platelet-activating factor (PAF)-induced neutrophil lung sequestration may require cell surface adhesion molecules (macrophage‐1 antigen (MAC‐1) and lymphocyte function-associated antigen‐1 (LFA‐1)). In this randomised, double-blinded, crossover study, theneutrophil kinetics after PAF and Lyso-PAF (L‐PAF) airway challenge were investigated in nine mild-intermittent asthmatics.Neutrophils were measured in peripheral blood (PB) before and at 5, 15, 45 and 240 min after bronchoprovocation, and in induced sputum before and at 240 min after challenge. MAC‐1 and LFA‐1 expression were assessed by immunocytochemistry, and leukotriene B4(LTB4) was measured by enzyme-immunoassay in induced-sputum supernatants.Compared with baseline, neutrophils in PB decreased 5 min after PAF, while at 240 min neutrophils in induced sputum increased. Compared with baseline and L‐PAF, PAF decreased the percentages of MAC‐1‐ and LFA‐1‐positive neutrophils in PB at 5 min, but increased the percentages of MAC‐1 and LFA‐1 in neutrophil-induced sputum. Moreover, compared with baseline and L‐PAF, PAF-induced sputum revealed higher LTB4levels, a finding that correlated with the elevated number of neutrophils in induced sputum.These findings suggest that macrophage‐1 antigen and lymphocyte function-associated antigen‐1 are involved in platelet-activating factor-induced neutrophil lung traffic, and that this process is modulated by enhanced leukotriene B4release within the airways.
Cyclosporin A, apoptosis of BAL T‐cells and expression of Bcl‐2 inasthmatics
Authors: Ying S. , Khan L.N. , Meng Q. , Barnes N.C. , Kay A.B. 
Published: July 2003

The late asthmatic reaction is characterised by elevated numbers of interleukin‐4/interleukin‐5/CD4‐positive T‐helper cells type 2 in bronchoalveolar lavage fluid (BALF). Cyclosporin A (CsA) is known to inhibit T‐cell proliferation, induce apoptosis of CD4‐positive T‐cells and downregulate cytokine gene expression.It was assessed whether CsA‐induced inhibition of the late asthmatic reaction was associated with apoptosis of BALF T‐lymphocytes and other cell types, as well as expression of the antiapoptotic protein B‐cell leukaemia/lymphoma 2 gene product (Bcl‐2). BALF cells were obtained from asthmatics at baseline and 24 h after allergen-inhalation challenge following prior administration of CsA (n=13) or placebo (n=11).The number of apoptotic CD3‐positive T‐lymphocytes increased in the CsA but not the placebo group. The numbers of Bcl‐2‐positive cells were significantly reduced in the CsA but not the placebo group. The majority of Bcl‐2‐positive cells were CD3‐positive T‐lymphocytes.The beneficial effect of cyclosporin A in asthma may be related to its inhibitory effect on the late asthmatic reactionviainduction of T‐cell apoptosis and decreased B‐cell leukaemia/lymphoma 2 gene product levels.
Prevalence of work-aggravated symptoms in clinically established asthma
Authors: Saarinen K. , Karjalainen A. , Martikainen R. , Uitti J. , Tammilehto L. , Klaukka T. , Kurppa K. 
Published: July 2003

This population-based cross-sectional survey assessed the prevalence of work-aggravated asthma symptoms and the effect of the work environment on the aggravation of symptoms of established asthma.A questionnaire was sent to 2,613 persons (aged 20–65 yrs) with asthma. The analyses were restricted to the 969 respondents who were currently employed. The effect of occupational exposure on the aggravation of asthma symptoms at work was assessed according to both self-reported and expert-evaluated exposure.Approximately 21% of the respondents reported work-aggravated asthma symptoms at least weekly during the past month. The prevalence of those with work-aggravated symptoms increased by age, self-reported occupational exposure to dusts, abnormal temperatures or poor indoor air quality, physically strenuous work, and chemicals, and expert-evaluated probability of daily occupational exposure to airborne dusts, gases or fumes.Aggravation of asthma symptoms at work is common among employed adults with asthma. Both self-reported and expert-evaluated exposure to dusts, abnormal temperatures or poor indoor air quality, physically strenuous work, and chemicals explained the significant worsening of symptoms. The findings suggest a marked role of the work environment in the aggravation of symptoms of established asthma.
BAL findings in idiopathic nonspecific interstitial pneumonia and usual interstitial pneumonia
Authors: Veeraraghavan S. , Latsi P.I. , Wells A.U. , Pantelidis P. , Nicholson A.G. , Colby T.V. , Haslam P.L. , Renzoni E.A. , du Bois R.M. 
Published: July 2003

Idiopathic pulmonary fibrosis (IPF), which has the histological pattern of usual interstitial pneumonia (UIP), is a progressive interstitial lung disease with a poor prognosis. Idiopathic interstitial pneumonias with a histological pattern of nonspecific interstitial pneumonia (NSIP) have a better prognosis than UIP, and may present with a clinical picture identical to IPF. The authors hypothesised that bronchoalveolar lavage (BAL) findings may distinguish between UIP and NSIP, and have prognostic value within disease subgroups.BAL findings were studied retrospectively in 54 patients with histologically proven (surgical biopsy) idiopathic UIP (n=35) or fibrotic NSIP (n=19), all presenting clinically as IPF. These findings were also compared with the BAL profile of patients with other categories of idiopathic interstitial pneumonias.BAL total and differential cell counts did not differ between the two groups. Survival was better in NSIP. In neither group were BAL findings predictive of survival or changes in lung function at 1 yr, even after adjustment for disease severity, smoking andtreatment. BAL differential counts in fibrotic NSIP differed from respiratory bronchiolitis-associated interstitial lung disease, but not from desquamative interstitial pneumonia or cellular NSIP.The authors conclude that bronchoalveolar lavage findings do not discriminate between usual interstitial pneumonia and nonspecific interstitial pneumonia in patients presenting with clinical features of idiopathic pulmonary fibrosis, and have no prognostic value, once the distinction between the two has been made histologically.
Modulation by cAMP of IL‐1β‐induced eotaxin and MCP‐1 expression and release in human airway smooth muscle cells
Authors: Wuyts W.A. , Vanaudenaerde B.M. , Dupont L.J. , Demedts M.G. , Verleden G.M. 
Published: July 2003

Inflammatory cells, such as eosinophils, seem to be key players in the inflammatory process of asthma. These cells are attracted by chemokines, for example eotaxin and monocyte chemotactic protein (MCP‐1).In this study, the authors investigated whether eotaxin and MCP‐1 expression and release in human airway smooth muscle cells could be modulated by an increase in intracellular cyclic adenosine monophosphate (cAMP) concentration. The possible involvement of cAMP‐dependent protein kinase A (PKA) was also studied.Forskolin, a direct stimulator of adenylyl cyclase, decreased the interleukin (IL)‐1β‐induced eotaxin and MCP‐1 release by 73±8 and 65±6%, respectively. 8Bromo‐cAMP, a cAMP analogue, similarly decreased the chemokine production by 58±9 and 63±8% for eotaxin and MCP‐1, respectively. Prostaglandin E2, known as an activator of the prostanoid receptors EP2and EP4, which are positively coupled to adenylyl cyclase, also decreased the IL‐1β‐induced eotaxin and MCP‐1 production by 57±17 and 53±4%, respectively. H‐89, an inhibitor of PKA, was able to inhibit the decrease in eotaxin and MCP‐1 protein release induced by forskolin. Using Western-blot analysis, no effect of cAMP was found on the IL‐1β‐induced p38 mitogen-activated protein kinase, extracellular signal-related kinase or cJunN‐terminal kinase activation.This study shows that an increase in intracellular cyclic adenosine monophosphate concentration may decrease the interleukin‐1β‐induced eotaxin and monocyte chemotactic protein‐1 expression and production. This can be inhibited by addition of H‐89, an inhibitor of cyclic adenosine monophosphate-dependent protein kinase. No decrease was observed in interleukin‐1β‐induced p38 mitogen-activated protein kinase, extracellular signal-related kinase or cJunN‐terminal kinase activation. These findings may be important for the further development of new anti-inflammatory drugs.
Inhaled corticosteroids and hospitalisation due to exacerbation of COPD
Authors: Bourbeau J. , Ernst P. , Cockcoft D. , Suissa S. 
Published: July 2003

Previous studies have provided conflicting evidence as to the possible benefits of inhaled corticosteroids in the treatment of chronic obstructive pulmonary disease (COPD).Using the Saskatchewan healthcare databases subjects were identified who were aged ≥55 yrs, initiating regular treatment for COPD but without any prior treatment for asthma. In the current nested case-control analysis, the authors concentrated on 1,742 subjects with a first hospitalisation for COPD after January 1, 1990 and examined whether the use of inhaled corticosteroids was associated with a change in the risk of a subsequent hospitalisation for COPD.The cases consisted of 846 patients with a subsequent hospitalisation for COPD. These were matched on age, time since the prior hospitalisation and use of other respiratory therapy to all possible person moments in the cohort without rehospitalisation. After further adjustment for comorbidity, sex, calendar year and intensity of other drug therapy, inhaled corticosteroids were not significantly associated with risk of a subsequent COPD hospitalisation. Even relatively high doses of inhaled corticosteroids, >800 µg of beclomethasone or the equivalent per day, were not associated with the risk of COPD hospitalisation.No reduction in chronic obstructive pulmonary disease exacerbations requiring hospitalisation, in relation to the use of inhaled corticosteroids, were observed.
Lymphoepithelioma-like carcinoma of the lung in a patient withsilicosis
Authors: Ho J.C. , Lam W.K. , Ooi G.C. , Wong M.P. , Lam J.C. , Ip M.S. , Tsang K.W.T. 
Published: July 2003

Silicosis is an important form of pneumoconiosis, which is caused by significant exposure to crystalline silica. The carcinogenicity of silica, despite traditional beliefs, in relation to lung cancer has been controversial. Lymphoepithelioma-like carcinoma of the lung, an Epstein-Barr virus-associated undifferentiated carcinoma, is a rare entity of pulmonary malignancy, which tends to affect young nonsmoking Asians.The first case of silicosis, initially complicated by pulmonary tuberculosis, which later developed into advanced lymphoepithelioma-like carcinoma of the lung is reported. A combination of 5‐fluorouracil, cisplatin and calcium folinate resulted in partial tumour response.
Is preparation for bronchoscopy optimal?
Authors: Pickles J. , Jeffrey M. , Datta A. , Jeffrey A.A. 
Published: July 2003

The results of a questionnaire survey, of the current preparation for and practice of diagnostic bronchoscopy in England and Wales, are reported in this paper. The British Thoracic Society (BTS) has recently published guidelines on bronchoscopy and these provide a consensus statement on the current evidence base. There is no specific guidance on drugs or techniques, although it is recommended that all patients should be offered sedation, except where there are contraindications.In the present survey, there was a response rate of 76% (344 responses to 452 questionnaires) and the median number of bronchoscopies performed per session was 5 (interquartile range 4–6). Most operators use lignocaine gel to the nose (65%), spray to the throat (70%), followed by the “spray as you go” method (84%), recommended by the BTS. Atropine is routinely used by 13% contrary to the guidelines and despite concerns about its side-effects. Most operators use sedation with midazolam (85%) or a wide variety of combinations of sedative, analgesic, and anaesthetic agents (27%), and 27% perform unsedated bronchoscopies, with only 0.1% routinely performing unsedated bronchoscopies. A total 251 (77%) responders stated they assessed adequacy of sedation, with most using patient observation alone (149 (46%)). Only three operators assessed sedation using a formal sedation score. Thus, most centres routinely perform sedated bronchoscopies and the systematic level of monitoring is poor.The current controversies about sedation and safe sedation practice are discussed. There is a need for more evidence to allow more specific guidance to be produced in this difficult area.
Sputum induction leads to a decrease of exhaled nitric oxide unrelated to airflow
Authors: Beier J. , Beeh K.M. , Kornmann O. , Buhl R. 
Published: July 2003

Measurement of exhaled nitric oxide (eNO) and analysis of induced sputum are both established noninvasive methods for studying airway inflammation in asthma. Both methods are often used sequentially within short time frames. The aim of the present study was to evaluate the influence of sputum induction on eNO in adults and to follow the kinetics of airway eNO production after induction in relation to forced expiratory volume in one second (FEV1).eNO and FEV1were measured in 41 adult patients (aged 29 (range 23–50) yrs, 56% male) with asymptomatic atopy or mild asthma (mean FEV197.2±3% predicted) prior to and immediately after sputum induction with hypertonic saline (4%). Sputum induction with isotonic saline was also performed in 13 subjects (control group). Repeatability of eNO decrease after sputum induction was also studied in 27 patients on separate occasions and kinetics of eNO production after sputum induction were followed over 24 h in another 10 patients.Sputum induction with hypertonic, but not isotonic, saline led to a marked decrease in eNO (log) immediately after the procedure (pre: 3.85±0.13 parts per billion (ppb); post: 3.24±0.14 ppb). This decrease was shown to be highly reproducible and not related to a fall in FEV1following sputum induction. While FEV1returned to baseline within 1 h, decreased eNO levels were observed over 4 h and returned to baseline after 24 h.Hypertonic saline sputum induction leads to a prolonged reduction in exhaled nitric oxide in adult atopics that is reproducible within subjects and not related to a reduction in airflow following sputum induction. This methodological interference should be taken into account when sputum induction and exhaled nitric oxide measurements are performed in the same subject.
The Borah Peak, Idaho Earthquake of October 28, 1983—Summary
Authors: Reaveley Lawrence D. 
Published: July 2003

The Borah Peak, Idaho earthquake of October 28, 1983 occurred at 8:07 a.m. Mountain Daylight Time. This earthquake, which had a Richter magnitude of 7.3, was the largest earthquake to occur in Idaho in recorded history (since 1872). The epicenter was located approximately 30 km northwest of the town of MacKay (Fig. 1), in central Idaho (see also Taylor, et al). The earthquake shook eight northwestern states. Some minor damage to buildings was reported as far away as Salt Lake City, Utah and Boise, Idaho. The epicenter is located in the center of large Zone 2 seismic area, as designated in the 1982 Uniform Building Code. This area was an area of low historic seismicity and had previously been designated a Zone 3 area in the 1979 UBC. Two small Idaho communities are located some distance beyond the ends of the fault scarp. MacKay is approximately 21 km (13 mi.) southeast of the earthquake epicenter and 24 km (15 mi.) from the southern end of the scarp. Challis is located approximately 60 km (40 mi.) north-northwest of the epicenter and 19 km (12 mi.) beyond the northern end of the surface faulting (Taylor et al). Challis has the largest population which varies from 1,000 to 2,500 depending on the time of the year. MacKay is the second largest, with a population of approximately 500. The balance of the 4,000 to 5,000 people that live in the area live on ranches and in small mining communities.