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Träfflista för sökning "L773:0903 1936 OR L773:1399 3003 srt2:(1990-1994)"

Sökning: L773:0903 1936 OR L773:1399 3003 > (1990-1994)

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1.
  • Forsberg, Bertil, et al. (författare)
  • Air pollution levels, meteorological conditions and asthma symptoms
  • 1993
  • Ingår i: European Respiratory Journal. - 0903-1936 .- 1399-3003. ; 6:8, s. 1109-1115
  • Tidskriftsartikel (refereegranskat)abstract
    • We wanted to assess relations between the daily occurrence of asthma symptoms and fluctuations of air pollution concentrations and meteorological conditions. In a panel of 31 asthmatic patients residing in the town of Piteå in northern Sweden, severe symptoms of shortness of breath, wheeze, cough and phlegm were recorded in an asthma diary together with suspected causes. Sulphur dioxide, nitrogen dioxide, black smoke, relative humidity and temperature were used to evaluate the relationship to the environment. By using multivariate analyses, we found that daily variations in the particulate pollution levels, indicated by black smoke levels below the criteria limits, had significant effects on the risk of developing severe symptoms of shortness of breath. This association was stronger among 10 subjects, who had at least five incident days with severe shortness of breath. Meteorological conditions were not significant in the multivariate models. Cough and phlegm did not show significant relationships to any environmental condition that was evaluated. Only one-third of the subjects reported, at least once during the study, symptoms believed to be related to air pollutants, although we found significant correlations between the pollution levels and the frequency of pollution-related symptoms. We conclude that an association has been established for black smoke as pollutant and shortness of breath as respiratory symptom, and that in certain asthmatics, effects were occurring at lower particulate levels than suggested previously.
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3.
  • Nilsson, Kristina, 1967-, et al. (författare)
  • Pulmonary clearance of tracers with different lipid and water solubility in experimental surfactant dysfunction.
  • 1993
  • Ingår i: European Respiratory Journal. - 0903-1936 .- 1399-3003. ; 6:4, s. 505-8
  • Tidskriftsartikel (refereegranskat)abstract
    • We measured the pulmonary clearance of inhaled 99mTc-diethylenetriamine penta-acetic acid (DTPA), 99mTc-sestamibi and 99mTc-dimethyliminodiacetic acid (HIDA) in normal rabbits, and rabbits with surfactant dysfunction induced by the detergent dioctyl sodium sulfosuccinate. The tracers differ widely in lipid/water partition coefficients, but have similar molecular radius and weight. Five animals in each group received the detergent in aerosol, and the other five a vehicle aerosol, before the administration of the tracer. Pulmonary clearance of the tracers was measured with a gamma camera. The half-life of 99mTc-DTPA was 94 +/- 16 min in normal lungs, and 10 +/- 1 min after detergent administration (p < 0.001). The half-life for 99mTc-sestamibi was 45 +/- 4 min and 39 +/- 4 min, respectively, (p < 0.05). There was no significant difference between the half-life of 99mTc-HIDA in normal lungs and in lungs with surfactant dysfunction. The half-life was 20 +/- 3 min and 17 +/- 2 min, respectively. The results indicate that the clearance rate limiting factors for the alveolocapillary transfer of water and lipid soluble substances are not the same. Surfactant dysfunction affects the transfer of water soluble substances (99mTc-DTPA) but not of substances with high lipid solubility (99mTc-HIDA).
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4.
  • Riise, Gerdt C., 1956, et al. (författare)
  • Circulating cell adhesion molecules in bronchial lavage and serum in COPD patients with chronic bronchitis
  • 1994
  • Ingår i: Eur Respir J. - 0903-1936. ; 7:9, s. 1673-1677
  • Tidskriftsartikel (refereegranskat)abstract
    • The initial phase of inflammation in bronchial asthma appears to be triggered by the expression of leucocyte-endothelial adhesion molecules on endothelial cell surfaces. Cell adhesion molecules (CAMs) cause adhesion of leucocytes to the endothelium prior to their subsequent extravasation into inflamed tissue. We wanted to determine whether circulating intercellular adhesion molecule-1 (cICAM-1) and circulating E-selectin (cE-selectin) could be detected in bronchial lavage fluid and serum in patients with stable chronic obstructive pulmonary disease (COPD) and chronic bronchitis. Bronchoscopy and small volume bronchial lavage was performed in 19 patients with COPD and chronic bronchitis and in 13 control subjects. We found increased mean levels of cICAM-1 both in serum (481 micrograms.l-1) and in bronchial lavage (24 micrograms.l-1) in the COPD patients as compared to the controls (321 micrograms.l-1 in serum, 15 micrograms.l-1 in lavage). We also found higher mean levels of cE-selectin in serum from the COPD patients (86 micrograms.l-1) compared to controls (50 micrograms.l-1). The serum levels of cE-selectin correlated significantly with lung function measured as forced expiratory volume in one second (FEV1) in percentage of predicted. Patients with significant intrabronchial bacterial colonization had increased levels of serum cE-selectin. Our results indicate that cCAMs may reflect an upregulation of CAMs on endothelial and epithelial airway cells in COPD.
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5.
  • Bjermer, Leif, et al. (författare)
  • Bronchoalveolar lavage fibronectin in patients with sarcoidosis: correlation to hyaluronan and disease activity
  • 1991
  • Ingår i: European Respiratory Journal. - 1399-3003. ; 4:8, s. 965-971
  • Tidskriftsartikel (refereegranskat)abstract
    • Bronchoalveolar lavage was performed in 51 patients with sarcoidosis and in 21 healthy nonsmokers. The concentration of fibronectin was significantly higher (p less than 0.001) in lavage fluid from sarcoid patients (median 267 micrograms.l-1) than in that of controls (46 micrograms.l-1). Furthermore, a significantly higher concentration of fibronectin was found in patients with active disease than in those in whom the disease was inactive (p less than 0.001). In a six month follow-up perspective, patients with a progressive disease course had significantly higher levels of fibronectin than those who had a stable or regressive disorder (p less than 0.01). Correspondingly, lavage hyaluronan was higher (p less than 0.001) in sarcoid patients (55 micrograms.l-1) than in controls (9 micrograms.l-1) and higher (p less than 0.01) in those with active than in those with inactive disease. Patients with progressive disease had higher (p less than 0.01) concentrations of hyaluronan than those in whom the disease was stable. A significant correlation was found between lavage fibronectin levels and hyaluronan (r = 0.81, p less than 0.001). The percentage of mast cells was also higher in patients with active than in those with inactive disease (p less than 0.01) and higher in progressive than in stable sarcoidosis (p less than 0.001). Ten out of 10 patients with progressive disease had mast cells greater than or equal to 0.5%, hyaluronan greater than or equal to 50 micrograms.l-1 and fibronectin greater than or equal to 350 micrograms.l-1 compared to eight out of 41 patients with stable or regressive disease.
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6.
  • Bjermer, Leif, et al. (författare)
  • Radiation-induced increase in hyaluronan and fibronectin in bronchoalveolar lavage fluid from breast cancer patients is suppressed by smoking
  • 1992
  • Ingår i: European Respiratory Journal. - 1399-3003. ; 5:7, s. 785-790
  • Tidskriftsartikel (refereegranskat)abstract
    • Bronchoalveolar lavage (BAL) fluid was analysed from 21 patients with breast cancer, stage T1N0M0, who had undergone tumour resection and post-operative local irradiation (accumulated dose 56 Gy). The lavage was performed two months after radiotherapy, in the anterior part of the lingula (left side) or of the right middle lobe (right side), depending on which side had been exposed to radiation. The patients had significantly increased concentrations of fibronectin (FN) (p less than 0.001), hyaluronan (HA) (p less than 0.01) and albumin (p less than 0.05) in BAL fluid compared with the healthy controls (n = 19). However, when the patients were separated, according to smoking history, it was obvious that the inflammatory reaction occurred entirely in the nonsmoking patient group (n = 10), whilst no difference could be found between the smoking patients (n = 11) and the controls. In the nonsmoking patient group, there was a sevenfold increase in BAL concentrations of FN and a threefold increase in HA. Moreover, four patients had detectable levels of procollagen III peptide in BAL, all were nonsmokers. The smoking habits of the controls had no influence on the BAL measurements. These findings indicate that smoking interferes with the radiation-induced early inflammatory connective tissue reaction of the lung. Finally, the results justify further investigation of interaction of smoking with cancer treatment, both from the view of therapy effectiveness and reduction of adverse effects.
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7.
  • Bjermer, Leif, et al. (författare)
  • Tobacco smoke exposure suppresses radiation-induced inflammation in the lung: a study of bronchoalveolar lavage and ultrastructural morphology in the rat
  • 1993
  • Ingår i: European Respiratory Journal. - 1399-3003. ; 6:8, s. 1173-1180
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous studies on patients with breast cancer, who received postsurgical irradiation, displayed a markedly suppressed inflammatory response in the lung of smoking patients compared to nonsmokers. The aim of the present study was to investigate further the effect of exposure to tobacco smoke on the development of irradiation-induced pneumonitis in the rat. Four groups of animals were used: controls (C); those exposed to tobacco smoke (S); those irradiated but not exposed to smoke (RNS); and those irradiated and exposed to tobacco smoke (RS). The rats were exposed to a diluted main stream of cigarette smoke, at a concentration of about 0.4 mg.l-1, in a nose-only exposure system for 1 h.day-1, 5 days.week-1 for 10 weeks. Exposure to tobacco smoke started 3 weeks before irradiation. The basal one third of both lungs was exposed to a single radiation dose of 28 Gy (6 MeV photons). All animals were killed 7 weeks after irradiation. We compared findings in bronchoalveolar lavage (BAL) and tissue morphology. The alveolar tissue showed less inflammation in the RS-group than in the RNS-group. Most strikingly, mast cells were increased one hundredfold in the lung interstitium and thirty fold in the peribronchial area in the RNS-group, whereas no increase was found in the RS-group or in the controls. The alveolar septa of the RNS-group were thickened, with occurrence of inflammatory cells and mast cells, whereas the RS-group displayed no difference as compared to the non-irradiated, nonsmoking group (C).
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8.
  • Hernnas, J, et al. (författare)
  • Alveolar accumulation of fibronectin and hyaluronan precedes bleomycin-induced pulmonary fibrosis in the rat
  • 1992
  • Ingår i: European Respiratory Journal. - 1399-3003. ; 5:4, s. 404-410
  • Tidskriftsartikel (refereegranskat)abstract
    • The development of bleomycin-induced pulmonary fibrosis in rats was studied over a period of 30 days after an intratracheal instillation of bleomycin. Fibronectin was visualized in histological sections and quantified in bronchoalveolar lavage fluid (BALF) and related to simultaneous measurements of hyaluronan, collagen and albumin in BALF and/or lung tissue extracts. An increase in BALF fibronectin levels was noted after 3 days and the peak value a sixty fold increase was noted at day 7. Thereafter, the fibronectin levels declined and reached control values on day 21. A pronounced, patchily distributed staining for fibronectin appeared in the injured alveolar tissue parallel to the increased lavage fluid fibronectin levels on days 3-7. A fainter, streakily distributed fibronectin staining remained within the alveolar walls in areas with proliferating fibroblasts on days 14-30. Albumin in BALF increased to a peak level, 20 times control values, after 3 days and then rapidly declined. Thus, the ratio of fibronectin to albumin increased to a peak value of 43 times control values on day 7, indicating that plasma leakage cannot be the only source of the observed increase in lavage fibronectin. Lung tissue hydroxyproline increased between days 7 and 30, whereas extractable hyaluronan in lung tissue and bronchoalveolar lavage fluid peaked on days 3-7 and then gradually declined towards normal values on days 21-30. These data demonstrate that fibronectin accumulates in the alveolar tissue during the early inflammatory phase of the bleomycin-induced lung injury, parallelling hyaluronan accumulation and preceding the development of pulmonary fibrosis.
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