Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Mucociliary clearance has been measured over a 6 h period by using the radioaerosol technique in seven normal male subjects lying supine, both during the day when awake, and during the night when asleep. 2. The percentage of radioaerosol cleared during the night, when asleep, was significantly less than during the day when awake (P less than 0.02). 3. A comparison of radioaerosol clearance before and after the time of onset of sleep demonstrates that reduced clearance occurred during sleep, indicating that this is probably a sleep-related phenomenon and not merely a result of diurnal variation. 4. This finding has important implications for patients with chronic bronchitis or asthma, in whom early morning cough or wheeze may be a predominant feature.
Clin Sci Mol Med Suppl 1978 Dec
PMID:The retention of lung secretions during the night in normal subjects. 28 43

1. Lung volumes, airway resistance and flow/volume curves were measured in ten asthmatic subjects at times when tightness in the chest was just sensed (threshold symptom). 2. These measurements when the threshold symptom was induced by methacholine inhalation were compared with those when a similar symptom occurred spontaneously, in the same subjects. 3. Values during the methacholine-induced thresholds were very similar to those observed when threshold symptoms developed spontaneously. 4. Controlled bronchial provocation mimics spontaneous asthma sufficiently well to allow this technique to be used in the study of sensations associated with breathing. This has some advantages over the already established models utilizing external hindrances to breathing.
Clin Sci Mol Med 1977 Apr
PMID:Bronchial provocation in the study of sensations associated with disordered breathing. 86 37

1. Needle acupuncture was performed at three sites in twenty patients in a clinical attack of bronchial asthma. 2. In all patients the symptoms of bronchoconstriction improved during the attacks when the correct site was stimulated, and in five patients wheezing was abolished. 3. Stimulation at the correct site produced a significant increase in the mean FEV1-0 (58%) and FVC (29%) but not in maximal mid-expiratory flow rate (MMFR; 76%), when compared with the findings before acupuncture, along with a significant fall in the Pa,CO2 and an insignificant fall in Pa,O2. A mild tachycardia was also observed. 4. After acupuncture a greater improvement in FEV1-0, FVC and MMFR was produced by inhalation of isoprenaline. 5. No significant changes in FEV1-0, FVC, MMFR, pulse rate or arterial blood gas tensions occurred after acupuncture at control sites. 6. In four of the patients during clinical remission acupuncture was performed before and after histamine aerosol challenge, but there was no effect on either the severity or the duration of the histamine-induced bronchoconstriction. 7. It is concluded that acupunture probably reduced the reflex component of the bronchoconstriction, but failed to influence direct smooth muscle constriction caused by histamine.
Clin Sci Mol Med 1976 Nov
PMID:Effect of acupuncture on bronchial asthma. 99 48

1. Changes in specific airway conductance after the inhalation of aerosols of prostaglandins (PG) E1, E2, and F2alpha were investigated in healthy and asthmatic subjects. 2. Inhalation of 155 nmol (55 mug) of PGE1 or 156 nmol (55 mug) of PGF2 resulted in consistent minor bronchodilatation in healthy subjects, but in asthmatic patients airway conductance increased significantly, along with subjective improvement. Isoprenaline (988 nmol; 550 mug) inhalation resulted in a similar increase in conductance to that obtained after these two prostaglandins, whereas a control aerosol had no effect. In contrast to the isoprenaline aerosol, both PGE1 and PGF2 were highly irritant to inhale. It was concluded that this made them unsuitable for therapeutic use. 3. Prostaglandin F2alpha inhalation resulted in a dose-related bronchoconstriction in healthy and asthmatic subjects. Asthmatics were approximately 150 than were the healthy subjects but there was very wide and significant variantion in the sensitivity of the asthmatic subjects. In contrast the asthmatic subjects were only 8-5 times more sensitive to histamine than the healthy subjects with less variation in response of individual subjects. The reasons for the hyper-reactivity of asthmatic subjects to PGF2alpha is unknown and no correlation could be drawn between increased sensitivity and age, type of asthma, or treatment. 4. The effects of disodium cromoglycate, flufenamic acid, atropine methonitrate, PGF2 and isoprenaline on PGF2alpha-induced bronchoconstriction were investigated in healthy subjects. Prostaglandin E2 reversed PGF2alpha-induced bronchoconstriction, as did isoprenaline, but prior treatment with the other drugs had no effect in preventing bronchoconstriction.
Clin Sci Mol Med 1975 May
PMID:Effects of inhaled prostaglandins E1, E2, and F2alpha on the airway resistance of healthy and asthmatic man. 112 33

1. A technique has been developed for assessing CO2 responsiveness by measuring the maximum rate of isometric inspiratory pressure change at the mouth [(dP/dt)max.]. 2. By use of a rebreathing technique, the (dP/dt)max. response to CO2 was shown to correlate well the ventilatory response in thirty-two normal subjects. 3. The addition of an external flow resistance sufficient to reduce the ventilatory response by a mean of 33.4% produced no significant mean change in the (dP/dt)max. response in thirty subjects. 4. In six patients recovering from bronchial asthma, reduction of airways obstruction led to a mean increase in the ventilatory response of 109% without any significant mean change in the (dP/dt)max. response. 5. An increase in lung volume did not reduce the (dP/dt)max. response in five normal subjects. 6. At very high lung volumes, six normal subjects were able to develop a higher (dP/dt)max. during voluntary inspiratory efforts than has been recorded during spontaneous breathing response to CO2. 7. It is believed that (dP/dt)max. represents the initial rate of development of force by the inspiratory muscles before this can be modified by mechanical loading, proprioceptive feedback mechanisms or conscious response and can therefore be used to study changes in the motor output of the respiratory centre in response to ventilatory stimuli independently of pulmonary mechanics.
Clin Sci Mol Med 1975 Jul
PMID:The rate of isometric inspiratory pressure development as a measure of responsiveness to carbon dioxide in man. 114 95

In previous reports, we have documented decreased in vitro airway smooth muscle responses to isoproterenol (ISO) in fresh postmortem trachea and bronchus from subjects with fatal asthma. One hypothesis to explain this finding is a decrease in beta-adrenergic receptor (beta AR) numbers on airway smooth muscle. We have now examined the autoradiographic distribution and density of beta AR using [125I]iodocyanopindolol on sections of airway smooth muscle adjacent to those studied functionally. The results have been compared with "normal" trachea and bronchi obtained from persons dying suddenly of nonpulmonary causes. In both trachea and bronchi, there was a 2.8-fold and 2.5-fold increase in specific grain counts, respectively, over smooth muscle from asthmatic airways (n = 6) compared with that determined in normal airways (n = 4, P less than 0.01, unpaired t test). The affinity of the beta AR for the agonist ISO, as determined by competitive binding experiments with increasing concentrations of (-)-ISO on tissue sections, was increased in asthmatic bronchi (IC50 = 80 +/- 13 nM; n = 3) compared with normal bronchi (IC50 = 562 +/- 144 nM; n = 4, P less than 0.05). We conclude that beta AR-mediated relaxant abnormalities in airway smooth muscle in fatal asthma cannot be explained by a decrease in receptor number and, surprisingly, beta AR expression is increased.
Am J Respir Cell Mol Biol 1992 Jun
PMID:A comparison of beta-adrenergic receptors and in vitro relaxant responses to isoproterenol in asthmatic airway smooth muscle. 131 93

c-fos, a proto-oncogene regulating the transcription of many genes, plays a critical role in the cell cycle and differentiation and may be involved in the regulation of inflammation in asthma. Very low levels of c-fos are detectable in most human cells, and its expression is rapidly and transiently increased by multiple factors, some of which are involved in the airways inflammation of asthma (histamine, eicosanoids, and cytokines). The presence of c-fos protein, as detected by immunofluorescence, and the immunoreactivity of PCNA, a cell proliferation marker, were examined in bronchial biopsies obtained from 12 asthmatics and 10 normal subjects. Biopsies of eight of 12 asthmatics expressed c-fos versus none of 10 normal subjects. The expression was heterogeneous and localized to cells positive for anti-cytokeratin monoclonal antibody, indicating their epithelial origin. On the other hand, PCNA immunoreactivity was only observed in one asthmatic and one control subject but it was not related with c-fos expression. This study demonstrates the induction of c-fos in epithelial cells of asthmatics, suggesting a role for this proto-oncogene in activation rather than in proliferation.
Am J Respir Cell Mol Biol 1992 Aug
PMID:c-fos proto-oncogene expression in bronchial biopsies of asthmatics. 135 73

Inflammation of the human airways in diseases such as chronic bronchitis, cystic fibrosis with Pseudomonas endobronchial infection, and possibly asthma during late-phase reactions involves a local influx of neutrophils (PMN) that may participate in airway epithelial injury. PMN-mediated cellular injury is most efficient under conditions of PMN-target cell adhesion. PMN express adhesive glycoproteins of the CD11/CD18 family that are counter-receptors for intercellular adhesion molecule-1 (ICAM-1), found on various cell types. We proposed that adherence by PMN to human airway epithelial cells via ICAM-1 might be an important mechanism in inflammatory airway diseases. We found that although PMN adhere poorly (less than 5%) to monolayers of human tracheal epithelial cells (TEC) in primary culture, they adhere readily (45 to 50%) to an SV40-immortalized line of human TEC, designated 9HTEo-. We also found 6-fold greater surface expression of ICAM-1 on 9HTEo- compared with primary TEC. Blocking surface ICAM-1 on 9HTEo- cells with specific monoclonal antibody inhibited PMN adherence by about 50%. Thus, ICAM-1 plays a major role in this adherence, although it is possible that other epithelial ligands contribute also. Antibodies to CD11a, CD11b, and CD18 on PMN also inhibited PMN-epithelial adherence. Treatment of primary TEC monolayers with the proinflammatory cytokines interleukin-1 (IL-1) or tumor necrosis factor-alpha (TNF-alpha) caused a 3- to 4-fold increase in both cell surface ICAM-1 expression and support of PMN adhesion.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Respir Cell Mol Biol 1992 Aug
PMID:Induction of ICAM-1 expression on human airway epithelial cells by inflammatory cytokines: effects on neutrophil-epithelial cell adhesion. 135 76

Dust mite allergens are considered as a major cause of allergic disease and as a risk factor for asthma. Der p I, a 222 amino-acid residue globular glycoprotein, is one of the major allergens from Dermatophagoides pteronyssinus (Dpt) mites. In this study, we have used predictive conventional algorithms (i.e. hydrophilicity, mobility, accessibility) and a three-dimensional model of Der p I derived from comparison to actinidin and papain to select continuous amino acid sequences as potential B cell epitopes. Four peptides, 52-71, 117-133, 176-187, 188-199 were synthesized. Their antigenic reactivity was investigated, mainly by measuring their capacity to induce in vitro histamine release. Results indicated that only Dpt-sensitive patients react specifically to Der p I-derived peptides and more frequently to 52-71 and 117-133. For each peptide, the intensity of response was dependent on the patient tested and on the peptide concn. The capacity of peptides to induce histamine release was demonstrated to be correlated with the serum level of anti-Der p I IgE (r = 0.86; p less than 10(-2)). Taken together these data emphasize, in Dpt-sensitive patients, the heterogeneity of the specific response to synthetic Der p I-derived peptides and underline the possible variety of epitopes belonging to the allergen Der p I.
Mol Immunol 1992 Jun
PMID:Specific histamine release capacity of peptides selected from the modelized Der p I protein, a major allergen of Dermatophagoides pteronyssinus. 137 13

Mounting evidence suggests that inflammatory cells recruited to the lung can contribute to the pathogenesis of asthma. The factors governing the activation and recruitment of circulating cells to the lung remain unknown, but an early step in this process is the interaction of adhesion molecules on circulating cells with those on endothelial cells. We used a segmental antigen challenge model followed 18 h later by bronchoalveolar lavage (BAL) to study granulocyte recruitment to the lung in 14 allergic subjects. Using immunofluorescence and flow cytometry, we determined the expression of the adhesion molecules CD11b, L-selectin (LECAM-1), and VLA-4 on BAL and peripheral blood granulocytes. Total cell count and percentages of recovered eosinophils and basophils were significantly increased in BAL fluids from antigen-challenged segments. Compared with their peripheral blood counterparts, CD11b expression was increased 2- to 3-fold on BAL eosinophils, basophils, and neutrophils (n = 9, P less than 0.05). In contrast, L-selectin expression was significantly decreased on BAL cells (n = 3 to 4, P less than 0.05). Similar phenotypic changes were observed on all three cell types, and on neutrophils recovered from saline-challenged control lung segments. In two subjects, VLA-4 alpha (CD49d) expression on BAL eosinophils was 78 +/- 5% of that seen on peripheral blood eosinophils. Because ELAM-1 (endothelial leukocyte adhesion molecule-1, E-selectin) expression occurs during allergic inflammation and is shed after endothelial activation, we used a sensitive enzyme-linked immunosorbent assay to analyze BAL supernatants for a soluble form of this molecule (sELAM-1).(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Respir Cell Mol Biol 1992 Sep
PMID:Altered adhesion molecule expression and endothelial cell activation accompany the recruitment of human granulocytes to the lung after segmental antigen challenge. 138 95


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