ReviewClinical reviews in allergy1985
Late asthmatic responses: inquiry into mechanisms and significance.
Review in Clinical reviews in allergy, 1985. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- TNF-induced IL-8 and MCP-1 production in the eosinophilic cell line, EOL-1.Mediators of inflammation · 1996Article
- Therapeutic approaches to asthma based on VLA-4 integrin and its counter receptors.Springer seminars in immunopathology · 1995Review
- Airway epithelial cell expression of interleukin-6 in transgenic mice. Uncoupling of airway inflammation and bronchial hyperreactivity.The Journal of clinical investigation · 1994Article
- Modification of allergen-induced airway obstruction and bronchial hyperresponsiveness in the allergic rabbit by theophylline aerosol.Agents and actions · 1992Article
- UCHL1+ (CD45RO+) 'memory' T cells predominate in the CD4+ cellular infiltrate associated with allergen-induced late-phase skin reactions in atopic subjects.Clinical and experimental immunology · 1991Article
- The abnormal in vitro response to aspirin of platelets from aspirin-sensitive asthmatics is inhibited after inhalation of nedocromil sodium but not of sodium cromoglycate.British journal of clinical pharmacology · 1990Article
- Inhibition of neutrophil and eosinophil induced chemotaxis by nedocromil sodium and sodium cromoglycate.British journal of pharmacology · 1990Article
- Inhibition of platelet-activating factor- and zymosan-activated serum-induced chemotaxis of human neutrophils by nedocromil sodium, BN 52021 and sodium cromoglycate.British journal of pharmacology · 1989Article
- Nedocromil sodium inhibits the A23187- and opsonized zymosan-induced leukotriene formation by human eosinophils but not by human neutrophils.British journal of pharmacology · 1989Article
- Article
- Rhinovirus upper respiratory infection increases airway hyperreactivity and late asthmatic reactions.The Journal of clinical investigation · 1989Article
- Late-phase IgE-mediated reactions.Journal of clinical immunology · 1988Review
- The effect of platelet activating factor on pulmonary beta-adrenoceptors.British journal of pharmacology · 1987Article
- Standardization of fungal allergens.Clinical reviews in allergy · 1987Review
- Platelet-activating factor. A potent chemotactic and chemokinetic factor for human eosinophils.The Journal of clinical investigation · 1986Article
- Platelet activating factor and asthma.Agents and actions · 1986Review
- Review
- Treatment of asthma and food allergy with herbal interventions from traditional chinese medicine.The Mount Sinai journal of medicine, New YorkReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Late asthmatic responses are common, simulate a chronic phase of asthma, and are associated with an influx of inflammatory cells. The precise sequence of events leading to late inflammatory responses and increased hyperresponsiveness of the airways is uncertain, but likely begins with the triggering of mediator release from local (luminal or interstitial) mast cells or, conceivably, alveolar macrophages. Consequent influx and activation of granulocytes, including eosinophils and neutrophils, possibly T lymphocytes, basophils, and platelets, and subsequently later-arriving monocytes and macrophages, may be responsible for a continuing inflammatory reaction, airways hyperresponsiveness, and continuing active bronchial asthma. Identification of the relative importance of responsible cells and mediators will help clarify pathogenesis of bronchial asthma and should lead to a better understanding and design of therapeutic regimens and preventive measures in the management of this common and important disease.
Indexed as
Identifiers
3886116What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.