This article reviews some main results and progress in distributed multi-agent coordination, focusing on papers published in major control systems and robotics journals since 2006. Distributed coordination of multiple vehicles, including unmanned aerial vehicles, unmanned ground vehicles and unmanned underwater vehicles, has been a very active research subject studied extensively by the systems and control community. The recent results in this area are categorized into several directions, such as consensus, formation control, optimization, task assignment, and estimation. After the review, a short discussion section is included to summarize the existing research and to propose several promising research directions along with some open problems that are deemed important for further investigations.

An Overview of Recent Progress in the Study of Distributed Multi-agent Coordination

▪ Abstract When asthma is diagnosed, eosinophilic inflammation and airway remodeling are established in the bronchial airways and can no longer be separated as cause and effect because both processes contribute to persistence and progression of disease, despite anti-inflammatory therapy. Th2 cells are continually active in the airways, even when disease is quiescent. IL-13 is the key effector cytokine in asthma and stimulates airway fibrosis through the action of matrix metalloproteinases on TGF-β and promotes epithelial damage, mucus production, and eosinophilia. The production of IL-13 and other Th2 cytokines by non-T cells augments the inflammatory response. Inflammation is amplified by local responses of the epithelium, smooth muscle, and fibroblasts through the production of chemokines, cytokines, and proteases. Injured cells produce adenosine that enhances IL-13 production. We review human and animal data detailing the cellular and molecular interactions in established allergic asthma that promote p...

Asthma: Mechanisms of Disease Persistence and Progression

Allergic rhinitis (AR) is a high-prevalence disease in many developed countries, affecting about 10±20% of the general population (1±5). Several studies based on questionnaire and objective testing or medical examination indicate an increasing prevalence of AR in European countries over the last decades (6, 7). AR is characterized by nasal itching, sneezing, watery rhinorrhoea, and nasal obstruction. Additional symptoms such as headache, impaired smell, and conjunctival symptoms can be associated. According to the time of exposure, AR can be subdivided into perennial, seasonal, and occupational disease. Perennial AR (PAR) is most frequently caused by dust mites and animal dander. Seasonal AR (SAR) is related to a wide variety of pollen allergens including grasses, Parietaria, Ambrosia, Artemisia, birch, olive, hazelnut, and cypress. The morbidity of SAR obviously depends on the geographic region, the pollen season of the plants, and the local climate. Several other conditions can cause similar symptoms and are referred to as nonallergic (noninfectious) rhinitis: NARES (nonallergic rhinitis with eosinophilia syndrome); aspirin sensitivity; endocrine, occupational, postinfectious, and side-effects of systemic drugs; abuse of topical decongestants (rhinitis medicamentosa); and idiopathic rhinitis. Furthermore, diseases such as nasal polyposis, chronic sinusitis, cystic ®brosis, Wegener's disease, benign or malignant tumours, etc. have to be excluded carefully. Therefore, current guidelines (4) emphasize the importance of an accurate diagnosis of patients presenting with rhinitis symptoms. In fact, several causes may commonly coexist in the same *European Academy of Allergology and Clinical Immunology. Allergy 2000: 55: 116±134 Printed in UK. All rights reserved Copyright # Munksgaard 2000

Consensus statement * on the treatment of allergic rhinitis

Background Erosion and rupture of coronary atheromas are the events preceding the vast majority of acute coronary syndromes. The shoulder regions of atheromas, the sites at which erosion or rupture is most likely to occur, are the sites at which mast cells accumulate. These cells are filled with neutral proteases capable of triggering extracellular matrix degradation via activation of matrix metalloproteinases. To obtain more direct evidence for the participation of mast cells in the acute coronary syndromes, we quantified the numbers of mast cells at eroded or ruptured sites of coronary atheromas in patients who died of myocardial infarction. Methods and Results In specimens of coronary arteries from 20 patients who had died of acute myocardial infarction, the site of atheromatous erosion or rupture was identified. The specimens were stained with monoclonal antibodies against the two major proteases of mast cells, tryptase and chymase, and against macrophages, T lymphocytes, and smooth muscle cells. At t...

Infiltrates of Activated Mast Cells at the Site of Coronary Atheromatous Erosion or Rupture in Myocardial Infarction

That mast cells and allergic mechanisms play at least some role in bronchial asthma has been suggested for at least 75 years [92]. The incidence of these mechanisms in a cross section of all asthmatics [31, 77], and the importance of allergic mechanisms as compared with neural mechanisms is controversial, however, and has been discussed and debated for at least as long [16, 113].

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Mast cells and basophils.

Exposure of mice to aerosolized ovalbumin (OA) once weekly for 5 min, or once weekly to 10 microgram OA in PBS intranasally, elicited transient IgE responses which declined by the seventh week. When these animals were challenged intraperitoneally (i.p.) with soluble or alum-precipitated OA, their subsequent IgE responses were markedly suppressed relative to controls. In contrast, i.p. challenge provoked hemaagglutinating antibody (HA) responses to OA in the same animals which were considerably more vigorous than in controls. Adoptive transfer experiments employing splenocytes from mice repeatedly exposed to OA via the respiratory tract revealed the presence of suppressor cells active against OA-specific IgE but not HA responses. Radiotracer studies employing 125I-OA, administered intranasally and by aerosol, indicated that much of the antigen rapidly became associated with the gut.

Inhibition of specific IgE responses in mice by pre-exposure to inhaled antigen.

Ieee transactions on control systems technology

A lambda gt11 library made with cDNA from the house dust mite Dermatophagoides pteronyssinus was screened with human allergic serum by IgE plaque radioimmunoassay. This resulted in the isolation of clones coding for the major allergen Der p II. The cDNA coded for a 129-residue protein of 14,131 daltons with no N-glycosylation sites. No sequence homology with other proteins was evident. The Der p II expressed in Escherichia coli reacted with IgE in 14 of 17 sera from mite-allergic patients giving clonal evidence for its designation as a major allergen. This, along with previous work, has resulted in the cloning of the two major mite allergens.

Isolation of cDNA Coding for the Major Mite Allergen Der p II by IgE Plaque Immunoassay

A cDNA clone coding for the major house dust mite allergen Der p 1 was isolated from a lambda gt 11 library. Its sequence correlates with known amino acid sequences of Der p 1 and it produces a fusion protein which reacts with rabbit anti-Der p 1 antiserum.

Cloning and expression of DNA coding for the major house dust mite allergen Der p 1 in Escherichia coli.

Human peripheral blood leucocytes (PBL), cultured in the presence of mitogen or antigen, yielded supernatants which contained a factor with histamine-releasing activity (HRA) This factor, analogous to the putative lymphokine HRA described by Thueson et al (1979a), was shown to promote the rapid release of histamine from PBL preparations containing basophils HRA production by PBL in response to co-culture with the skin test antigens Candida and SK-SD was shown to reflect the in vivo immune status of the PBL donor Experiments with isolated cell populations from PBL implicated T cells as the prime source of HRA, production of the factor being macrophage-dependent HRA activity failed to synergize anti-IgE-mediated histamine release, and was not species-restricted

K.J. Turner

Papers

Inhibition of specific IgE responses in mice by pre-exposure to inhaled antigen.

Ieee transactions on control systems technology

Isolation of cDNA Coding for the Major Mite Allergen Der p II by IgE Plaque Immunoassay

Cloning and expression of DNA coding for the major house dust mite allergen Der p 1 in Escherichia coli.

Production of a histamine-releasing lymphokine by antigen- or mitogen-stimulated human peripheral T cells.