Asthma is a disease whose ability to cause episodic symptomatology has been appreciated since antiquity. Although the fine points of the definition can be debated, it is reasonable to think of asthma as a pulmonary disorder characterized by the generalized reversible obstruction of airflow and to define reversibility as a greater than 12% increase in the patient's forced expiratory volume in 1 second (FEV 1 ) that occurs either spontaneously or with therapy. Airway hyperresponsiveness, an exaggerated bronchospastic response to nonspecific agents such as methacholine and histamine or specific antigens, is the physiologic cornerstone of this disorder. A diagnosis of asthma is established based on a history of recurrent wheeze, cough, or shortness of breath, reversible airway obstruction demonstrated by pulmonary-function testing, and, in cases where questions exist, a methacholine challenge demonstrating airway hyperresponsiveness. It has long been assumed that patients with asthma experience intermittent attacks and have relatively normal lung function during intervening periods. More recent studies have demonstrated that asthma can cause progressive lung impairment and, in some patients, eventuate in partially reversible or irreversible airway obstruction.Any discussion of asthma must take into account the recent increase in its prevalence. Since approximately 1980, the frequency of this disorder has almost doubled. As a result of this "epidemic," asthma now affects approximately 8-10% of the population in the US, is the leading cause of hospitalization among children less than 15 years of age, and costs society billions of dollars annually. This increase in prevalence is not simply due to diagnostic transference or increased diagnostic awareness, since asthma mortality rates have also increased during this interval.An aerosol antigen challenge of an appropriately sensitized asthmatic patient can induce two types of airway responses. The early response is an acute bronchospastic event that occurs 15-30 minutes after exposure and resolves over time. The late-phase response peaks 4-6 hours after exposure and can cause prolonged symptomatology. Over the years, a variety of concepts of pathogenesis have been put forth in an attempt to explain one or both of these responses (Table 1). Early investigators postulated that there was an intrinsic airway smooth muscle abnormality at the root of the asthmatic diathesis. However, many studies with airway myocytes in culture have not corroborated this contention. This was followed by the contention that asthma is an autonomic dysfunction syndrome characterized by excess cholinergic and/or tachykinin pathway activity. This was never proven or disproven. Instead, IgE-mediated mast cell and/or basophil degranulation with the release of leukotrienes, histamine, prostaglandins, tryptase, cytokines (such as IL-4 and IL-5), and other mediators was appreciated to be a key event in the acute response. The prominent eosinophil-, macrophage-, and lymphocyte-rich inflammatory response i...

This paper describes a self-learning ULR fuzzy controller using temporal back propagation. The ULR fuzzy controller is a multi-layer feed-forward network in which each node performs an unidirectional linear response (ULR) function (node function) on incoming weighted signals. In order to achieve a desired input-output mapping, the weight parameters are updated with a temporal back propagation such that the state variables can follow a given desired trajectory as closely as possible. The temporal back prop agation algorithm is used to train the ULR fuzzy controller to a variety of problems. We demonstrate the effectiveness of the self-learning ULR fuzzy controller by applying it to a benchmark problem in in telligent control-the inverted pendulum system. Experiments show a very good control performance and self-learning capability of the ULR fuzzy controllers.

IntroductionTissue remodeling responses are prominent features of inflammatory disorders of the airway and parenchyma of the lung. These responses are readily apparent in chronic obstructive pulmonary disease (COPD), asthma, and interstitial lung diseases: in which remodeling causes the alveolar septal destruction and changes in compliance that are characteristic of pulmonary emphysema (1), the subepithelial fibrosis, mucus metaplasia, and other structural alterations seen in asthmatic airway remodeling (2), and the pulmonary fibrosis that characterizes the interstitial disorders (3). Elevated levels of matrix metalloproteinases (MMPs) have been noted in patients with these disorders (4-12). In addition, studies from our laboratories and others demonstrated that MMP-12 plays an essential role in the pathogenesis of cigarette smoke-induced emphysema in mice (13) and that pretreatment with broad-spectrum MMP antagonists decreases the inflammation and airway hyperresponsiveness in murine models of asthma and the fibrosis in murine models of interstitial lung disorders (14,15). Surprisingly, little else is known about the roles that individual MMPs play in the pathogenesis of these important pulmonary disorders.IL-13 is a pleiotropic 12-kDa product of a gene on chromosome 5 at q31 that is produced in large quantities by Th2 cells and in lesser quantities by Th1 cells. IL-13 potently stimulates eosinophilic and lymphocytic inflammation and alveolar remodeling in the lung, effects that depend on the induction of various matrix metalloproteinases (MMPs).Here, we compared the remodeling and inflammatory effects of an IL-13 transgene in lungs of wild-type, MMP-9-deficient, or MMP-12-deficient mice. IL-13-induced alveolar enlargement, lung enlargement, compliance alterations, and respiratory failure and death were markedly decreased in the absence of MMP-9 or MMP-12. Moreover, IL-13 potently induced MMPs-2, -12, -13, and -14 in the absence of MMP-9, while induction of MMPs-2, -9, -13, and -14 by IL-13 was diminished in the absence of MMP-12. A deficiency in MMP-9 did not alter eosinophil, macrophage, or lymphocyte recovery, but increased the recovery of total leukocytes and neutrophils in bronchoalveolar lavage (BAL) fluids from IL-13 transgenic mice. In contrast, a deficiency in MMP-12 decreased the recovery of leukocytes, eosinophils, and macrophages, but not lymphocytes or neutrophils. These studies demonstrate that IL-13 acts via MMPs-9 and -12 to induce alveolar remodeling, respiratory failure, and death and that IL-13 induction of MMPs-2, -9, -13, and -14 is mediated at least partially by an MMP-12-dependent pathway. The also demonstrate that MMPs-9 and -12 play different roles in the generation of IL-13-induced inflammation, with MMP-9 inhibiting neutrophil accumulation and MMP-12 contributing to the accumulation of eosinophils and macrophages.

Guaranteed-cost consensus for high-order nonlinear multiagent networks with switching topologies is investigated. By constructing a time-varying nonsingular matrix with a specific structure, the whole dynamics of multiagent networks is decomposed into the consensus and disagreement parts with nonlinear terms, which is the key challenge to be dealt with. An explicit expression of the consensus dynamics, which contains the nonlinear term, is given and its initial state is determined. Furthermore, by the structure property of the time-varying nonsingular transformation matrix and the Lipschitz condition, the impacts of the nonlinear term on the disagreement dynamics are linearized, and the gain matrix of the consensus protocol is determined on the basis of the Riccati equation. Moreover, an approach to minimize the guaranteed cost is given in terms of linear matrix inequalities. Finally, the numerical simulation is shown to demonstrate the effectiveness of theoretical results. KEYWORDS guaranteed-cost consensus, Lipschitz nonlinearity, multiagent network, Riccati equation, switching topology INTRODUCTIONConsensus is a typical collection behavior of multiagent networks consisting of a number of autonomous dynamic agents and has been extensively investigated recently due to its wide applications in different fields such as formation and containment control for unmanned aerial vehicles, 1-4 synchronization control for sensor networks, 5,6 and reconfiguration for spacecraft clusters. 7,8 For leadless multiagent networks, the whole dynamics contains 2 parts: the consensus dynamics and the disagreement dynamics, which describe the macroscopical and microcosmic behaviors of multiagent networks, respectively. The consensus dynamics is often described by the consensus function, and the disagreement dynamics is used to determine the consensus and consensualization criteria.According to the dynamics of each agent, multiagent networks can be classified 3 types: first-order ones, second-order ones, and high-order ones. The dynamics of each agent in first-order and second-order multiagent networks is usually described as the first-order and second-order integrators, respectively, whose consensus analysis and design problems can be simplified by these structure features (see other works 9-14 and references therein). Each agent in high-order multiagent networks is often modeled by a general high-order linear system, whose consensus and consensualization criteria are more difficult to be determined since each agent does not have specific structure features compared with first-order Int J Robust Nonlinear Control. 2018;28:2841-2852.wileyonlinelibrary.com/journal/rnc

No abstract

The rate of reduction reactions of zero-valent metal nanoparticles is restricted by their agglomeration. Hydrodynamic cavitation was used to overcome the disadvantage in this study. Experiments for decolorization of methyl orange azo dye by zero-valent copper nanoparticles were carried out in aqueous solution with and without hydrodynamic cavitation. The results showed that hydrodynamic cavitation greatly accelerated the decolorization rate of methyl orange. The size of nanoparticles was decreased after hydrodynamic cavitation treatment. The effects of important operating parameters such as discharge pressure, initial solution pH, and copper nanoparticle concentration on the degradation rates were studied. It was observed that there was an optimum discharge pressure to get best decolorization performance. Lower solution pH were favorable for the decolorization. The pseudo-first-order kinetic constant for the degradation of methyl orange increased linearly with the copper dose. UV-vis spectroscopic and Fourier transform infrared (FT-IR) analyses confirmed that many degradation intermediates were formed. The results indicated hydroxyl radicals played a key role in the decolorization process. Therefore, the enhancement of decolorization by hydrodynamic cavitation could due to the deagglomeration of nanoparticles as well as the oxidation by the in situ generated hydroxyl radicals. These findings greatly increase the potential of the Cu(0)/hydrodynamic cavitation technique for use in the field of treatment of wastewater containing hazardous materials.

No abstract

No abstract