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Gastroesophageal reflux disease (GERD) is clearly explained as the unintentional passage of stomach contents through the esophagus that takes place many times during the day both in children and in adults. GERD leads to symptoms of heartburn and regurgitation, these defined esophageal symptoms are in dichotomy with extraesophageal symptoms of GERD. These extra-esophageal symptoms include several respiratory manifestations that include chronic cough, bronchoconstriction and inflammation of airway, main features of asthma. Asthma is a chronic disease defined by variable degree of airflow obstruction, bronchial hyper-responsiveness (AHR) and chronic airway inflammation. Recent papers demonstrated an association between GERD and asthma. There are a lot of mechanisms through GERD can alter the reactivity of airway and lead to bronchoconstriction. Two hypotheses are proposed to explain this effect and different mechanisms may be involved. However many authors suggest bidirectional effect between asthma and GERD. In fact, asthma can lead to onset of GERD through an increase of intrathoracic pressure during breathing and a reduction of lower esophageal sphincter (LES) pressure due to asthma therapy. The correlation between GERD and asthma is more complicated and has not yet been fully elucidated and understood, leaving this field of research open to further investigations.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pulmonary emphysema is a respiratory condition characterized by alveolar destruction that leads to airflow limitation and reduced lung function. Although with extensive research, the pathophysiology of emphysema is poorly understood and effective treatments are still missing. Evidence suggests that mesenchymal stem cells (MSCs) possess the ability to engraft the injured tissues and induce repair via a paracrine effect. Thus, the aim of this study was to test the effects of the intratracheal administration of lung-derived mouse MSCs in a model of elastase-induced emphysema. Pulmonary function (static lung compliance) showed an increased stiffness induced by elastase, while morphometric findings (mean linear intercept and tissue/alveolar area) confirmed the severity of alveolar disruption. Contrarily, MSC administration partially restored lung elasticity and alveolar architecture. In the absence of evidence that MSCs acquired epithelial phenotype, we detected an increased proliferative activity of aquaporin 5-and surfactant protein C-positive lung cells, suggesting MSC-driven paracrine mechanisms. The data indicate the mediation of hepatocyte growth factor in amplifying MSC-driven tissue response after injury. Our study shed light on supportive properties of lung-derived MSCs, although the full identification of mechanisms orchestrated by MSCs and responsible for epithelial repair after injury is a critical aspect yet to be achieved. Copyright © 2018 Donato Cappetta et al. Pulmonary emphysema is a respiratory condition characterized by alveolar destruction that leads to airflow limitation and reduced lung function. Although with extensive research, the pathophysiology of emphysema is poorly understood and effective treatments are still missing. Evidence suggests that mesenchymal stem cells (MSCs) possess the ability to engraft the injured tissues and induce repair via a paracrine effect. Thus, the aim of this study was to test the effects of the intratracheal administration of lung-derived mouse MSCs in a model of elastase-induced emphysema. Pulmonary function (static lung compliance) showed an increased stiffness induced by elastase, while morphometric findings (mean linear intercept and tissue/alveolar area) confirmed the severity of alveolar disruption. Contrarily, MSC administration partially restored lung elasticity and alveolar architecture. In the absence of evidence that MSCs acquired epithelial phenotype, we detected an increased proliferative activity of aquaporin 5- and surfactant protein C-positive lung cells, suggesting MSC-driven paracrine mechanisms. The data indicate the mediation of hepatocyte growth factor in amplifying MSC-driven tissue response after injury. Our study shed light on supportive properties of lung-derived MSCs, although the full identification of mechanisms orchestrated by MSCs and responsible for epithelial repair after injury is a critical aspect yet to be achieved.

A small scale tri-rotor test bed with tilting propellers has been built to test flight control laws in view of the construction of a larger tilt rotor UAV. As a first step to achieve autonomous flight capabilities, a nonlinear dynamic inversion based flight controller is developed. This controller is designed on the basis of a time-scale principle with two levels. A lower level, fast control action, designed to achieve attitude control and stability goals, is driven by a higher level trajectory tracking control law. To achieve robust stability and performance in the presence of parametric variations and modelling uncertainties, an adaptive flight control law correction based on neural networks is investigated. A RBF neural network is implemented to mitigate the effects of imprecise inverse dynamics. The overall proposed flight controller performance are tested via numerical simulations on the mathematical model of the small scale tri-rotor. Preliminary results on the full tilt rotor are also shown. © 2015, IFAC (International Federation of Automatic Control) Hosting by Elsevier Ltd. All rights reserved

Structural changes contribute to airway hyperresponsiveness and airflow obstruction in asthma. Emerging evidence points to the involvement of c-kit+ cells in lung homeostasis, although their potential role in asthma is unknown. Our aim was to isolate c-kit+ cells from normal mouse lungs and to test whether these cells can interfere with hallmarks of asthma in an animal model. Adult mouse GFP-tagged c-kit+ cells, intratracheally delivered in the ovalbumin-induced airway hyperresponsiveness, positively affected airway remodeling and improved airway function. In bronchoalveolar lavage fluid of cell-treated animals, a reduction in the number of inflammatory cells and in IL-4, IL-5, and IL-13 release, along with an increase of IL-10, was observed. In MSC-treated mice, the macrophage polarization to M2-like subset may explain, at least in part, the increment in the level of anti-inflammatory cytokine IL-10. After in vitro stimulation of c-kit+ cells with proinflammatory cytokines, the indoleamine 2,3-dioxygenase and TGFβ were upregulated. These data, together with the increased apoptosis of inflammatory cells in vivo, indicate that c-kit+ cells downregulate immune response in asthma by influencing local environment, possibly by cell-to-cell contact combined to paracrine action. In conclusion, intratracheally administered c-kit+ cells reduce inflammation, positively modulate airway remodeling, and improve function. These data document previously unrecognized properties of c-kit+ cells, able to impede pathophysiological features of experimental airway hyperresponsiveness.

Epidemiological data suggest that obesity represent an important risk factor for asthma, but the link between excess fat and airway hyperresponsiveness (AHR) and inflammation is not fully understood. Recently, a key role in physiopathologic conditions of lungs has been given to adiponectin (Acrp30). Acrp30 is one of the most expressed adipokines produced and secreted by adipose tissue, showing an intriguing relationship with metabolism of sphingolipids. Sphingosine-1-phosphate (S1P) has been proposed as an important inflammatory mediator implicated in the pathogenesis of airway inflammation and asthma. In the present study we analyze the effects of recombinant Acrp30 administration in an experimental model of S1P-induced AHR and inflammation. The results show that S1P is able to reduce endogenous Acrp30 serum levels and that recombinant Acrp30 treatment significantly reduce S1P-induced AHR and inflammation. Moreover, we observed a reduction of Adiponectin receptors (AdipoR1, AdipoR2 and T-cadherin) expression in S1P treated mice. Treatment with recombinant Acrp30 was able to restore Acrp30 serum levels and adiponectin receptors expression. These results could indicate the ability of S1P to modulate the Acrp30 action, by modulating not only the serum levels of the protein, but also its receptors. Taken together, these data suggest that adiponectin could represent a possible biomarker in obesity-associated asthma. Epidemiological data suggest that obesity represent an important risk factor for asthma, but the link between excess fat and airway hyperresponsiveness (AHR) and inflammation is not fully understood. Recently, a key role in physiopathologic conditions of lungs has been given to adiponectin (Acrp30). Acrp30 is one of the most expressed adipokines produced and secreted by adipose tissue, showing an intriguing relationship with metabolism of sphingolipids. Sphingosine-1-phosphate (SIP) has been proposed as an important inflammatory mediator implicated in the pathogenesis of airway inflammation and asthma. In the present study we analyze the effects of recombinant Acrp30 administration in an experimental model of S1P-induced AHR and inflammation. The results show that SIP is able to reduce endogenous Acrp30 serum levels and that recombinant Acrp30 treatment significantly reduce S1P-induced AHR and inflammation. Moreover, we observed a reduction of Adiponectin receptors (AdipoR1, AdipoR2 and T-cadherin) expression in S1P treated mice. Treatment with recombinant Acrp30 was able to restore Acrp30 serum levels and adiponectin receptors expression. These results could indicate the ability of SIP to modulate the Acrp30 action, by modulating not only the serum levels of the protein, but also its receptors. Taken together, these data suggest that adiponectin could represent a possible biomarker in obesity-associated asthma. (C) 2015 Elsevier Ltd. All rights reserved.

This paper presents the application of a distributed attitude and position estimation algorithm to a swarm of cooperating UAVs with heterogeneous sensors on board. The algorithm, based on a Consensus Extended Kalman Filtering (CEKF) to account for nonlinearities, is implemented assuming kinematic relationships. Numerical simulations are presented on different flight scenarios to evaluate the benefits of dealing with prior and novel information in a separate way on the basis of recent theoretical results on CEKF. Inertial and vision sensors are supposed to be mounted on board of the aircraft. Realistic flight scenarios are analyzed in the light of possible time communication delays among the agents. © 2015 IEEE.