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Computer-Aided Diagnosis of Chronic Obstructive Pulmonary Disease Using Accurate Lung Air Volume Estimation in Computed Tomographic Imaging
Published in Ayman El-Baz, Jasjit S. Suri, Lung Imaging and CADx, 2019
Hadi Moghadas-Dastjerdi, Mohammad Reza Ahmadzadeh, Abbas Samani
According to World Health Organization reports, lung diseases are among the leading causes of death around the world. The death rate due to lung diseases is still on the rise, while other causes of death, such as cancer and stroke, are declining. Among all pulmonary disorders, chronic obstructive pulmonary disease (COPD) is one of the most prevalent and fatal diseases. About 7% of the global population is affected by this disease, leading to an economic burden estimated at $2.1 trillion in 2010 [1]. The main effect of COPD is the lung's air ventilation reduction, which may occur due to two different mechanisms. The first mechanism is the obstruction of small airways as a result of clogging by mucus or as a consequence of shape change. The second mechanism, emphysema, involves destruction of the alveoli's wall and a reduction of the elasticity of the alveoli sacs and consequently a reduction of the gas–blood exchange surface. In general, these two mechanisms lead to the limitation of airflow throughout respiration and immobility of old inhaled air in the lungs, referred to as air trapping. The trapped air has no beneficial function in the pulmonary system, as it includes a low amount of oxygen and a high amount of carbon dioxide.
Lung Mechanobiology
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Daniel J. Tschumperlin, Francis Boudreault, Fei Liu
The mechanical challenge in distributing gas and blood in suitable proportions is great: the lung's delicate structure must be compliant and elastic to allow lung inflation and deflation with minimal effort, yet stable to prevent collapse of the airway and alveoli. The stability of this arrangement depends crucially on pulmonary surfactant, a complex mixture of phospholipids and proteins synthesized by specialized cells within the epithelial lining of the alveoli.3 Pulmonary surfactant lowers surface tension in alveoli, and possesses the unique characteristic that it drives surface tension toward zero during dynamic film compression, helping to stabilize alveoli during lung deflation.4 Both acute and chronic derangements of the lung's delicate microstructure and surfactant system ultimately lead to inadequate gas exchange and, in extreme cases, to respiratory failure. Understanding the physical origin of lung mechanical function, and the mechanism of failure in various disease states, is central to the study of respiratory physiology and medicine. In this chapter, we focus on efforts to elucidate the cellular, molecular, and microstructural mechanisms underpinning mechanobiological function of the lung in health and disease.
Noninvasive Tests Involving the Input of Audible Sound Energy
Published in Robert B. Northrop, Non-Invasive Instrumentation and Measurement in Medical Diagnosis, 2017
It is well known that various anatomical and physical changes happen to the bronchioles and alveoli of the lungs in obstructive lung diseases (e.g., asthma, atelectasis, byssinosis, cystic fibrosis, emphysema, pneumonia, silicosis, asbestosis, tuberculosis, etc.). These changes alter the acoustic impedance of the lungs as measured orally through the tracheal airway. For example, in emphysema, the walls separating adjacent alveoli break down, producing larger alveolar spaces with walls having less elasticity. In cystic fibrosis, the alveoli and bronchioles become clogged with mucus, increasing airway resistance and reducing lung volume, etc. Different physical changes in lung tissues will lead to different ZA(jω) plots. Hereafter, we will refer to the ZA of the respiratory system “seen” through the pharynx and trachea as Zrs.
Microplastics and human health: Integrating pharmacokinetics
Published in Critical Reviews in Environmental Science and Technology, 2023
While sizes >5 µm may rarely reach the alveoli through air, larger microplastics may be found more frequently in lungs from the entrapment of circulating particles in the narrow pulmonary capillary network (Slack et al., 1981). Indeed, only microplastics <5.5 µm were found in human lung biopsies, while fibers presented sizes 8.1–16.8 µm (Amato-Lourenço et al., 2021). In dogs, PS >8 µm were not able to cross pulmonary capillaries and became entrapped (Ring et al., 1961). Internalization of particles in the alveoli could occur by: (i) vesicular migration in type I pneumocytes and capillary endothelium (transcytosis); (ii) crossing in intercellular spaces; (iii) phagocytosis by any of the alveolar cells, but most importantly by alveolar macrophages which remove particles to the ciliated airways; (iv) removal of fluid and/or particles from alveoli by anterior ciliary movement or lymphatic drainage (generally ≤10 µm) (Morrow, 1973). Indeed, 0.2 µm PS could be found incorporated in type I pneumocytes, type II pneumocytes, and alveolar macrophages after intratracheal instillation of rats, suggesting transcytosis (Kato et al., 2003). Similarly, alveolar macrophages are able to phagocytize microplastics (e.g. PS) in the lung, especially of 1 µm in size (Makino et al., 2003). Presence of microplastics in the lungs can also change microvascular permeability, modulating internalization (Hamoir et al., 2003). Internalization is also supported by the redistribution of inhaled 0.02, 0.1, and 1 µm PS to internal tissues (e.g. liver, spleen, gut, kidney, and uterus) in rats (Sarlo et al., 2009).
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A. Zeki, Christopher M. Royer, Urmila P. Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E. Pinkerton
Patients diagnosed with emphysema exhibit mucous cell hyperplasia, resembling manifestations of chronic bronchitis. These individuals exhibit destruction of lung parenchymal tissues and alveolar septal walls, which result in airspace enlargement. Destruction of alveolar walls includes loss of the alveolar capillary bed and alveolar surface area, which impairs gas exchange. One potential mechanism underlying alveolar loss involves proteases released by the sustained recruitment, retention, and activation of inflammatory cells, or by alveolar and bronchial epithelial cells following exposure to toxic irritants, allergens, or TS (Churg, Zhou, and Wright 2012; Fischer, Voynow, and Ghio 2015). Loss of alveolar septa reduces lung function, increases compliance (reduces elastance), and induces breathlessness and hyperventilation (Boutou et al. 2015; Suki et al. 2013). In smokers, the loss contributes to persistent airway inflammation (Barnes 2016b; Gamble et al. 2007) and airflow obstruction. Host genetic predisposition also induces COPD pathogenesis and symptoms (Alam et al. 2014; Silverman 2020; Sorroche et al. 2015).
Assessing the in vitro toxicity of airborne (nano)particles to the human respiratory system: from basic to advanced models
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Maria João Bessa, Fátima Brandão, Fernanda Rosário, Luciana Moreira, Ana Teresa Reis, Vanessa Valdiglesias, Blanca Laffon, Sónia Fraga, João Paulo Teixeira
Another important aspect to take into consideration is how physiological fluids might change the physicochemical properties and behavior of (nano)particles (Urban et al. 2016). Upon contact with the biological pulmonary milieu, (nano)particles may become surrounded by biomolecules such as albumin and proteins in the surfactant, which significantly contribute to the formation of a corona around them and change particle size and kinetics in the airways (Monopoli et al. 2012). In the alveolar region, (nano)particles interact with the lipids present in the surfactant film located at the air-liquid interface (ALI) in the epithelial lining fluid covering the internal surface of the lung (Raesch et al. 2015). The surfactant helps to stabilize the alveoli and promotes clearance of inhaled particles to maintain alveoli in a sterile- and inflammation-free environment (Kendall and Holgate 2012). Accordingly, characterization of nano-sized materials in relevant pulmonary biological fluids is of utmost importance (Wohlleben et al. 2016).