Relevant bibliographies by topics / Pulmonary alveoli Bronchioles

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Academic literature on the topic 'Pulmonary alveoli Bronchioles'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Pulmonary alveoli Bronchioles"

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Kitaoka, Hiroko, Shinichi Tamura, and Ryuji Takaki. "A three-dimensional model of the human pulmonary acinus." Journal of Applied Physiology 88, no. 6 (June 1, 2000): 2260–68. http://dx.doi.org/10.1152/jappl.2000.88.6.2260.

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A three-dimensional (3-D) model of the human pulmonary acinus, a gas exchange unit, is constructed with a labyrinthine algorithm generating branching ducts that fill a given space completely. Branching down to the third respiratory bronchioles is generated with the proposed algorithm. A subacinus, a region supplied by the last respiratory bronchiole, is approximated to be a set of cubic cells with a side dimension of 0.5 mm. The labyrinthine algorithm is used to determine a pathway through all cells only once, except at branching points with the smallest path lengths. In choosing each step of a pathway, random variables are used. Resulting labyrinths have equal mean path lengths and equal surface areas of inner walls. An alveolus can be generated by attaching alveolar septa, 0.25 mm long and 0.1 mm wide, to the inner walls. Total alveolar surface area and numbers of alveolar ducts, alveolar sacs, and alveoli in our 3-D acinar model are in good accordance with those reported in the literature.
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Ravaglia, Claudia, and Venerino Poletti. "Bronchiolitis and Bronchiolar Disorders." Seminars in Respiratory and Critical Care Medicine 41, no. 02 (April 2020): 311–32. http://dx.doi.org/10.1055/s-0039-3402728.

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AbstractBronchioles are noncartilaginous small airways with internal diameter of 2 mm or less, located from approximately the eighth generation of purely air conducting airways (membranous bronchioles) down to the terminal bronchioles (the smallest airways without alveoli) and respiratory bronchioles (which communicate directly with alveolar ducts and are in the range of 0.5 mm or less in diameter). Bronchiolar injury, inflammation, and fibrosis may occur in myriad disorders including connective tissue diseases, inflammatory bowel diseases, lung transplant allograft rejection, graft versus host disease in allogeneic stem cell recipients, neuroendocrine cell hyperplasia, infections, drug toxicity (e.g., penicillamine, busulfan), inhalation injury (e.g., cigarette smoke, nylon flock, mineral dusts, hard metals, Sauropus androgynous); idiopathic, common variable immunodeficiency disorder, and a host of other disorders or insults. The spectrum of bronchiolar disorders is wide, ranging from asymptomatic to fatal obliterative bronchiolitis. In this review, we discuss the salient clinical, radiographic, and histological features of these diverse bronchiolar disorders, and discuss a management approach.
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Conhaim, R. L. "Airway level at which edema liquid enters the air space of isolated dog lungs." Journal of Applied Physiology 67, no. 6 (December 1, 1989): 2234–42. http://dx.doi.org/10.1152/jappl.1989.67.6.2234.

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To identify lung units associated with liquid leakage into the air space in high-pressure pulmonary edema, we perfused air-inflated dog lung lobes with albumin solution to fill the loose peribronchovascular interstitium. Next, we perfused the lobes for 90 s with fluorescent albumin solution then froze the lobes in liquid nitrogen. This procedure confined the fluorescent perfusate to the liquid flux pathway between the circulation and the air space and eliminated the previously filled peribronchovascular cuffs as a source of the fluorescence that entered the air space. We divided each frozen lobe into three horizontal layers and prepared fluorescence-microscopic sections of each layer. In the most apical layers where alveolar flooding was minimal, 10.6 +/- 21.0% (SD) of alveolar ducts were either fluorescence filled or air filled and continuous with fluorescence-filled alveoli. In the same layers, 11.0 +/- 19.0% of respiratory bronchioles were similarly labeled. No terminal bronchioles in these layers were fluorescence labeled. This suggested that the fluorescent albumin entered the air space across the epithelium of respiratory bronchioles, alveolar ducts, or their associated alveoli. To simulate an alternative explanation, i.e., that fluorescence first entered central airways then flowed into peripheral air spaces, we prepared two additional lobes that we first partially inflated with fluorescent albumin then filled to capacity with air. This pushed the fluorescent solution along the airways into the lung periphery. In these lobes the ciliary lining of bronchi and terminal bronchioles was fluorescence coated. By comparison, cilia in fluorescence-perfused lobes were not coated. We conclude that alveolar flooding in hydrostatic pulmonary edema occurs across the epithelium of alveolar ducts, respiratory bronchioles, or their associated alveoli.(ABSTRACT TRUNCATED AT 250 WORDS)
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Tokman, Sofya, M. Frances Hahn, Hesham Abdelrazek, Tanmay S. Panchabhai, Vipul J. Patel, Rajat Walia, and Ashraf Omar. "Lung Transplant Recipient with Pulmonary Alveolar Proteinosis." Case Reports in Transplantation 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/4628354.

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Pulmonary alveolar proteinosis (PAP) is a progressive lung disease characterized by accumulated surfactant-like lipoproteinaceous material in the alveoli and distal bronchioles. This accumulation is the result of impaired clearance by alveolar macrophages. PAP has been described in 11 solid organ transplant recipients, 9 of whom were treated with mammalian target of rapamycin inhibitors. We report a case of a lung transplant recipient treated with prednisone, mycophenolate mofetil (MMF), and tacrolimus who ultimately developed PAP, which worsened when MMF was replaced with everolimus.
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Mokhtar, Doaa M., Manal T. Hussein, Marwa M. Hussein, Enas A. Abd-Elhafez, and Gamal Kamel. "New Insight into the Development of the Respiratory Acini in Rabbits: Morphological, Electron Microscopic Studies, and TUNEL Assay." Microscopy and Microanalysis 25, no. 3 (February 14, 2019): 769–85. http://dx.doi.org/10.1017/s1431927619000059.

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AbstractThis study investigated the histomorphological features of developing rabbit respiratory acini during the postnatal period. On the 1st day of postnatal life, the epithelium of terminal bronchiole consisted of clear cells which intercalated between few ciliated and abundant non-ciliated (Clara) cells. At this age, the rabbit lung was in the alveolar stage. The terminal bronchioles branched into several alveolar ducts, which opened into atria that communicated to alveolar sacs. All primary and secondary inter-alveolar septa were thick and showed a double-capillary network (immature septa). The primitive alveoli were lined largely by type-I pneumocytes and mature type-II pneumocytes. The type-I pneumocytes displayed an intimate contact with the endothelial cells of the blood capillaries forming the blood–air barrier (0.90 ± 0.03 µm in thickness). On the 3rd day, we observed intense septation and massive formation of new secondary septa giving the alveolar sac a crenate appearance. The mean thickness of the air–blood barrier decreased to reach 0.78 ± 0.14 µm. On the 7th day, the terminal bronchiole epithelium consisted of ciliated and non-ciliated cells. The non-ciliated cells could be identified as Clara cells and serous cells. New secondary septa were formed, meanwhile the inter-alveolar septa become much thinner and the air–blood barrier thickness was 0.66 ± 0.03 µm. On the 14th day, the terminal bronchiole expanded markedly and the pulmonary alveoli were thin-walled. Inter-alveolar septa become much thinner and single capillary layers were observed. In the 1st month, the secondary septa increased in length forming mature cup-shaped alveoli. In the 2nd month, the lung tissue grew massively to involve the terminal respiratory unit. In the 3rd month, the pulmonary parenchyma appeared morphologically mature. All inter-alveolar septa showed a single-capillary layer, and primordia of new septa were also observed. The thickness of the air–blood barrier was much thinner; 0.56 ± 0.16 µm. TUNEL assay after birth revealed that the apoptotic cells were abundant and distributed in the epithelium lining of the pulmonary alveoli and the interstitium of the thick interalveolar septa. On the 7th day, and onward, the incidence of apoptotic cells decreased markedly. This study concluded that the lung development included two phases: the first phase (from birth to the 14th days) corresponds to the period of bulk alveolarization and microvascular maturation. The second phase (from the 14th days to the full maturity) corresponds to the lung growth and late alveolarization.
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Crestani, Bruno. "Are Bronchioles Fueling Burning Alveoli in Lung Fibrosis?" Respiration 79, no. 4 (2010): 277–78. http://dx.doi.org/10.1159/000268621.

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7

Federspiel, W. J., and J. J. Fredberg. "Axial dispersion in respiratory bronchioles and alveolar ducts." Journal of Applied Physiology 64, no. 6 (June 1, 1988): 2614–21. http://dx.doi.org/10.1152/jappl.1988.64.6.2614.

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The mixing of gases in the pulmonary acinus was characterized by analyzing axial gas dispersion during steady flow in models of respiratory bronchioles and alveolar ducts. An analysis (method of moments) developed for addressing dispersion in porous media was used to derive an integral expression for the axial dispersion coefficient (D*). Evaluation of D* required solving the Navier-Stokes equations for the flow field and a convection-diffusion type equation arising from the analysis. D* was strongly dependent on alveolar volume per central duct volume, the aperture size through which the alveoli communicate with the central duct, and the Peclet number (Pe). At smaller Pe (flow rate) D* was substantially smaller than the molecular diffusion coefficient, whereas at larger Pe (flow rate) D* was much greater than the Taylor-Aris result for flow-enhanced dispersion in straight tubes. Also, flow-enhanced dispersion became appreciable at smaller Pe than indicated by the Taylor-Aris result. These behaviors transcend both the lower and upper limits established previously for gas mixing in the pulmonary acinus.
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Sojka, Peter A., Christina L. Ploog, Michael M. Garner, Matti Kiupel, Jane Kuypers, and Thanhthao Huynh. "Acute human orthopneumovirus infection in a captive white-handed gibbon." Journal of Veterinary Diagnostic Investigation 32, no. 3 (March 13, 2020): 450–53. http://dx.doi.org/10.1177/1040638720910521.

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We report herein a fatal case of acute human orthopneumovirus (formerly respiratory syncytial virus) infection in a captive white-handed gibbon ( Hylobates lar). Other members of the housing group had mild respiratory signs. Gross examination revealed bilateral pulmonary congestion and froth in the bronchi. Microscopically, the lungs had lymphocytic, neutrophilic infiltration of the interstitium and alveolar walls. There was necrosis of terminal bronchiolar epithelium and terminal bronchioles, and surrounding alveoli contained necrotic and exfoliated epithelial cells admixed with histiocytes and syncytial cells. Additional lesions included nonsuppurative meningoencephalitis, and epidermal hyperkeratosis and hyperplasia with syncytial cell formation. PCR screening for 12 human respiratory viruses was positive for orthopneumovirus in multiple tissues, including lung, and immunohistochemical staining for human orthopneumovirus detected viral antigen within bronchial epithelial cells. IHC and PCR for measles virus on preserved sections were negative. White-handed gibbons have not been previously reported as hosts for human orthopneumovirus, an important respiratory pathogen of both primates and humans.
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Oliveira, Diego Medeiros de, João Marcos Araújo Medeiros, Ana Lucélia de Araújo, Luciano da Anunciação Pimentel, Felipe Pierezan, Eldinê Gomes Miranda Neto, Antônio Flávio Medeiros Dantas, and Franklin Riet-Correa. "Pulmonary choristoma associated with calf meningocele." Ciência Rural 39, no. 9 (December 2009): 2652–54. http://dx.doi.org/10.1590/s0103-84782009000900045.

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Pulmonary choristoma is a rare malformation reported in different animal species defined as a mass of normal histological pulmonary tissue in an abnormal location. A case of pulmonary choristoma and meningocele is reported in a calf that presented a fluctuating subcutaneous fluid containing mass, measuring 15 x 15 x 20cm in the skull frontal region. The skin covering the sac was surgically removed. Macroscopically, subcutaneous nodules up to 2cm in diameter with irregular whitish areas mixed with red areas were observed. In the histological examination, pulmonary lobules tissue composed by alveoli, bronchi, bronchioles and cartilage were observed. Dilated blood vessels and hemorrhages were present between the lobules. In this case the pulmonary choristoma was associated with meningocele, and probably was the mechanical cause for the failure of the skull closure.
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Khaleel, Hadeel Kamil. "Investigating the Histological Changes in Heart, Lung, Liver and Kidney of Male Albino Mice Treated with Ivabradine." Baghdad Science Journal 16, no. 3(Suppl.) (September 22, 2019): 0719. http://dx.doi.org/10.21123/bsj.2019.16.3(suppl.).0719.

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The present study aimed to investigate the histological changes of heart, lung, liver and kidney which caused by different concentrations (10, 20 and 40 mg/kg) of Ivabradine. Results of the study revealed some histological changes represented by aggregation of the lymphocytes around respiratory bronchioles of the lung. In the liver, the drug caused hepatocyte necrosis and infiltration of the lymphocytes. In Kidney, there are no histopathological modifications in the tissue after the animals treated with 10 mg\kg of Ivabradine. When the animals treated with Ivabradine drug at 20mg/kg of bw, dose showed vascular congestion between myocardial fibers of heart. Emphysematous changes of the alveoli and infiltration of lymphocytes around respiratory bronchioles of lung. In the liver there were dilated blood sinusoids. Also, there are vascular congestion and congestion of capillaries in the glomerular of kidney. Male mice treated with Ivabradine drug at 40 mg/kg of bw cause increase spaces between myocardial fibers, cardiac atrophy and myocardial degeneration in the heart. In addition, there are infiltration of lymphocytes around respiratory bronchioles, pulmonary congestion and emphysematous changes of the alveoli in lung. In the liver, the drug cause amyloid deposition and degeneration of hepatocytes. Furthermore, the drug caused vascular congestion in the kidney. Conclusion: From the current study, we conclude that the different concentrations of Ivabradine caused tissue changes in the heart, lung, liver and kidneys. The study should continue using different drugs and concentrations.
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Dissertations / Theses on the topic "Pulmonary alveoli Bronchioles"

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Chhabra, Sudhaker. "Fluid flow and particle dispersion in lung acini." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 195 p, 2009. http://proquest.umi.com/pqdweb?did=1691646821&sid=8&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Book chapters on the topic "Pulmonary alveoli Bronchioles"

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M. Jelic, Tomislav. "Emphysema." In Update in Respiratory Diseases. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.83273.

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Emphysema (Greek word meaning to inflate/to blow) is an increase in the size of airspace distal to the terminal bronchiolus, that is, hyperinflation of the alveoli due to the destruction of the gas-exchanging structures: alveolar walls, alveolar ducts, and respiratory bronchioles with coalescence of airspaces into the abnormal, much larger airspaces. The main consequences are the reduction of alveolar surface for gas exchange and the chronic obstructive pulmonary disease due to the destruction and disappearance of respiratory bronchioles with decreased total small airway diameter sum. Both decreased alveolar surface for gas exchange and chronic obstructive pulmonary disease lead to difficulty in breathing with dyspnea varying from mild to very severe. Two main pathohistologic types of emphysema are centriacinar and panacinar. Centriacinar emphysema involves the central portion of the acinus, and inflation mainly involves respiratory bronchioles and adjacent alveoli, and not all alveoli inside the acinus are involved. Panacinar (panlobular) emphysema is characterized by uniform enlargement and destruction of alveoli throughout the entire acinus. The panacinar emphysema is rare and its most common cause is hereditary alpha-1 antitrypsin deficiency. The centriacinar emphysema is the most frequent emphysema. It is mainly caused by smoking but also by coal dust exposure and advanced age.
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Bourke, S. J., and G. P. Spickett. "Hypersensitivity pneumonitis." In Oxford Textbook of Medicine, edited by Pallav L. Shah, 4244–56. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0424.

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Hypersensitivity pneumonitis is an immune-mediated lung disease in which the repeated inhalation of certain antigens provokes a hypersensitivity response, with granulomatous inflammation in the distal bronchioles and alveoli of susceptible people. A diverse range of antigens including bacteria (Thermophilic actinomycetes), fungi (Trichosporon cutaneum), animal proteins (bird antigens), mycobacteria, and chemicals may cause the disease. The commonest forms are bird fancier’s lung, farmer’s lung, humidifier lung, and metal-working fluid pneumonitis. In some cases no antigen is identified. Acute disease is characterized by recurrent episodes of breathlessness, cough, fevers, malaise, and flu-like symptoms occurring 4–8 hours after antigen exposure. Fever and basal crackles are the main physical signs. Chronic disease is characterized by the insidious development of dyspnoea and persistent pneumonitis, sometimes progressing to lung fibrosis. Clinical features are similar to those of other varieties of pulmonary fibrosis, but clubbing is uncommon.
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Henry, Travis S., and Brent P. Little. "Emphysema." In Chest Imaging, 325–29. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199858064.003.0056.

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Emphysema is the abnormal, permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by destruction of alveolar walls, but without obvious fibrosis. Chronic obstructive pulmonary disease (COPD) is a spectrum of obstructive lung diseases that includes emphysema and chronic bronchitis – diseases that frequently coexist, especially in smokers. Emphysema is an extremely common disease and in most cases the diagnosis is established with clinical data including pulmonary function tests (PFTs). CT may be helpful for clarifying the diagnosis in mild cases or if another disease process (such as interstitial lung disease) is suspected. The three different types of emphysema (centrilobular, paraseptal, and panlobular) affect different parts of the secondary pulmonary lobule and are easily distinguished on CT. Emphysema distorts the normal lung anatomy and can cause superimposed processes (e.g. pneumonia or pulmonary edema) to look atypical on chest radiography and CT. Similarly, lung cancer may have an unusual morphology when it arises within emphysematous lung. Cystic lung disease and honeycombing in pulmonary fibrosis should not be confused with emphysema. Cysts and honeycombing have defined walls on CT, whereas centrilobular emphysema manifests as areas of low attenuation without perceptible walls.
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DEVEREUX, THEODORA R., BARBARA A. DOMIN, and RICHARD M. PHILPOT. "XENOBIOTIC METABOLISM BY ISOLATED PULMONARY BRONCHIOLAR AND ALVEOLAR CELLS." In Metabolic Activation and Toxicity of Chemical Agents to Lung Tissue and Cells, 25–40. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-08-041177-4.50007-9.

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Conference papers on the topic "Pulmonary alveoli Bronchioles"

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Imai, Yohsuke, Takahito Miki, Masanori Nakamura, Takuji Ishikawa, Shigeo Wada, and Takami Yamaguchi. "Image Based Simulation of Pulmonary Airflow Using Multi-Level Voxel Modeling." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176529.

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Chronic Obstructive Pulmonary Disease (COPD) refers to a group of diseases that are characterized by airflow obstruction. Currently, COPD is the fourth leading cause of death worldwide, but fluid dynamics in airways of COPD patients has not been well understood. Multi-slice Computer Tomography (CT) images provide three-dimensional realistic geometry of patient airways. Computational Fluid Dynamics (CFD) analysis using the patient-specific geometry will greatly help the understanding of the mechanism of COPD. However, few studies have performed such a patient-specific pulmonary airflow simulation. Our aim is to develop a patient-specific CFD method applicable to multi-scale airways, involving trachea, bronchi, bronchioles, and alveoli. We propose a CFD method using multi-level voxel modeling of airway geometry, in which voxel size in a local domain is adaptively refined or coarsened to the local flow scale.
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Wang, Xiao, Keith Walters, Greg W. Burgreen, and David S. Thompson. "Cyclic Breathing Simulations: Pressure Outlet Boundary Conditions Coupled With Resistance and Compliance." In ASME/JSME/KSME 2015 Joint Fluids Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/ajkfluids2015-26569.

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A patient-specific non-uniform pressure outlet boundary condition was developed and used in unsteady simulations of cyclic breathing in a large-scale model of the lung airway from the oronasal opening to the terminal bronchioles. The computational domain is a reduced-geometry model, in which some airway branches in each generation were truncated, and only selected paths were retained to the terminal generation. To characterize pressure change through airway tree extending from the truncated outlets to pulmonary zone, virtual airways represented by extended volume mesh zones were constructed in order to apply a zero-dimensional airway resistance model. The airway resistances were prescribed based on a precursor steady simulation under constant ventilation condition. The virtual airways accommodate the use of patient-specific alveolar pressure conditions. Furthermore, the time-dependent alveolar pressure profile was composed with the physiologically accurate pleural pressure predicted by the whole-body simulation software HumMod, and the transpulmonary pressure evaluated based on lung compliance and local air volume change. To investigate airway flow patterns of healthy and diseased lungs, unsteady breathing simulations were conducted with varying lung compliances accounting for healthy lungs, and lungs with emphysema or interstitial fibrosis. Results show that the simulations using this patient-specific pressure boundary condition are capable of reproducing physiologically realistic flow patterns corresponding to abnormal pulmonary compliance in diseased lungs, such as the hyperventilation in lungs with emphysema, and the demand of more mechanic work for breathing in lungs with fibrosis.
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