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Idiopathic pulmonary fibrosis (IPF) affects 200,000 patients in the United States of America. IPF is responsible for changes in the micro-architecture of the lung parenchyma, such as thickening of the alveolar walls, which reduces compliance and elasticity. In this study, we verify the hypothesis that changes in the micro-architecture of the lung parenchyma can be characterized by exploiting multiple scattering of ultrasound waves by the alveolar structure. Ultrasound propagation in a highly scattering regime follows a diffusion process, which can be characterized using the Diffusion Constant. We hypothesize that in a fibrotic lung, the thickening of the alveolar wall reduces the amount of air (compared to a healthy lung), thereby minimizing the scattering events. Pulmonary fibrosis is created in Sprague-Dawley rats by instilling bleomycin into the airway. The rats are studied within 3 week after bleomycin administration. Using a 128-element linear array transducer operating at 7.8 MHz, in-vivo experimental data is obtained from Sprague-Dawley rats and the transport mean free path (L*) and Backscatter Frequency Shift (BFS) are evaluated. Significant differences (p<0.05) in the L* values between control and fibrotic rats and in the BFS values between fibrotic and edematous rats showcase the potential of these parameters for diagnosis and monitoring of IPF.
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?:doi
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?:doi
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10.1109/tuffc.2020.3023611
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IEEE_transactions_on_ultrasonics,_ferroelectrics,_and_frequency_control
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In-Vivo Assessment of Pulmonary Fibrosis and Pulmonary Edema in Rodents Using Ultrasound Multiple Scattering.
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