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dc.contributor.authorShick, Amanda E.
dc.contributor.authorLiu, Guanyun
dc.contributor.authorMenezes, Amor A.
dc.date.accessioned2026-08-23T07:59:31Z
dc.date.available2026-08-23T07:59:31Z
dc.date.copyright2026/04/01
dc.date.issued2026
dc.identifier.issn2689-6117
dc.identifier.otheraldsc-25-1070.pdf
dc.identifier.urihttp://yetl.yabesh.ir/yetl1/handle/yetl/4315912
dc.description.abstractAbstract. Pulmonary fibrin accumulation is caused by aberrant cascade interactions that promote fibrin protein deposits in the lung. Fibrin buildup stiffens the lungs, decreases gas exchange, and impairs lung function. Unregulated fibrin accumulation can devolve into irreversible scarring, called fibrosis, and ultimately lung failure. Diseases with pulmonary fibrin accumulation such as acute respiratory distress syndrome (ARDS) have no known cure. Supportive care that is open-loop and nonpersonalized is the only treatment option. Here, we propose closing the loop for ARDS with a feedback treatment regimen of a novel protein therapeutic, activated protein C (APC). We show the observability, controllability, and feedback linearizability of a single-input, single-output control-affine nonlinear system that captures the simplified dynamics of pulmonary fibrin accumulation during virally-induced ARDS. We then apply our developed input-state feedback linearizing APC controller to our simplified system and demonstrate the return of a diseased patient to a healthy reference.
dc.publisherThe American Society of Mechanical Engineers (ASME)
dc.titleDynamic Therapy for Pulmonary Fibrin Accumulation
dc.typeJournal Paper
dc.journal.volume6
dc.journal.issue2
dc.journal.titleASME Letters in Dynamic Systems and Control
dc.identifier.doi10.1115/1.4070146
dc.journal.fristpage247
dc.journal.lastpage299
dc.page53
dc.treeASME Letters in Dynamic Systems and Control:;2026:;volume( 006 ):;issue:002
dc.contenttypeFulltext


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