@phdthesis{clarelli_mathematical_2007, title = {Mathematical {Modeling} for lung infections}, abstract = {The main purpose of this work is to investigate mathematical models able to describe problems arising in human lungs. We shall focus our attention specifically on the first human immune response due to the infection of tuberculosis, and on the nitric oxide-gas exchange in the lungs, as a non-invasive marker of lung infections. Hereby, this thesis work is composed by two parts. In the first one, we develop two deterministic differential models describing the immune response to mycobacterium tuberculosis (M.TB.) infection, i.e. the formation of granulomas. We make an analytical validation of the models and we build up numerical algorithms able to simulate this process under different conditions. In the second one, we develop a model describing the nitric oxide (NO) exchange in the lungs for healthy and ill patients; here, we find exact solutions and we build up numerical algorithms able to simulate this process by theoretical and experimental data.}, author = {Clarelli, Fabrizio}, month = feb, year = {2007}, doi = {10.13140/RG.2.1.2594.4805} } @article{le_rolle_mathematical_2013, title = {Mathematical {Modeling} of {Respiratory} {System} {Mechanics} in the {Newborn} {Lamb}}, volume = {61}, issn = {0001-5342, 1572-8358}, url = {http://link.springer.com/10.1007/s10441-013-9175-7}, doi = {10.1007/s10441-013-9175-7}, abstract = {In this paper, a mathematical model of the respiratory mechanics is used to reproduce experimental signal waveforms acquired from three newborn lambs. As the main challenge is to determine specific lamb parameters, a sensitivity analysis has been realized to find the most influent parameters, which are identified using an evolutionary algorithm. Results show a close match between experimental and simulated pressure and flow waveforms obtained during spontaneous ventilation and pleural pressure variations acquired during the application of positive pressure, since Root Mean Square Errors (RMSE) equal to 0.0119, 0.0052 and 0.0094. The identified parameters were discussed in light of previous knowledge of respiratory mechanics in the newborn.}, language = {en}, number = {1}, urldate = {2018-10-22}, journal = {Acta Biotheoretica}, author = {Le Rolle, Virginie and Samson, Nathalie and Praud, Jean-Paul and Hernández, Alfredo I.}, month = mar, year = {2013}, pages = {91--107} } @article{saini_mathematical_nodate, title = {Mathematical {Modeling} of {Lung} {Mechanics}-{A} {Review}}, language = {en}, author = {Saini, Anju and Katiyar, V K}, pages = {4} } @article{racheal_analysis_nodate, title = {Analysis of {Mathematical} {Models} of the {Human} {Lung}}, language = {en}, author = {Racheal, Cooper}, pages = {37} } @article{noauthor_chronic_nodate, title = {{CHRONIC} {OBSTRUCTIVE} {PULMONARY} {DISEASE} {Model} of {Care}}, language = {en}, pages = {51} } @article{groneberg_models_2004, title = {Models of chronic obstructive pulmonary disease}, volume = {5}, issn = {1465-993X}, url = {https://doi.org/10.1186/1465-9921-5-18}, doi = {10.1186/1465-9921-5-18}, abstract = {Chronic obstructive pulmonary disease (COPD) is a major global health problem and is predicted to become the third most common cause of death by 2020. Apart from the important preventive steps of smoking cessation, there are no other specific treatments for COPD that are as effective in reversing the condition, and therefore there is a need to understand the pathophysiological mechanisms that could lead to new therapeutic strategies. The development of experimental models will help to dissect these mechanisms at the cellular and molecular level. COPD is a disease characterized by progressive airflow obstruction of the peripheral airways, associated with lung inflammation, emphysema and mucus hypersecretion. Different approaches to mimic COPD have been developed but are limited in comparison to models of allergic asthma. COPD models usually do not mimic the major features of human COPD and are commonly based on the induction of COPD-like lesions in the lungs and airways using noxious inhalants such as tobacco smoke, nitrogen dioxide, or sulfur dioxide. Depending on the duration and intensity of exposure, these noxious stimuli induce signs of chronic inflammation and airway remodelling. Emphysema can be achieved by combining such exposure with instillation of tissue-degrading enzymes. Other approaches are based on genetically-targeted mice which develop COPD-like lesions with emphysema, and such mice provide deep insights into pathophysiological mechanisms. Future approaches should aim to mimic irreversible airflow obstruction, associated with cough and sputum production, with the possibility of inducing exacerbations.}, number = {1}, urldate = {2018-10-22}, journal = {Respiratory Research}, author = {Groneberg, David A. and Chung, K. Fan}, month = nov, year = {2004}, pages = {18} } @article{b_moore_animal_2013, title = {Animal models of fibrotic lung disease}, volume = {49}, issn = {1535-4989}, doi = {10.1165/rcmb.2013-0094TR}, abstract = {Interstitial lung fibrosis can develop as a consequence of occupational or medical exposure, as a result of genetic defects, and after trauma or acute lung injury leading to fibroproliferative acute respiratory distress syndrome, or it can develop in an idiopathic manner. The pathogenesis of each form of lung fibrosis remains poorly understood. They each result in a progressive loss of lung function with increasing dyspnea, and most forms ultimately result in mortality. To better understand the pathogenesis of lung fibrotic disorders, multiple animal models have been developed. This review summarizes the common and emerging models of lung fibrosis to highlight their usefulness in understanding the cell-cell and soluble mediator interactions that drive fibrotic responses. Recent advances have allowed for the development of models to study targeted injuries of Type II alveolar epithelial cells, fibroblastic autonomous effects, and targeted genetic defects. Repetitive dosing in some models has more closely mimicked the pathology of human fibrotic lung disease. We also have a much better understanding of the fact that the aged lung has increased susceptibility to fibrosis. Each of the models reviewed in this report offers a powerful tool for studying some aspect of fibrotic lung disease.}, language = {eng}, number = {2}, journal = {American Journal of Respiratory Cell and Molecular Biology}, author = {B Moore, Bethany and Lawson, William E. and Oury, Tim D. and Sisson, Thomas H. and Raghavendran, Krishnan and Hogaboam, Cory M.}, month = aug, year = {2013}, pmid = {23526222}, pmcid = {PMC3824038}, keywords = {Animals, Cell Communication, Disease Models, Animal, Epithelial Cells, Genetic Diseases, Inborn, Humans, Lung Diseases, Interstitial, Pulmonary Alveoli, Pulmonary Fibrosis, Respiratory Distress Syndrome, Adult, Respiratory Mucosa}, pages = {167--179} }