Fibrosis results from a number of idiopathic and defined origins.  As chronic inflammation and radiation are both known causes of fibrosis, Biomodels has developed a number of approaches to look at fibrosis as an endpoint in our cancer supportive care and inflammatory disease models.  Additionally, Biomodels has developed several models of fibrosis to reflect common pathologies of the liver, skin, kidney, and lungs.  One of the main interests at Biomodels in this space was to develop a pre-clinical animal model of pulmonary fibrosis that closely recapitulates the clinical condition in patients. To evaluate the response to a clients’ treatment we use a combination of clinically translatable endpoints such as weight loss, lung mechanics (flexiVent) analysis, and histopathology in addition to downstream tissue analysis. Pulmonary fibrosis occurs when the tissue around the alveoli in the lung becomes scarred and thickened making it difficult for oxygen to diffuse into the blood stream resulting in symptoms of dyspnea, dry cough, fatigue, unexplained weight loss, and aching muscles and joints. Pulmonary fibrosis may be caused by occupational and environmental factors such as silica dust and asbestos fibers, radiation therapy, medications such as certain chemotherapy drugs, heart medications, antibiotics, and medical conditions such as tuberculosis and pneumonia. Complications of pulmonary fibrosis may include pulmonary hypertension, ventricular heart failure, respiratory failure and lung cancer. Pulmonary fibrosis cannot be reversed and no current treatment is able to completely stop the progression of the disease. 

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