The inflammatory response is accompanied by increases in various inflammatory markers such as CXCL1, GM-CSF, IL-6, and VEGF. In addition, chlorine exposure results in the recruitment of inflammatory neutrophils and macrophages ( Balakrishna et al., 2014). Both of those compounds can result in oxidative injury following the formation of reactive oxygen species, which can result in edema, inflammation, and immediate airway constriction. The mouse model will evaluate survival, clinical outcomes, body weight, lung weight, and upper respiratory tract histopathology after exposure to chlorine gas and MN-166 or control.Ĭhlorine inhalation results in the formation of hydrochloric acid (HCl) and hypochlorous acid (HOCl) as it dissolves into the airway surface liquid. control in an ovine model of chlorine-induced acute lung injury through evaluation of pulmonary function, lung injury and edema formation, cardiopulmonary hemodynamics, and systemic vascular permeability. The partnership is set up to test the potential for MN-166 (ibudilast) as a medical countermeasure (MCM) for the treatment of chlorine gas-induced acute respiratory distress syndrome (ARDS) and acute lung injury (ALI).
(NASDAQ:MNOV) announced it initiated a sheep study and also reached an agreement to conduct a mouse study as part of its partnership with the Biomedical Advanced Research and Development Authority (BARDA).
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