Thrombosis and Hemostasis
Thrombogenesis is a natural process by which the body acts on an injury to stop bleeding and heal the injured tissues. However, a growing thrombus may block a blood vessel preventing blood from reaching vital organs. Further, parts of a thrombus may detach and travel through the circulatory system causing heart attack and stroke. While the roles of cells and molecules that contribute to thrombus formation have been identified, and the steps that lead to thrombus formation, the so-called coagulation cascade, are fairly well known, the effect of blood flow on thrombus formation and transport of thrombogenic products is less understood.
Thrombus formation on thrombogenic surfaces has been shown to consist of 3 phases: (I) initial, slow growth; (II) linear growth; (III) plateau, during which the thrombus stops growing. Phase three may not be observed if the thrombus occludes the vessel. While phases one and two are somewhat understood, the mechanisms by which the thrombus stops growing are not well understood. Several factors, such as blood and thrombus-surface chemistry as well as blood flow might play a role. The Rugonyi Lab focuses on understanding the effect of blood flow on thrombus growth, with the ultimate goal of elucidating the mechanisms by which thrombi break lose or stop growing.
Pulmonary Surfactant Biophysics
Pulmonary surfactant is essential for normal breathing. The lack of sufficient amount of mature surfactant causes respiratory distress syndrome (RDS) in premature infants, and can worsen the patient condition in adults with acute respiratory distress syndrome (ARDS). In the lungs, pulmonary surfactant forms a thin surface film, generally believed to be a monolayer, at the interface between air and a thin liquid layer that coats the alveoli. This surfactant film reduces surface tension, a force that tends to collapse the alveoli causing lung injury.
In situ experiments demonstrate that surface tension reaches very low values (~1 mN/m) during exhalation. However, these very low values are difficult to reproduce in vitro. Unlike in the lungs, during in vitro compression of pulmonary surfactant monolayers, surface tension decreases until the monolayer starts to thicken forming multi-layer films, process that is usually referred to as monolayer collapse and that occurs at a constant surface tension (the collapse or equilibrium surface tension, ~ 24 mN/m). Why pulmonary surfactant film responds differently to compression in situ and in vitro is not well understood. Dr. Rugonyi's research has focused on the kinetics of surfactant collapse - the formation of multi-layers from a monolayer film - and how collapse rates are affected by (I) the rate of film compression; (II) the film surface tension; and (III) the sub-phase liquid thickness. The ultimate goal is to understand the mechanisms by which proper surfactant function is achieved.