Abstract: 

In the path of finding therapies and solutions to selective problematic issues of human life, carbon monoxide (CO) poisoning is a subject of study. CO poisoning is a crucial cause of human mortality and does not have any approved antidotal therapy up to date. The only current treatments have debatable efficacy with short and long-term side effects. Our long-term goal is to find a point-of-care device for intravenous injections of treatments to the poisoned victims promptly after diagnosis. A successful antidote will rapidly bind and slowly release CO so that it consumes CO in the blood. Laser pulse flash photolysis technique which fully releases CO from its binding molecule, heme, has been employed to measure the binding association rates of proposed antidotes. Due to the high affinity of Nitric Oxide (NO) molecules for hemoglobin, NO becomes a suitable choice for measuring the dissociation rates of CO replacement with NO in the targeted protein antidotes. We successfully showed the beneficial candidacy of two hemoproteins [StHb and NEMHb] in comparison with R-state hemoglobin and equine myoglobin. Our data highlighted their therapeutic potential for point-of-care antidotal therapy of CO poisoning.  

Another persisting problem is the daily and possibly fatal occurrence of unwanted blood clot formation in the blood-contacting devices in modern medicine. Formation of blood clots is often a beneficial process to stop bleeding and repair damage after a wound. However, clot formation when there is no wound can lead to a great degree of morbidity and mortality; this process is called thrombosis. Despite all of the advances made, failure rates are still as high as 6%, and up to 1/3 of neonates and children suffer thrombosis complications from extracorporeal circulation devices. Thus, device thrombosis is a significant complication in otherwise life-saving interventions, and methods to locally reduce thrombosis would be advantageous. NO is a known anti-platelet agent that can prevent thrombosis.  We hypothesize that nitrite increases NO bioavailability through a mechanism involving RBC bioactivation, and this action is potentiated with red light illumination that can be used for treatments aimed at decreasing device thrombosis. The collected data from our innovative macroscale prototype shows that dual nitrite/light therapy has the potential to prevent device thrombosis and to lead new clinical therapeutic applications and practices.

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