Bio-Organometallic systems for the hydrogen economy: engineering of electrode materials and light-driven devices

International audienceHydrogen is an energy vector with great potential, and the large‐scale development of hydrogen technologies currently relies on the catalytic properties of noble metals, making them both unsustainable and economically questionable. Alternative catalytic materials can be derived from hydrogenase enzymes or bio‐inspired molecular catalysts mimicking either the structure of their active site or their functioning. In this chapter, we describe how surface science and nanotechnologies provide means to produce biological and bio‐inspired types of noble metal‐free electrode materials for implementation in electrolyzers and fuel cells. We also show how the combination of H2‐evolving catalysts with light‐harvesting centers, as part of the artificial photosynthesis approach, can provide a solution to the energetic transition toward a solar fuel‐based econo

Interleukin-18 Delays Neutrophil Apoptosis following Alcohol Intoxication and Burn Injury

Studies have shown that burn patients who are intoxicated at the time of injury are more susceptible to infection and have a higher incidence of mortality. A major cause of death in burn and trauma patients regardless of their alcohol (EtOH) exposure is multiple organ dysfunction, which is driven in part by the systemic inflammatory response and activated neutrophils. Neutrophils are short lived and undergo apoptosis to maintain homeostasis and resolution of inflammation. A delay in apoptosis of neutrophils is one important mechanism which allows for their prolonged presence and the release of potentially harmful enzymes. The purpose of this study was to examine whether EtOH intoxication combined with burn injury influences neutrophil apoptosis and whether IL-18 plays any role in this setting. To accomplish this investigation, rats were gavaged with EtOH (3.2 g/kg) 4 h before being subjected to sham or burn injury of ~12.5% of the total body surface area, and then killed on d 1 after injury. Peripheral blood neutrophils were isolated and lysed. The lysates were analyzed for pro- and antiapoptotic proteins. We found that EtOH combined with burn injury prolonged neutrophil survival. This prolonged neutrophil survival was accompanied by a decrease in the levels of the neutrophil proapoptotic protein Bax, and an increase in antiapoptotic proteins Mcl-1 and Bcl-xl. Administration of IL-18 antibody following burn injury normalized the levels of Bax, Mcl-1 and Bcl-xl. The decrease in caspase-3 and DNA fragmentation observed following EtOH and burn injury was also normalized in rats treated with anti–IL-18 antibody. These findings suggest that IL-18 delays neutrophil apoptosis following EtOH and burn injury by modulating the pro- and antiapoptotic proteins