The latter are chemically stable because they are water soluble but lipophilic, strongly acidic, and enzymatically non-degradable compounds. Some differences between published chemical profiles and our results might also be due to misidentifications. Apart from specific taxonomic problems with individual taxa, the identification of sawfly larvae, including those in Pergidae and Argidae, still is generally hampered by the lack of suitable identification keys. The combination of the unusual chemical properties and high toxicity of the peptides has provoked reservations against using certain pergid species as biological control agents. In contrast, the argid C. janthina has been introduced on Reunion Island to control the invasive Rubus alceifolius. We have not seen reports of this argid affecting the local fauna, although in our analyses Tioxolone larvae of C. janthina contain high amounts of Perg and LGln. Considering the functioning of ecosystems, the poisoning of livestock following the ingestion of toxin-containing sawfly larvae is merely an epiphenomenon. On the scale of the larvae, the value of the toxic peptides probably lies in defense against natural enemies such as predators. The peptides were not detected in species of the pergid subfamily Perginae, but these larvae exhibit another defensive mechanism. Once disturbed, they discharge a viscous oral fluid, perhaps as an alternative defensive strategy. In laboratory bioassays, extracts from several isolated body parts of A. pagana and A. pullata proved to be effective as feeding deterrents against ants, and the extracts also rapidly paralyzed feeding ants; both of these bioactivities are ascribed to the Cryptochlorogenic-acid action of peptides. The taming of aggressive behavior by ants has been documented also for oligopeptides recently isolated from frogs. It is likely that predators are strongly deterred from ingesting sawfly larvae that contain toxins. In turn, this fact should keep the peptides from being disseminated widely in the food webs of natural environments. Despite great advances in treatment strategies over the last years, myocardial infarction remains a major cause of death and disability worldwide. To reduce myocardial damage and improve clinical outcome, restoration of blood flow to the heart, either by thrombolytic therapy or percutaneous coronary intervention, is vital. Paradoxically, the process of reperfusion itself greatly contributes to myocardial injury, and has been suggested to account for up to 50% of the final infarct size. Significant improvements in future treatments of MI are therefore likely to combine current therapy and targeting of molecular pathways involved in ischemia/reperfusion injuries. The mechanisms involved in I/R injury are complex and not yet fully understood. The changes that occur upon ischemia followed by reperfusion involve an array of biochemical and metabolic changes that mediate detrimental effects within the myocardium. These changes include mitochondrial reenergization, generation of reactive oxygen species, intracellular Ca2+-overload and rapid restoration of physiological pH; all of which act in concert and cause opening of mitochondrial permeability transitioning pore and subsequent cellular death. A consequence of I/R injury is activation of innate and subsequent adaptive immune responses which is important for adequate healing following MI. However, strong evidence points to detrimental consequences if such activity is unbalanced or sustained.