The elucidation of factors that activate the regeneration of the adult mammalian heart is of major scientific and therapeutic importance. Here we found that epicardial cells contain a potent cardiogenic activity identified as follistatin-like 1 (Fstl1). Epicardial Fstl1 declines following myocardial infarction and is replaced by myocardial expression. Myocardial Fstl1 does not promote regeneration, either basally or upon transgenic overexpression. Application of the human Fstl1 protein (FSTL1) via an epicardial patch stimulates cell cycle entry and division of pre-existing cardiomyocytes, improving cardiac function and survival in mouse and swine models of myocardial infarction. The data suggest that the loss of epicardial FSTL1 is a maladaptive response to injury, and that its restoration would be an effective way to reverse myocardial death and remodelling following myocardial infarction in humans.

We show that quantum interference in graphene can result in antilocalization of charge carriers--an increase of the conductance, which is detected by a negative magnetoconductance. We demonstrate that depending on experimental conditions one can observe either weak localization or antilocalization of carriers in graphene. A transition from localization to antilocalization occurs when the carrier density is decreased and the temperature is increased. We show that quantum interference in graphene can survive at high temperatures, up to T approximately 200 K, due to weak electron-phonon scattering.