Keystone symposium: The role of microenvironment in tumor induction and progression, Banff, Canada, 5–10 February 2005

The first Keystone symposium on the role of microenvironment in tumor induction and progression attracted 274 delegates from 13 countries to Banff in the heart of the Canadian Rockies. The meeting was organized by Mina Bissell, Ronald DePinho and Luis Parada, and was held concurrently with the Keystone symposium on cancer and development, chaired by Matthew Scott and Roeland Nusse. The 30 oral presentations and over 130 posters provided an excellent forum for discussing emerging data in this rapidly advancing field

Teaching: Natural or Cultural?

In this chapter I argue that teaching, as we now understand the term, is historically and cross-culturally very rare. It appears to be unnecessary to transmit culture or to socialize children. Children are, on the other hand, primed by evolution to be avid observers, imitators, players and helpers—roles that reveal the profoundly autonomous and self-directed nature of culture acquisition (Lancy in press a). And yet, teaching is ubiquitous throughout the modern world—at least among the middle to upper class segment of the population. This ubiquity has led numerous scholars to argue for the universality and uniqueness of teaching as a characteristically human behavior. The theme of this chapter is that this proposition is unsustainable. Teaching is largely a result of recent cultural changes and the emergence of modern economies, not evolution

Role for mitochondrial reactive oxygen species in brain lipid sensing: redox regulation of food intake

0012-1797 (Print) Journal Article Research Support, Non-U.S. Gov'tThe ability for the brain to sense peripheral fuel availability is mainly accomplished within the hypothalamus, which detects ongoing systemic nutrients and adjusts food intake and peripheral metabolism as needed. Here, we hypothesized that mitochondrial reactive oxygen species (ROS) could trigger sensing of nutrients within the hypothalamus. For this purpose, we induced acute hypertriglyceridemia in rats and examined the function of mitochondria in the hypothalamus. Hypertriglyceridemia led to a rapid increase in the mitochondrial respiration in the ventral hypothalamus together with a transient production of ROS. Cerebral inhibition of fatty acids-CoA mitochondrial uptake prevented the hypertriglyceridemia-stimulated ROS production, indicating that ROS derived from mitochondrial metabolism. The hypertriglyceridemia-stimulated ROS production was associated with change in the intracellular redox state without any noxious cytotoxic effects, suggesting that ROS function acutely as signaling molecules. Moreover, cerebral inhibition of hypertriglyceridemia-stimulated ROS production fully abolished the satiety related to the hypertriglyceridemia, suggesting that hypothalamic ROS production was required to restrain food intake during hypertriglyceridemia. Finally, we found that fasting disrupted the hypertriglyceridemia-stimulated ROS production, indicating that the redox mechanism of brain nutrient sensing could be modulated under physiological conditions. Altogether, these findings support the role of mitochondrial ROS as molecular actors implied in brain nutrient sensing