The spread of a novel behaviour in wild chimpanzees : new insights into the ape cultural mind

TP was funded by the Canadian Research Chair in Continental Ecosystem Ecology, and received computational support from the Theoretical Ecosystem Ecology group at UQAR. The research leading to these results has received funding from the People Programme (Marie Curie Actions) and from the European Research Council under the European Union's Seventh Framework Programme (FP7/2007–2013) REA grant agreement n°329197 awarded to TG, ERC grant agreement n° 283871 awarded to KZ. WH was funded by a BBSRC grant (BB/I007997/1).For years, the animal culture debate has been dominated by the puzzling absence of direct evidence for social transmission of behavioural innovations in the flagship species of animal culture, the common chimpanzee. Although social learning of novel behaviours has been documented in captivity, critics argue that these findings lack ecological validity and therefore may not be relevant for understanding the evolution of culture. For the wild, it is possible that group-specific behavioural differences emerge because group members respond individually to unspecified environmental differences, rather than learning from each other. In a recent paper, we used social network analyses in wild chimpanzees (Pan troglodytes schweinfurthii) to provide direct evidence for social transmission of a behavioural innovation, moss-sponging, to extract water from a tree hole. Here, we discuss the implications of our findings and how our new methodological approach could help future studies of social learning and culture in wild apes.Publisher PDFPeer reviewe

Targeting Vascular NADPH Oxidase 1 Blocks Tumor Angiogenesis through a PPARα Mediated Mechanism

Reactive oxygen species, ROS, are regulators of endothelial cell migration, proliferation and survival, events critically involved in angiogenesis. Different isoforms of ROS-generating NOX enzymes are expressed in the vasculature and provide distinct signaling cues through differential localization and activation. We show that mice deficient in NOX1, but not NOX2 or NOX4, have impaired angiogenesis. NOX1 expression and activity is increased in primary mouse and human endothelial cells upon angiogenic stimulation. NOX1 silencing decreases endothelial cell migration and tube-like structure formation, through the inhibition of PPARα, a regulator of NF-κB. Administration of a novel NOX-specific inhibitor reduced angiogenesis and tumor growth in vivo in a PPARα dependent manner. In conclusion, vascular NOX1 is a critical mediator of angiogenesis and an attractive target for anti-angiogenic therapies