Quasi-steady state aerodynamics of the cheetah tail

During high-speed pursuit of prey, the cheetah (Acinonyx jubatus) has been observed to swing its tail while manoeuvring (e.g. turning or braking) but the effect of these complex motions is not well understood. This study demonstrates the potential of the cheetah's long, furry tail to impart torques and forces on the body as a result of aerodynamic effects, in addition to the well-known inertial effects. The first-order aerodynamic forces on the tail are quantified through wind tunnel testing and it is observed that the fur nearly doubles the effective frontal area of the tail without much mass penalty. Simple dynamic models provide insight into manoeuvrability via simulation of pitch, roll and yaw tail motion primitives. The inertial and quasi-steady state aerodynamic effects of tail actuation are quantified and compared by calculating the angular impulse imparted onto the cheetah's body and its shown aerodynamic effects contribute to the tail's angular impulse, especially at the highest forward velocities

Rac signaling in osteoblastic cells is required for normal bone development but is dispensable for hematopoietic development

Hematopoietic stem cells (HSCs) interact with osteoblastic, stromal, and vascular components of the BM hematopoietic microenvironment (HM) that are required for the maintenance of long-term self-renewal in vivo. Osteoblasts have been reported to be a critical cell type making up the HSC niche in vivo. Rac1 GTPase has been implicated in adhesion, spreading, and differentiation of osteoblast cell lines and is critical for HSC engraftment and retention. Recent data suggest a differential role of GTPases in endosteal/osteoblastic versus perivascular niche function. However, whether Rac signaling pathways are also necessary in the cell-extrinsic control of HSC function within the HM has not been examined. In the present study, genetic and inducible models of Rac deletion were used to demonstrate that Rac depletion causes impaired proliferation and induction of apoptosis in the OP9 cell line and in primary BM stromal cells. Deletion of Rac proteins caused reduced trabecular and cortical long bone growth in vivo. Surprisingly, HSC function and maintenance of hematopoiesis in vivo was preserved despite these substantial cell-extrinsic changes. These data have implications for therapeutic strategies to target Rac signaling in HSC mobilization and in the treatment of leukemia and provide clarification to our evolving concepts of HSC-HM interactions