Secondary flows and loss caused by blade row interaction in a turbine stage

A study of the three-dimensional stator-rotor interaction in a turbine stage is presented. Experimental data reveal vortices downstream of the rotor which are stationary in the absolute frame - indicating that they are caused by the stator exit flowfield. Evidence of the rotor hub passage vortices is seen, but additional vortical structures away from the endwalls, which would not be present if the rotor were tested in isolation, are also identified. An unsteady computation of the rotor row is performed using the measured stator exit flowfield as the inlet boundary condition. The strength and location of the vortices at rotor exit are predicted. A formation mechanism is proposed whereby stator wake fluid with steep spanwise gradients of absolute total pressure is responsible for all but one of the rotor exit vortices. This mechanism is then verified computationally using a passive-scalar tracking technique. The predicted loss generation through the rotor row is then presented and a comparison made with a steady calculation where the inlet flow has been mixed out to pitchwise uniformity. The loss produced in the steady simulation, even allowing for the mixing loss at inlet, is 10% less than that produced in the unsteady simulation. This difference highlights the importance of the time-accurate calculation as a tool of the turbomachine designer.

Blocking central opiate function modulates hedonic impact and anterior cingulate response to rewards and losses.

Reward processing is linked to specific neuromodulatory systems with a dopaminergic contribution to reward learning and motivational drive being well established. Neuromodulatory influences on hedonic responses to actual receipt of reward, or punishment, referred to as experienced utility are less well characterized, although a link to the endogenous opioid system is suggested. Here, in a combined functional magnetic resonance imaging-psychopharmacological investigation, we used naloxone to block central opioid function while subjects performed a gambling task associated with rewards and losses of different magnitudes, in which the mean expected value was always zero. A graded influence of naloxone on reward outcome was evident in an attenuation of pleasure ratings for larger reward outcomes, an effect mirrored in attenuation of brain activity to increasing reward magnitude in rostral anterior cingulate cortex. A more striking effect was seen for losses such that under naloxone all levels of negative outcome were rated as more unpleasant. This hedonic effect was associated with enhanced activity in anterior insula and caudal anterior cingulate cortex, areas implicated in aversive processing. Our data indicate that a central opioid system contributes to both reward and loss processing in humans and directly modulates the hedonic experience of outcomes.

Differential encoding of losses and gains in the human striatum.

Studies on human monetary prediction and decision making emphasize the role of the striatum in encoding prediction errors for financial reward. However, less is known about how the brain encodes financial loss. Using Pavlovian conditioning of visual cues to outcomes that simultaneously incorporate the chance of financial reward and loss, we show that striatal activation reflects positively signed prediction errors for both. Furthermore, we show functional segregation within the striatum, with more anterior regions showing relative selectivity for rewards and more posterior regions for losses. These findings mirror the anteroposterior valence-specific gradient reported in rodents and endorse the role of the striatum in aversive motivational learning about financial losses, illustrating functional and anatomical consistencies with primary aversive outcomes such as pain.