Kinematic and hydrodynamic analyses of turning manoeuvres in penguins: body banking and wing upstroke generate centripetal force.

Penguins perform lift-based swimming by flapping their wings. Previous kinematic and hydrodynamic studies have revealed the basics of wing motion and force generation in penguins. Although these studies have focused on steady forward swimming, the mechanism of turning manoeuvres is not well understood. In this study, we examined the horizontal turning of penguins via 3D motion analysis and quasi-steady hydrodynamic analysis. Free swimming of gentoo penguins (Pygoscelis papua) at an aquarium was recorded, and body and wing kinematics were analysed. In addition, quasi-steady calculations of the forces generated by the wings were performed. Among the selected horizontal swimming manoeuvres, turning was distinguished from straight swimming by the body trajectory for each wingbeat. During the turns, the penguins maintained outward banking through a wingbeat cycle and utilized a ventral force during the upstroke as a centripetal force to turn. Within a single wingbeat during the turns, changes in the body heading and bearing also mainly occurred during the upstroke, while the subsequent downstroke accelerated the body forward. We also found contralateral differences in the wing motion, i.e. the inside wing of the turn became more elevated and pronated. Quasi-steady calculations of the wing force confirmed that the asymmetry of the wing motion contributes to the generation of the centripetal force during the upstroke and the forward force during the downstroke. The results of this study demonstrate that the hydrodynamic force of flapping wings, in conjunction with body banking, is actively involved in the mechanism of turning manoeuvres in penguins.

Kinematics and hydrodynamics analyses of swimming penguins: wing bending improves propulsion performance.

Penguins are adapted to underwater life and have excellent swimming abilities. Although previous motion analyses revealed their basic swimming characteristics, the details of the 3D wing kinematics, wing deformation and thrust generation mechanism of penguins are still largely unknown. In this study, we recorded the forward and horizontal swimming of gentoo penguins (Pygoscelis papua) at an aquarium with multiple underwater action cameras and then performed a 3D motion analysis. We also conducted a series of water tunnel experiments with a 3D printed rigid wing to obtain lift and drag coefficients in the gliding configuration. Using these coefficients, the thrust force during flapping was calculated in a quasi-steady manner, where the following two wing models were considered: (1) an 'original' wing model reconstructed from 3D motion analysis including bending deformation and (2) a 'flat' wing model obtained by flattening the original wing model. The resultant body trajectory showed that the penguin accelerated forward during both upstroke and downstroke. The motion analysis of the two wing models revealed that considerable bending occurred in the original wing, which reduced its angle of attack during the upstroke in particular. Consequently, the calculated stroke-averaged thrust was larger for the original wing than for the flat wing during the upstroke. In addition, the propulsive efficiency for the original wing was estimated to be 1.8 times higher than that for the flat wing. Our results unveil a detailed mechanism of lift-based propulsion in penguins and underscore the importance of wing bending.

Inhibition of Recombinant Human Acetylcholinesterase Activity by Antipsychotics.

BACKGROUND/AIMS: Extrapyramidal symptoms (EPS) are representative side effects of antipsychotics, caused by their inhibitory action on dopaminergic nerves in nigrostriatal pathways. EPS could be also caused by direct augmentation of cholinergic effects, for example, by acetylcholinesterase (AChE) inhibition. We investigated the potential inhibitory effects of 26 clinically available antipsychotics on the activity of recombinant human AChE (rhAChE) to predict the role of antipsychotic-induced AChE inhibition in EPS onset. METHOD: The degree of rhAChE activity inhibition was calculated using the 5,5'-dithio-bis-(2-nitrobenzoic acid) method. RESULTS: At a concentration of 10-5 mol/L, haloperidol, bromperidol, timiperone, nemonapride, pimozide, risperidone, blonanserin, aripiprazole, and brexpiprazole inhibited rhAChE activity by >20%. Risperidone, aripiprazole, and brexpiprazole inhibited rhAChE activity in a concentration-dependent manner, and their effects were more potent than those of other antipsychotics. The inhibitory effects of these 3 drugs were evident from 10-6 mol/L, and their pIC50 values were 4.74 ± 0.04, 4.80 ± 0.04, and 4.93 ± 0.06, respectively. Notably, the concentration range in which aripiprazole inhibited rhAChE activity (≥10-6 mol/L) overlapped with its clinically achievable blood levels. CONCLUSION: Aripiprazole may cause EPS at clinical dosages by augmenting cholinergic effects via AChE inhibition, in addition to its suppressive effect on dopaminergic neurons.