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Successful reactive balance control requires coordinated modulation of hip, knee, and ankle torques. Stabilizing joint torques arise from neurally-mediated feedforward tonic muscle activation that modulates muscle short-range stiffness, which provides instantaneous "mechanical feedback" to the perturbation. In contrast, neural feedback pathways activate muscles in response to sensory input, generating joint torques after a delay. However, the specific contributions from feedforward and feedback pathways to the balance-correcting torque response are poorly understood. As feedforward- and feedback-mediated torque responses to balance perturbations act at different delays, we modified the sensorimotor response model (SRM), previously used to analyze the muscle activation response, to reconstruct joint torques using parallel feedback loops. Each loop is driven by the same information, center of mass (CoM) kinematics, but each loop has an independent delay. We evaluated whether a torque-SRM could decompose the reactive torques during balance-correcting responses to backward support surface translations at four magnitudes into the instantaneous "mechanical feedback" torque modulated by feedforward neural commands before the perturbation and neurally-delayed feedback components. The SRM accurately reconstructed torques at the hip, knee, and ankle, across all perturbation magnitudes (R2 > 0.84 and VAF > 0.83). Moreover, the hip and knee exhibited feedforward and feedback components, while the ankle only exhibited feedback components. The lack of a feedforward component at the ankle may occur because the compliance of the Achilles tendon attenuates muscle short-range stiffness. Our model may provide a framework for evaluating changes in the feedforward and feedback contributions to balance that occur due to aging, injury, or disease. NEW & NOTEWORTHY: Reactive balance control requires coordination of neurally-mediated feedforward and feedback pathways to generate stabilizing joint torques at the hip, knee, and ankle. Using a sensorimotor response model, we decomposed reactive joint torques into feedforward and feedback contributions based on delays relative to the center of mass kinematics. Responses across joints were driven by the same signals, but contributions from feedforward versus feedback pathways differed, likely due to differences in musculotendon properties between proximal and distal muscles. [ABSTRACT FROM AUTHOR]

Herein, we investigate the effects of ligand design on the nuclearity and reactivity of metal-ligand multiply bonded (MLMB) complexes to access an exclusively bimetallic reaction pathway for C-H bond functionalization. To this end, the diiron alkoxide [Fe 2 ( Ph Dbf) 2 ] ( 1 ) was treated with 3,5-bis(trifluoromethyl)phenyl azide to access the diiron imido complex [Fe 2 ( Ph Dbf) 2 (μ-NC 8 H 3 F 6 )] ( 2a ) that promotes hydrogen atom abstraction (HAA) from a variety of C-H and O-H bond containing substrates. A diiron bis(amide) complex [Fe 2 ( Ph Dbf) 2 (μ-NHC 8 H 3 F 6 )(NHC 8 H 3 F 6 )] ( 3 ) was generated, prompting the isolation of the analogous bridging amide terminal alkoxide [Fe 2 ( Ph Dbf) 2 (μ-NHC 8 H 3 F 6 )(OC 19 H 15 )] ( 4 ) and the asymmetric pyridine-bound diiron imido [Fe 2 ( Ph Dbf) 2 (μ-NC 8 H 3 F 6 )(NC 5 H 5 )] ( 6a ). We found that 6a is competent for toluene amination, indicating the effect of Lewis base-enhanced C-H bond functionalization. Mechanistic investigations suggest that the bimetallic bridging imido complex is the reactive intermediate as no monometallic species is detected during the time course of the reaction.