Midfoot passive stiffness affects foot and ankle kinematics and kinetics during the propulsive phase of walking.

The midfoot joint complex (MFJC) is related to the mechanics and efficiency of the walking propulsive phase and low midfoot passive stiffness may require compensatory foot and ankle joint moments to avoid excessive pronation and inefficient propulsion. This study aimed to investigate the kinematics and kinetics of the MFJC and ankle during the propulsive phase of walking in subjects with larger and smaller midfoot passive stiffness. MFJC passive stiffness of 20 healthy adult participants, and the kinematics and kinetics of the MFJC (forefoot-rearfoot) and ankle (rearfoot-shank) during the stance phase of walking were measured. The participants were divided equally into two groups according to the MFJC passive stiffness. Ranges of motion (ROM) and mean joint moments were computed for the late stance. Independent t-tests (α = 0.05) revealed that subjects with lower midfoot passive stiffness showed an increased MFJC sagittal ROM (flattened longitudinal arch) (p = 0.002), increased ankle frontal ROM (more everted positions) (p = 0.002), increased MFJC frontal ROM (more inverted positions) (p = 0.019), as well as a tendency for larger ankle sagittal ROM (p = 0.056). They also showed increased MFJC (p = 0.021) and ankle (p = 0.018) moments in the sagittal plane, increased MFJC moment in the frontal plane (p = 0.047) and a tendency for a predominant ankle moment in the frontal (p = 0.058). Foot and ankle joint moments are possible strategies to reduce pronation and improve propulsion, but not sufficient to prevent the altered kinematics related to low midfoot stiffness. Therefore, midfoot passive stiffness is critical for foot and ankle kinematics and kinetics during walking propulsive phase and is a potential target of interventions.

Evidence for the involvement of opioid and cannabinoid systems in the peripheral antinociception mediated by resveratrol.

Despite all the development of modern medicine, around 100 compounds derived from natural products were undergoing clinical trials only at the end of 2013. Among these natural substances in clinical trials, we found the resveratrol (RES), a pharmacological multi-target drug. RES analgesic properties have been demonstrated, although the bases of these mechanisms have not been fully elucidated. The aim of this study was to evaluate the involvement of opioid and cannabinoid systems in RES-induced peripheral antinociception. Paw withdrawal method was used and hyperalgesia was induced by carrageenan (200 µg/paw). All drugs were given by intraplantar injection in male Swiss mice (n = 5). RES (100 µg/paw) administered in the right hind paw induced local antinociception that was antagonized by naloxone, non-selective opioid receptor antagonist, and clocinnamox, µOR selective antagonist. Naltrindole and nor-binaltorfimine, selective antagonists for δOR and kOR, respectively, did not reverse RES-induced peripheral antinociception. CB1R antagonist AM251, but not CB2R antagonist AM630, antagonized RES-induced peripheral antinociception. Peripheral antinociception of RES intermediate-dose (50 µg/paw) was increased by: (i) bestatin, inhibitor of endogenous opioid degradation involved-enzymes; (ii) MAFP, inhibitor of anandamide amidase; (iii) JZL184, inhibitor of 2-arachidonoylglycerol degradation involved-enzyme; (iv) VDM11, endocannabinoid reuptake inhibitor. Acute and peripheral administration of RES failed to affect the amount of µOR, CB1R and CB2R. Experimental data suggest that RES induces peripheral antinociception through µOR and CB1R activation by endogenous opioid and endocannabinoid releasing.