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Objective: Ankle braces can affect the kinematics of the ankle joint during landing tasks. Previous studies were primarily relied on traditional marker-based motion capture systems, which pose limitations in non-invasively capturing the motion of the talus bone. The effect of ankle braces on the in vivo kinematics of the tibiotalar and subtalar joints during landing remains unknown. This study used a high-speed dual fluoroscopic imaging system (DFIS) and magnetic resonance imaging (MRI) to investigate effect of ankle braces on the in vivo kinematics of the tibiotalar and subtalar joints during landing.Methods: Fourteen healthy participants were recruited for this study. During the experiment, static three-dimensional MRI data were collected for each participant, and 3D ankle joint models for the calcaneus, talus, and tibia were constructed. The DFIS was used to capture the images of each participant performing a single-leg landing-jump task at a height of 40 cm. The images were captured once with and without a brace in the fatigue condition, which was induced by running. The six-degree-of-freedom (6DOF) kinematic data were obtained by 2D-3D registration.Results: The flexion-extension range of motion (ROM) (42.73 ± 4.76° vs. 38.74 ± 5.43°, p = 0.049) and anterior-posterior translation ROM (16.86 ± 1.74 mm vs. 15.03 ± 1.73 mm, p = 0.009) of the tibiotalar joint were decreased. The maximum inversion angle (−3.71 ± 2.25° vs. 2.11 ± 1.83°, p = 0.047) of the subtalar joint was decreased.Conclusion: The ankle brace limited the flexion-extension ROM of the tibiotalar joints and the inversion angle of the subtalar joint during landing.

Objective: Fatigue can affect the ankle kinematic characteristics of landing movements. Traditional marker-based motion capture techniques have difficulty in accurately obtaining the kinematics of the talocrural and subtalar joints. This study aimed to investigate the effects of fatigue on the talocrural and subtalar joints during the landing using dual fluoroscopic imaging system (DFIS).Methods: This study included fourteen healthy participants. The foot of each participant was scanned using magnetic resonance imaging to create 3D models. High-speed DFIS was used to capture images of the ankle joint during participants performing a single-leg landing jump from a height of 40 cm. Fatigue was induced by running and fluoroscopic images were captured before and after fatigue. Kinematic data were obtained by 3D/2D registration in virtual environment software. The joint kinematics in six degrees of freedom and range of motion (ROM) were compared between the unfatigued and fatigued conditions.Results: During landing, after the initial contact with the ground, the main movement of the talocrural joint is extension and abduction, while the subtalar joint mainly performs extension, eversion, and abduction. Compared to unfatigued, during fatigue the maximum medial translation (1.35 ± 0.45 mm vs. 1.86 ± 0.69 mm, p = 0.032) and medial-lateral ROM (3.19 ± 0.60 mm vs. 3.89 ± 0.96 mm, p = 0.029) of the talocrural joint significantly increased, the maximum flexion angle (0.83 ± 1.24° vs. 2.11 ± 1.80°, p = 0.037) of the subtalar joint significantly increased, and the flexion-extension ROM (6.17 ± 2.21° vs. 7.97 ± 2.52°, p = 0.043) of the subtalar joint significantly increased.Conclusion: This study contributes to the quantitative understanding of the normal function of the talocrural and subtalar joints during high-demand activities. During landing, the main movement of the talocrural joint is extension and abduction, while the subtalar joint mainly performs extension, eversion, and abduction. Under fatigue conditions, the partial ROM of the talocrural and subtalar joints increases.

Background: Chronic stress promotes cancer growth. Antidepressant fluoxetine (FLX) is usually prescribed for cancer patients with comorbid depression. FLX displays inhibition on cancer cell proliferation, however, the in vivo activity has not been investigated.Methods: We explored the antitumor effect of FLX in subcutaneous transplanted lung cancer cells in a tumor-bearing mouse model. Fifty-six C57BL/6 mice were randomly divided into group A (blank control), group B (tumor-bearing control), group C (tumor-bearing + FLX), group D (CUMS control), group E (CUMS + FLX), group F (tumor-bearing + CUMS), and group G (tumor-bearing + CUMS + FLX). 5-HT, tryptophane (Trp), kynurenine, IFN-γ, TNF-α, IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-17A levels were measured by ELISA. T helper (Th), cytotoxic T (Tc) and regulatory T cells (Tregs) subtype were measured by flow cytometry. The antitumor effects of FLX were evaluated by tumor weight. The expression of kynurenine pathway related genes TDO, IDO1, IDO2, and apoptosis-related genes caspase1, 3, 4, 5, 7, 12 in tumor tissues were measured by western blotting and qRT-PCR. A549 cells were exposed with FLX (15 μmol/L) and its effect on cell proliferation, migration, and clonal formation were detected. Kynurenine pathway and apoptosis related gene expression were also measured.Results:In vivo, chronic stress promoted tumor growth in C57BL/6 mice. FLX administration not only significantly reversed chronic unpredictable mild stress (CUMS)-induced reduction of 5-HT and Trp, increment of kynurenine, but increased CD4+ Th and CD8+ Tc cells, and reduced CD25+ FOXP3+ Tregs. FLX promoted Th to differentiate into Th1 cells and increased IL-2 and IFN-γ, meanwhile inhibited Th differentiate into Th2 and Th17 cells and decreased the concentrations of IL-4, IL-6, IL-10, and IL-17A. Chronic stress obviously up-regulated IDO1 and IDO2 expression, down-regulated caspase 4, 7, and 12 expression, meanwhile FLX administration reversed this regulation. However, there was no significant change in TDO, caspase 1, 3, 5. Similarly, in vitro, FLX administration significantly inhibited the proliferation, migration, and clonal formation of A549 cells and induced cell apoptosis. FLX administration down-regulated the expression of IDO1, IDO2, and up-regulated caspase 4, 5, and 7.Conclusion: Fluoxetine administration could inhibit tumor growth. The inhibition might be via suppressing kynurenine pathway and enhancing cellular immunity.