Locomotion recovery after a spinal cord injury (SCI) includes axon regeneration, myelin preservation and increased plasticity in propriospinal and descending spinal circuitries. The combined effects of tamoxifen and exercise after a SCI were analyzed in this study to determine whether the combination of both treatments induces the best outcome in locomotion recovery. In this study, the penetrating injury was provoked by a sharp projectile that penetrates through right dorsal and ventral portions of the T13-L1 spinal segments, affecting propriospinal and descending/ascending tracts. Intraperitoneal application of Tamoxifen and a treadmill exercise protocol, as rehabilitation therapies, separately or combined, were used. To evaluate the functional recovery, angular patterns of the hip, knee and ankle joints as well as the leg pendulum-like movement (PLM) were measured during the unrestricted gait of treated and untreated (UT) animals, previously and after the traumatic injury (15 and 30days post-injury (dpi)). A pattern (curve) comparison analysis was made by using a locally designed Matlab script that determines the Frechet dissimilarity. The SCI magnitude was assessed by qualitative and quantitative histological analysis of the injury site 30days after SCI. Our results showed that all treated groups had an improvement in hindlimbs kinematics compared to the UT group, which showed a poor gait locomotion recovery throughout the rehabilitation period. The group with the combined treatment (tamoxifen+exercise (TE)) presented the best outcome. In conclusion, tamoxifen and treadmill exercise treatments are complementary therapies for the functional recovery of gait locomotion in hemi-spinalized rats.
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http://dx.doi.org/10.1016/j.neuroscience.2016.07.023 | DOI Listing |
J Orthop Res
January 2025
Department of Biomedical Engineering, Columbia University, New York, New York, USA.
Enthesitis, or inflammation specific to sites in the body where tendon inserts into bone, can arise in isolated joints from overuse or in multiple joints as a complication of an autoimmune condition such as psoriatic arthritis or spondyloarthritis. However, the pathogenesis of enthesitis is not well understood, so treatment strategies are limited. A clinically relevant animal model of enthesitis would allow investigators to determine mechanisms driving the disease and evaluate novel therapies.
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October 2024
Department of Animal Sciences, Purdue University, West Lafayette, Indiana, USA.
Skelet Muscle
June 2024
Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Gronostajowa 7, 30-387, Kraków, Poland.
Background: Adult muscle-resident myogenic stem cells, satellite cells (SCs), that play non-redundant role in muscle regeneration, are intrinsically impaired in Duchenne muscular dystrophy (DMD). Previously we revealed that dystrophic SCs express low level of anti-inflammatory and anti-oxidative heme oxygenase-1 (HO-1, HMOX1). Here we assess whether targeted induction of HMOX1 affect SC function and alleviates hallmark symptoms of DMD.
View Article and Find Full Text PDFBiomedicines
August 2023
Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, 2-26-1 Muraoka-Higashi, Fujisawa-shi, Kanagawa 251-8555, Japan.
Facioscapulohumeral muscular dystrophy (FSHD), one of the most common muscular dystrophies, is caused by an abnormal expression of the DUX4 gene in skeletal muscles, resulting in muscle weakness. In this study, we investigated MT-DUX4-ASO, a novel gapmer antisense oligonucleotide (ASO). MT-DUX4-ASO decreased the expression of DUX4 and its target genes in FSHD patient-derived myoblasts.
View Article and Find Full Text PDFFunction (Oxf)
December 2022
William Harvey Heart Centre, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
We aimed to determine the pathophysiological impact of heart rate (HR) slowing on cardiac function. We have recently developed a murine model in which it is possible to conditionally delete the stimulatory heterotrimeric G-protein (Gα) in the sinoatrial (SA) node after the addition of tamoxifen using cre-loxP technology. The addition of tamoxifen leads to bradycardia.
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