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Thoracolumbar spine muscle size and composition changes in long-duration space missions.

Life Sci Space Res (Amst)

February 2025

Department of Biomedical Engineering, Center for Injury Biomechanics, Wake Forest University School of Medicine. 575 N. Patterson Avenue, Suite 530. Winston-Salem, NC 27101, USA. Electronic address:

Muscle atrophy occurs with extended exposure to microgravity. This study quantified the overall muscle size, lean muscle area and fat infiltration changes pre- to post-flight that occur in the thoracic and lumbar spine with long-duration spaceflight. Pre- and post-flight magnetic resonance imaging (MRI) scans were obtained from 9 crewmembers on long-duration (≥6 months) International Space Station (ISS) missions.

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Background: Vaginal childbirth is one of the main risk factors for pelvic floor dysfunction. Magnetic resonance imaging (MRI) can facilitate quantitative evaluation of the morphology and function of the pelvic floor in static and dynamic environments. The objective of this study was to investigate the changes in pelvic floor morphology and function in primigravida women before pregnancy (BP) and after vaginal delivery.

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Background: Spinal muscular atrophy (SMA) is caused by reduced expression of survival motor neuron (SMN) protein. Previous studies indicated SMA causes not only lower motor neuron degeneration but also extensive brain involvement. This study aimed to investigate the changes of brain white matter and structural network using diffusion tensor imaging (DTI) in children with type 2 and 3 SMA.

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Unlabelled: Congenital titinopathy has recently emerged as one of the most common congenital muscle disorders.

Objective: To better understand the presentation and clinical needs of the under-characterized extreme end of the congenital titinopathy severity spectrum.

Methods: We comprehensively analyzed the clinical, imaging, pathology, autopsy, and genetic findings in 15 severely affected individuals from 11 families.

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Duchenne muscular dystrophy (DMD) is a severe genetic muscle disease occurring due to mutations of the dystrophin gene. There is no cure for DMD. Using a dystrophinutrophin (DKO-Hom) mouse model, we investigated the PGE2/EP2 pathway in the pathogenesis of dystrophic muscle and its potential as a therapeutic target.

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