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Muscle and bone plasticity after spinal cord injury: review of adaptations to disuse and to electrical muscle stimulation

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TLDR
The paralyzed musculoskeletal system retains a remarkable degree of plasticity after spinal cord injury, and physiological levels of electrically induced muscular loading hold promise for preventing post-SCI BMD decline.
Abstract
The paralyzed musculoskeletal system retains a remarkable degree of plasticity after spinal cord injury (SCI). In response to reduced activity, muscle atrophies and shifts toward a fast-fatigable phenotype arising from numerous changes in histochemistry and metabolic enzymes. The loss of routine gravitational and muscular loads removes a critical stimulus for maintenance of bone mineral density (BMD), precipitating neurogenic osteoporosis in paralyzed limbs. The primary adaptations of bone to reduced use are demineralization of epiphyses and thinning of the diaphyseal cortical wall. Electrical stimulation of paralyzed muscle markedly reduces deleterious post-SCI adaptations. Recent studies demonstrate that physiological levels of electrically induced muscular loading hold promise for preventing post-SCI BMD decline. Rehabilitation specialists will be challenged to develop strategies to prevent or reverse musculoskeletal deterioration in anticipation of a future cure for SCI. Quantifying the precise dose of stress needed to efficiently induce a therapeutic effect on bone will be paramount to the advancement of rehabilitation strategies.

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Neuromuscular electrical stimulation: implications of the electrically evoked sensory volley

TL;DR: A goal of this work is to identify the best way to utilize the electrically evoked sensory volley generated during NMES to exploit mechanisms inherent to the neuromuscular system and enhance neuromoscular function for rehabilitation.
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Bone and muscle loss after spinal cord injury: organ interactions

TL;DR: Adiposity and marrow fat are increased after SCI with intriguing, though poorly understood, implications for the function of skeletal muscle and bone cells.
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Acute complications of spinal cord injuries

TL;DR: An overview of acute complications of spinal cord injury (SCI) is given to give an overview of possible complications during the acute phase because they may be life threatening and/ or may lead to prolonged rehabilitation.
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Multiple organ dysfunction and systemic inflammation after spinal cord injury: a complex relationship

TL;DR: Current evidence demonstrating the relevance of inflammatory conditions and immune suppression in several complications frequently seen following SCI are summarized and the potential pathways by which inflammatory and immune cues contribute to multiple organ failure and dysfunction are highlighted.
References
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Bone “mass” and the “mechanostat”: A proposal

TL;DR: The observed fit of bone mass to a healthy animal's typical mechanical usage indicates some mechanism or mechanisms monitor that usage and control the three longitudinal growth, bone modeling, and BMU‐based remodeling activities that directly determine bone mass.

Report of the Task Group on Reference Man

W S Snyder
TL;DR: As this report of the task group on reference man, it will really give you the good idea to be successful.
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GDNF: a potent survival factor for motoneurons present in peripheral nerve and muscle

TL;DR: Glial cell line-derived neurotrophic factor (GDNF), originally identified as a trophic factor specific for dopaminergic neurons, was found to be 75-fold more potent than the neurotrophins in supporting the survival of purified embryonic rat motoneurons in culture and to be a good candidate for treatment of motoneuron disease.
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Bone's mechanostat: A 2003 update

TL;DR: The mechanostat hypothesis predicts 32 things that occur, including the gross anatomical bone abnormalities in osteogenesis imperfecta; it distinguishes postnatal situations from baseline conditions at birth, and it provides functional definitions of mechanical bone competence, bone quality, osteopenias, and osteoporoses.
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