Publications by authors named "Nicoletta Adami"

Objective: To compare the effects of isokinetic (ISO-K) and vibrational-proprioceptive (VIB) trainings on muscle mass and strength.

Methods: In 29 ISO-K- or VIB-trained young athletes we evaluated: force, muscle fiber morphometry, and gene expression of muscle atrophy/hypertrophy cell signaling.

Results: VIB training increased the maximal isometric unilateral leg extension force by 48·1%.

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Background: Spinal cord injury causes muscle wasting and loss of function, which are especially severe after complete and permanent damage to lower motor neurons. In a previous cross-sectional study, long-standing denervated muscles were rescued by home-based functional electrical stimulation (h-bFES) training.

Objective: To confirm results by a 2-year longitudinal prospective study of 25 patients with complete conus/cauda equina lesions.

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Objective: Spinal cord injury (SCI) causes muscle atrophy, which is particularly severe, due to inability to perform tetanic contractions, when lower motor neurons (LMN) are involved. We performed a longitudinal study in 25 Europeans suffering from complete conus cauda syndrome from 0.7 to 8.

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To define the time course and potential effects of electrical stimulation on permanently denervated muscle, we evaluated excitation-contraction coupling (ECC) of rat leg muscles during progression to long-term denervation by ultrastructural analysis, specific binding to dihydropyridine receptors, ryanodine receptor 1 (RYR-1), Ca channels and extrusion Ca pumps, gene transcription and translation of Ca-handling proteins, and in vitro mechanical properties and electrophysiological analyses of sarcolemmal passive properties and L-type Ca current (ICa) parameters. We found that in response to long-term denervation: 1) isolated muscle that is unable to twitch in vitro by electrical stimulation has very small myofibers but may show a slow caffeine contracture; 2) only roughly half of the muscle fibers with "voltage-dependent Ca channel activity" are able to contract; 3) the ECC mechanisms are still present and, in part, functional; 4)ECC-related gene expression is upregulated; and 5) at any time point, there are muscle fibers that are more resistant than others to denervation atrophy and disorganization of the ECC apparatus. These results support the hypothesis that prolonged "resting" [Ca] may drive progression of muscle atrophy to degeneration and that electrical stimulation-induced [Ca] modulation may mimic the lost nerve influence, playing a key role in modifying the gene expression of denervated muscle.

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Contrary to general expectation, in humans, we have recently shown that after complete conus cauda lesion, the lower motoneuron denervated myofibers may survive several years. In adult rats, the sciatectomized muscle progresses in 4-6 months from severe atrophy to a dystrophic stage and undergoes a dramatic weight loss; during this process, myofiber death/regeneration processes maintain a decreasing population of very small, but vital myofibers. At the same time, in vitro electrophysiologic recordings show that denervated fibers can maintain membrane excitability longer than they can retain contractile properties.

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Idiopathic inflammatory myopathies such as polymyositis (PM) and dermatomyositis (DM) are a group of rare autoimmune diseases, characterized by an inflammatory infiltrate within the skeletal muscle and high titer of circulating autoantibodies in the patient's serum. The etiopathogenesis of these diseases is not known and the relationship between the specific muscle involvement and the ubiquitary presence of the targeted antigens is still unclear. The enhanced expression of myositis specific autoantigens in regenerating muscle fibers from biopsies of PM and DM patients compared to normal muscle has been recently demonstrated.

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Objective: Human muscle fibers usually undergo severe atrophy/degeneration as a result of long-term peripheral denervation. However, some biopsies from paraplegic patients suffering complete conus cauda syndrome display the presence of a small percentage of muscle fibers with a very large diameter (big fibers). The objective of the present study is to determine if these big fibers are the result of residual innervation/reinnervation, or if instead they are fibers resistant to atrophy.

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