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We began analyzing https://link.springer.com/article/10.1007/s00424-009-0643-5, but it redirected us to https://link.springer.com/article/10.1007/s00424-009-0643-5. The analysis below is for the second page.

Title[redir]:
Differential skeletal muscle gene expression after upper or lower motor neuron transection | Pflügers Archiv - European Journal of Physiology
Description:
Causes of disuse atrophy include loss of upper motor neurons, which occurs in spinal cord injury (SCI) or lower motor neurons (denervation). Whereas denervation quickly results in muscle fibrillations, SCI causes delayed onset of muscle spasticity. To compare the influence of denervation or SCI on muscle atrophy and atrophy-related gene expression, male rats had transection of either the spinal cord or sciatic nerve and were sacrificed 3, 7, or 14 days later. Rates of atrophy increased gradually over the first week after denervation and then were constant. In contrast, atrophy after SCI peaked at 1 week, then declined sharply. The greater atrophy after SCI compared to denervation was preceded by high levels of ubiquitin ligase genes, MAFbx and MuRF1, which then also markedly declined. After denervation, however, expression of these genes remained elevated at lower levels throughout the 2-week time course. Interestingly, expression of the muscle growth factor, IGF-1 was increased at 3 days after denervation when fibrillation also peaks compared to SCI. Expression of IGF-1R, GADD45, myogenin, and Runx1 were also initially increased after denervation or SCI, with later declines in expression levels which correlated less well with rates of atrophy. Thus, there were significant time-dependent differences in muscle atrophy and MAFbx, MuRF1, and IGF-1 expression following SCI or denervation which may result from distinct temporal patterns of spontaneous muscle contractile activity due to injury to upper versus lower motor neurons.

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Fitness & Wellness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,420 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We don't see any clear sign of profit-making.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Doi.org might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

google, scholar, pubmed, cas, muscle, article, atrophy, skeletal, expression, spinal, denervation, physiol, cord, gene, sci, cell, ubiquitin, zhao, growth, injury, motor, murf, factor, zhang, bauman, access, rat, denervated, biol, function, cardozo, nerve, ligase, effects, metab, usa, privacy, cookies, content, journal, lower, zeman, pan, genes, igf, protein, testosterone, glass, ligases, goldberg,

Topics {✒️}

phosphatidylinositol 3-kinase/akt/mammalian target month download article/chapter nerve activity-independent regulation atrophy-related ubiquitin ligases atrophy-related gene expression significant time-dependent differences weightlessness-induced musculoskeletal losses guinea-pig skeletal muscle dexamethasone-treated skeletal muscle lower motor neurons activity-unrelated neural control pituitary-testicular hormone axis beta 2-receptor agonist degrades cardiac troponin spinal cord injury upper motor neurons real-time quantitative pcr testosterone dose–response relationships ikkbeta/nf-kappab activation nf-kappab mediated escape stress induced proteolysis body protein kinetics suppressing protein breakdown satellite cells full article pdf skeletal muscle atrophy pi3k/akt/mtor ubiquitin ligases required gene expression profile testosterone deficiency european economic area multiple ubiquitin ligases privacy choices/manage cookies skeletal muscle plasticity skeletal muscle mass ubiquitin ligase genes muscle fibre loss burn-induced increase muscle denervation atrophy skeletal muscle igf spinal shock revisited united spinal association related subjects muscle growth factor stimulates muscle growth slow skeletal muscle hyatt jp severe muscle wasting runx1 prevents wasting denervated soleus muscle

Schema {🗺️}

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         headline:Differential skeletal muscle gene expression after upper or lower motor neuron transection
         description:Causes of disuse atrophy include loss of upper motor neurons, which occurs in spinal cord injury (SCI) or lower motor neurons (denervation). Whereas denervation quickly results in muscle fibrillations, SCI causes delayed onset of muscle spasticity. To compare the influence of denervation or SCI on muscle atrophy and atrophy-related gene expression, male rats had transection of either the spinal cord or sciatic nerve and were sacrificed 3, 7, or 14 days later. Rates of atrophy increased gradually over the first week after denervation and then were constant. In contrast, atrophy after SCI peaked at 1 week, then declined sharply. The greater atrophy after SCI compared to denervation was preceded by high levels of ubiquitin ligase genes, MAFbx and MuRF1, which then also markedly declined. After denervation, however, expression of these genes remained elevated at lower levels throughout the 2-week time course. Interestingly, expression of the muscle growth factor, IGF-1 was increased at 3 days after denervation when fibrillation also peaks compared to SCI. Expression of IGF-1R, GADD45, myogenin, and Runx1 were also initially increased after denervation or SCI, with later declines in expression levels which correlated less well with rates of atrophy. Thus, there were significant time-dependent differences in muscle atrophy and MAFbx, MuRF1, and IGF-1 expression following SCI or denervation which may result from distinct temporal patterns of spontaneous muscle contractile activity due to injury to upper versus lower motor neurons.
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      headline:Differential skeletal muscle gene expression after upper or lower motor neuron transection
      description:Causes of disuse atrophy include loss of upper motor neurons, which occurs in spinal cord injury (SCI) or lower motor neurons (denervation). Whereas denervation quickly results in muscle fibrillations, SCI causes delayed onset of muscle spasticity. To compare the influence of denervation or SCI on muscle atrophy and atrophy-related gene expression, male rats had transection of either the spinal cord or sciatic nerve and were sacrificed 3, 7, or 14 days later. Rates of atrophy increased gradually over the first week after denervation and then were constant. In contrast, atrophy after SCI peaked at 1 week, then declined sharply. The greater atrophy after SCI compared to denervation was preceded by high levels of ubiquitin ligase genes, MAFbx and MuRF1, which then also markedly declined. After denervation, however, expression of these genes remained elevated at lower levels throughout the 2-week time course. Interestingly, expression of the muscle growth factor, IGF-1 was increased at 3 days after denervation when fibrillation also peaks compared to SCI. Expression of IGF-1R, GADD45, myogenin, and Runx1 were also initially increased after denervation or SCI, with later declines in expression levels which correlated less well with rates of atrophy. Thus, there were significant time-dependent differences in muscle atrophy and MAFbx, MuRF1, and IGF-1 expression following SCI or denervation which may result from distinct temporal patterns of spontaneous muscle contractile activity due to injury to upper versus lower motor neurons.
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         Muscle atrophy
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         Cell Biology
         Receptors
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      name:Department of Medicine, Mount Sinai School of Medicine, New York, USA
      name:Department of Veterans Affairs, Center of Excellence for the Medical Consequences of SCI, James J. Peters VA Medical Center, New York, USA
      name:Department of Veterans Affairs, Center of Excellence for the Medical Consequences of SCI, James J. Peters VA Medical Center, New York, USA
      name:Department of Cell Biology and Anatomy, New York Medical College, New York, USA
      name:Department of Veterans Affairs, Center of Excellence for the Medical Consequences of SCI, James J. Peters VA Medical Center, New York, USA
      name:Department of Veterans Affairs, Center of Excellence for the Medical Consequences of SCI, James J. Peters VA Medical Center, New York, USA
      name:Department of Veterans Affairs, Center of Excellence for the Medical Consequences of SCI, James J. Peters VA Medical Center, New York, USA
      name:Department of Medicine, Mount Sinai School of Medicine, New York, USA
      name:Department of Rehabilitation Medicine, Mount Sinai School of Medicine, New York, USA
      name:Department of Veterans Affairs, Center of Excellence for the Medical Consequences of SCI, James J. Peters VA Medical Center, New York, USA
      name:Department of Medicine, Mount Sinai School of Medicine, New York, USA
      name:Department of Rehabilitation Medicine, Mount Sinai School of Medicine, New York, USA
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