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sarcopenia/feber

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This study aimed to evaluate the association of sarcopenia and Clinical Outcomes with esophageal cancer under neoadjuvant chemoradiotherapy (CRT).A retrospective study assessing patients with esophageal cancer who underwent CRT between 2001 and 2014 was

Increased store-operated Ca2+ entry in skeletal muscle with reduced calsequestrin-1 expression.

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Store-operated Ca(2+) entry (SOCE) contributes to Ca(2+) handling in normal skeletal muscle function, as well as the progression of muscular dystrophy and sarcopenia, yet the mechanisms underlying the change in SOCE in these states remain unclear. Previously we showed that calsequestrin-1 (CSQ1)

Skeletal Muscle Cell Behavior After Physical Agent Treatments.

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Apoptosis is essential for skeletal muscle development and homeostasis. It has been frequently involved in several muscle myopathies and sarcopenia, as well as in denervation, in disuse and acute strenuous or eccentric physical exercise. In this work skeletal muscle cell death, induced in vitro by a
Prostaglandin E(2) (PGE(2)), a prostanoid synthesized from arachidonic acid via the cyclooxygenase pathway, is a modulator of physiological responses including inflammation, fever, and muscle regeneration. Several patents have been filed that are related to PGE(2), one of them being directly related
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