Publications by authors named "G Sarah Power"

Rate of torque development (RTD) measures how rapidly one can generate torque and is crucial for balance and athletic performance. Fast RTD depends on the rapid recruitment of high threshold motor units (MUs). Cutaneous electrical stimulation has been shown to alter MU excitability, favoring high threshold MUs via reduced recruitment thresholds.

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The Lim Kinase (LIMK) family of serine/threonine kinases is comprised of LIMK1 and LIMK2, which are central regulators of cytoskeletal dynamics via their well-characterized roles in promoting actin polymerization and destabilizing the cellular microtubular network. The LIMKs have been demonstrated to modulate several fundamental physiological processes, including cell cycle progression, cell motility and migration, and cell differentiation. These processes play important roles in maintaining cardiovascular health.

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Introduction: The menopausal decline in ovarian estrogen production is thought to increase the risk of Alzheimer's disease; however, this link requires further investigation. The chronological development of this connection is not well defined because of the lack of animal models that recapitulate the time course of menopause. This study characterized the cognitive and neuronal effects of the 4-vinylcyclohexene diepoxide (VCD) model of ovarian failure in female mice and assessed whether high-intensity interval training (HIIT) would attenuate impairments.

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Residual force enhancement (rFE) and residual force depression (rFD) are history-dependent properties of muscle which refer to increased and decreased isometric force following a lengthening or shortening contraction, respectively. The history dependence of force is greater in older than in younger human adults when assessed at the joint level. However, it is unclear whether this amplification of the history dependence of force in old age is owing to cellular mechanisms or is a consequence of age-related remodelling of muscle architecture.

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Article Synopsis
  • Endothelial dysfunction in type 2 diabetes (T2D) may be caused by stiffening of cell structures, possibly linked to polymerization of filamentous actin (F-actin) and its regulation by the protein cofilin.
  • Oxidative stress in endothelial cells from T2D patients and diabetic mice leads to increased F-actin and cell stiffness, with reactive oxygen species promoting F-actin formation and inactivating cofilin.
  • Genetic silencing or inhibiting LIM kinase 1, which inactivates cofilin, can decrease F-actin levels and reduce cell stiffness, suggesting a novel mechanism for endothelial stiffening in T2D.
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