Susan V. Brooks

Modular flexibility of dystrophin: implications for gene therapy of Duchenne muscular dystrophy.

Muscle inflammatory cells after passive stretches, isometric contractions, and lengthening contractions.

Functional correction of adult mdx mouse muscle using gutted adenoviral vectors expressing full-length dystrophin.

Passive stretches protect skeletal muscle of adult and old mice from lengthening contraction-induced injury.

Current topics for teaching skeletal muscle physiology.

Susceptibility to sarcomere injury induced by single stretches of maximally activated muscles of mdx mice.

Muscles of mice deficient in alpha-sarcoglycan maintain large masses and near control force values throughout the life span.

Activation of Akt as a potential mediator of adaptations that reduce muscle injury.

Protection from contraction-induced injury provided to skeletal muscles of young and old mice by passive stretch is not due to a decrease in initial mechanical damage.

Age-related changes in the structure and function of skeletal muscles.

Direct observation of failing fibers in muscles of dystrophic mice provides mechanistic insight into muscular dystrophy.

Neutrophil accumulation following passive stretches contributes to adaptations that reduce contraction-induced skeletal muscle injury in mice.

Force deficits and breakage rates after single lengthening contractions of single fast fibers from unconditioned and conditioned muscles of young and old rats.

Repeated bouts of aerobic exercise lead to reductions in skeletal muscle free radical generation and nuclear factor kappaB activation.

The aging of elite male athletes: age-related changes in performance and skeletal muscle structure and function.

Conditional knockout of Mn-SOD targeted to type IIB skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity.

Inhibition of calpain prevents muscle weakness and disruption of sarcomere structure during hindlimb suspension.

Increased superoxide in vivo accelerates age-associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degeneration.

The age-related failure of adaptive responses to contractile activity in skeletal muscle is mimicked in young mice by deletion of Cu,Zn superoxide dismutase.

Reactive oxygen species on bone mineral density and mechanics in Cu,Zn superoxide dismutase (Sod1) knockout mice.

Decreased specific force and power production of muscle fibers from myostatin-deficient mice are associated with a suppression of protein degradation.

Regional stiffening with aging in tibialis anterior tendons of mice occurs independent of changes in collagen fibril morphology.

Skeletal muscle weakness due to deficiency of CuZn-superoxide dismutase is associated with loss of functional innervation.

Physiological loading of tendons induces scleraxis expression in epitenon fibroblasts.

Neb: a zebrafish model of nemaline myopathy due to nebulin mutation.

Transforming growth factor-beta induces skeletal muscle atrophy and fibrosis through the induction of atrogin-1 and scleraxis.

Oxidative stress and successful antioxidant treatment in models of RYR1-related myopathy.

Rapamycin slows aging in mice.

Weakness of whole muscles in mice deficient in Cu, Zn superoxide dismutase is not explained by defects at the level of the contractile apparatus.

Muscle-specific expression of LARGE restores neuromuscular transmission deficits in dystrophic LARGE(myd) mice.

Age-related changes in structure and extracellular matrix protein expression levels in rat tendons.

Eccentric exercise in aging and diseased skeletal muscle: good or bad?

CuZnSOD gene deletion targeted to skeletal muscle leads to loss of contractile force but does not cause muscle atrophy in adult mice.

Targeted inhibition of TGF-β results in an initial improvement but long term deficit in force production after contraction-induced skeletal muscle injury.

The role of oxidative stress in nervous system aging.

Reactive oxygen species generation is not different during isometric and lengthening contractions of mouse muscle.

Murine Fig4 is dispensable for muscle development but required for muscle function.

Neuron-specific expression of CuZnSOD prevents the loss of muscle mass and function that occurs in homozygous CuZnSOD-knockout mice.

RNAi-mediated Gene Silencing of Mutant Myotilin Improves Myopathy in LGMD1A Mice.

Intrinsic stiffness of extracellular matrix increases with age in skeletal muscles of mice.

Ten weeks of treadmill running decreases stiffness and increases collagen turnover in tendons of old mice.

Age affects the contraction-induced mitochondrial redox response in skeletal muscle.

Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype.