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Neuromuscular Disorders : NMD|September 1, 1994
Evidence of two mechanisms of prostaglandin release in an in vitro model of muscle damage. Possible therapeutic implicationsR Majumdar, V A Cwik, M H BrookeNeurology|November 1, 1989
Two dissimilar brothers with Becker's dystrophy have an identical genetic defectR Medori, M H Brooke, R H WaterstonNeurology|February 1, 1986
Inosine monophosphate production is proportional to muscle force in vitroM H Brooke, R Choksi, K K KaiserJournal of Neurology, Neurosurgery, and Psychiatry|June 1, 1982
Forearm exercise increases plasma hypoxanthineV H Patterson, K K Kaiser, M H BrookeNeurology|January 1, 1985
Defective [U-14 C] palmitic acid oxidation in Duchenne muscular dystrophyJ E Carroll, B J Norris, M H BrookeNeurology|June 1, 1983
Exercising muscle does not produce hypoxanthine in adenylate deaminase deficiencyV H Patterson, K K Kaiser, M H BrookeNeurology|November 1, 1980
Endurance exercise training in a patient with central core diseaseJ M Hagberg, J E Carroll, M H BrookeMuscle & Nerve|March 1, 1983
Hypoxanthine and Mcardle disease: a clue to metabolic stress in the working forearmM H Brooke, V H Patterson, K K KaiserActa Physiologica Scandinavica|November 1, 1993
Relationship of oxypurine release to contractile failure in dinitrophenol-treated rat skeletal muscleR Majumdar, V A Cwik, G Solonynko, et al.Pageof 7