Effect of Aerobic Physical Exercise in an Animal Model of Duchenne Muscular Dystrophy.

Duchenne muscular dystrophy (DMD) is a condition caused by an amendment to the X chromosome, inherited as a recessive trait, and affects 1:3500 live births, especially males. Low-intensity exercise is known to decrease certain parameters associated with muscular degeneration in animal models of progressive muscular dystrophies. In the present study, 28-day-old male mdx and wild-type (wild) mice were used.

Early fragmentation of polyester urethane sheet neither causes persistent oxidative stress nor alters the outcome of normal tissue healing in rat skin.

Silicone breast implant is associated with complications inherent to the surgical procedure. Prosthesis coating with polyurethane, however, commonly reduces the incidence of such complications. In this paper, the authors evaluated the inflammatory histomorphometric profile and oxidative damage associated to the implant of polyester urethane sheets.

Activity of Krebs cycle enzymes in mdx mice.

Introduction: Duchenne muscular dystrophy (DMD) is a degenerative disease of skeletal, respiratory, and cardiac muscles caused by defects in the dystrophin gene. More recently, brain involvement has been verified. Mitochondrial dysfunction and oxidative stress may underlie the pathophysiology of DMD.

Neurotrophins, cytokines, oxidative parameters and funcionality in Progressive Muscular Dystrophies.

We investigated the levels of brain derived-neurotrophic factor (BDNF), cytokines and oxidative parameters in serum and tried to correlate them with the age and functionality of patients with Progressive Muscle Dystrophies (PMD). The patients were separated into six groups (case and controls pared by age and gender), as follows: Duchenne Muscular Dystrophy (DMD); Steinert Myotonic Dystrophy (SMD); and Limb-girdle Muscular Dystrophy type-2A (LGMD2A). DMD patients (± 17.