RESUMEN
BACKGROUND: Children with spastic hemiplegic cerebral palsy are restricted in their daily activities due to limited active ranges of motion of their involved upper limb, specifically at the elbow. Their impaired muscles are frequently targeted by anti-spastic treatments that reduce muscle tone. But these treatments do not necessarily improve the limb function. There is a lack of comprehensive knowledge of the quantitative relations between muscle activation and joint active ranges of motion. Consequently, the objective of this study is to quantify the impact of muscle activation on the elbow active ranges of motion. METHODS: During voluntary elbow pronation/supination and extension/flexion movements, kinematic and electromyographic measurements were collected from the involved upper limb of 15 children with spastic hemiplegic cerebral palsy (mean age=8.7 years, standard deviation=2.2) and the dominant upper limb of 15 age-matched children who are typically developing. Representative indicators of the muscle activation, such as the muscle co-activation, were extracted from the electromyographic measurements. FINDINGS: Muscle co-activation in the involved upper limb accounted for 78% and 59% of the explained variance of the supination and extension limited active ranges of motion respectively. The agonist and antagonist muscle activations were both longer in the involved upper limb. INTERPRETATIONS: This study succeeded in quantifying the impact of longer antagonist muscle activation on decreased elbow active ranges of motion in children with spastic hemiplegic cerebral palsy. Longer agonist muscle activation suggests that strengthening agonist muscles could increase the extension and supination ranges of motion, which constitutes a perspective of future clinical studies.
Asunto(s)
Parálisis Cerebral/fisiopatología , Codo/fisiopatología , Músculo Esquelético/fisiopatología , Fenómenos Biomecánicos , Niño , Preescolar , Electromiografía , Femenino , Humanos , Masculino , Movimiento/fisiología , Espasticidad Muscular/fisiopatología , Rango del Movimiento Articular/fisiología , Extremidad Superior/fisiopatologíaRESUMEN
Paraoxonase 1 (PON1) is a serum enzyme closely associated with high-density lipoprotein (HDL), which may protect against atherosclerosis by hydrolyzing lipid peroxides and several organophosphorus compounds. The purpose of the present study was to test the hypothesis that lipid peroxidation modifies the activity and protein mass of PON1 in humans and rats. Our findings revealed that the bulk of the activity monitored by the hydrolysis of paraoxon and phenyl acetate was confined to liver intracellular endoplasmic reticulum-derived microsomes and was mostly recovered in circulating HDL3. Confirmation was obtained by the determination of PON1 expression by Western blot. It is noteworthy that PON1 levels were consistently decreased in human sera, HDL, and liver microsomes compared with rat counterparts. Concomitant with iron-ascorbate-mediated lipid peroxidation, there was a decline in PON1 activity and protein in both HDL3 and microsomes, which was attenuated by butylated hydroxytoluene antioxidant treatment. The current data indicate that PON1 localization in microsomes and HDL3 could represent a selective cellular and lipoprotein response to oxidative stress. This was tested by the iron-ascorbate oxygen-radical generating system. It is also proposed that the increased PON1 level may have a function related to the well-known atherosclerosis resistance of rats.