Effect of clofibric acid on desmin and vimentin contents in rat myocardiocytes.

The aim of this experimental study was to analyze in vitro effects of clofibric acid on vimentin and desmin contents in rat myocardiocytes, which was carried out in primary myocardiocyte cells that were treated only with clofibric acid at 0.1 mM. The measurement of vimentin and desmin were done by Western blotting and densitometry.

[Relations between delayed diagnosis and forms of onset in Duchenne muscular dystrophy].

Duchenne Muscular Dystrophy (DMD) is usually diagnosed several years after the onset of symptoms. The relatives of the patients with DMD frequently consult family physicians when they notice the first symptom. The purpose of this study was to determine the cause that influence the delayed diagnosis of DMD.

Molecular changes in erythrocyte membranes induced by long-term administration of clofibrate.

It has been reported that an enantiomer ((S)-(-)-4) of clofibric acid, and the racemate, can block the chloride conductance of skeletal muscle membrane. It has also been reported that several analogs of clofibric acid inhibit the HCO3(-)-Cl- exchange of erythrocytes. Since the two effects are probably similar biophysical membrane phenomena, the possibility of a common molecular mechanism arises.

Abscence of changes in the protein profile of erythrocyte membranes in Duchenne patients.

Numerous authors have suggested an impairement in protein synthesis as a possible cause for the failure in growth with degeneration of the skeletal muscles protein content present in Duchenne muscular dystrophy (DMD). Others have supported the use of in vitro erythrocyte membranes as a model of the sarcolemmal changes in DMD. Very recently, in vitro decrease in protein synthesis of ribosomal proteins of skeletal muscle cells, fibroblasts and erythrocytes of DMD patients have been reported.