Does rhythmic arm cycling suppress hyperactive soleus H-reflex amplitude after stroke?
Neural activity related to arm cycling can still access interlimb pathways after stroke and activate spinal control mechanisms leading to suppression of H-reflex amplitudes.
Our data show that MAPK cascades regulate COX-2 gene expression and PGE2 production in LPS-stimulated Mphi through NFkappaB independent pathways. The regulatory mechanism is likely to be mediated through CRE.