The main difference between the two alleles resides in a tract of b-satellite repeats present in 4qA but not 4qB. This difference may bear consequences either in the predisposition to deletions occurring within the D4Z4 repeat array or in the pathological consequences thereof. Another surprising observation was that, in both normal and FSHD cells, the D4Z4 marker interacted only with its related sequence DUX4c among the various segments tested. No interactions were detected with the promoter regions of ANT1, FRG1 or FRG2. In accordance, the hypothesis of a transcriptional regulation through a direct contact of the D4Z4 array with the promoters of these three genes appears unlikely. DUX4 and DUX4c are two genes that have been shown to be transcribed within the D4Z4 repeats. Thus, our results suggest that the D4Z4 enhancer, within the D4Z4 repeat array, may directly regulate the transcription of the DUX4 and DUX4c genes. We then found that DUX4c crosslinked with the FRG1 and FRG2 promoter regions in both normal and FSHD myoblasts. We therefore postulate that DUX4c plays a key role in the three-dimensional organization of the locus. Further studies are needed to elucidate the underlying mechanisms linking complement activation on platelets to cardiovascular disease. Xenotropic murine leukemia virus-related virus was first identified through microarray analysis of human prostate cancer samples from patients with an inherited defect in RNASEL, a downstream effector of the antiviral interferon defense pathway.However, a protective role of astrocytes after ischemia through multiple mechanisms has previously been posited. The presence of reactive astrocytes in the animals receiving only the preconditioning stimulus could be explained by the role of these cells in reducing excess glutamate in the brain and so limiting excitotoxic cell death.