The primary mechanism for clustering of metabolic abnormalities has yet to be elucidated, but insulin resistance or accumulation of visceral fat is believed as an encouraging candidate [ 3, 4].
We and others have demonstrated multiple alterations in chromatin structure arising as a consequence of EtOH exposure, but linking these epigenetic changes to alterations in the developmental program, and ultimately to the acquisition of congenital abnormalities, has yet to be achieved [ 2, 3].
Although a substantial number of gene alterations have been identified, the mechanism by which these abnormalities interact has yet to be elucidated.
To our knowledge, however, this morphologic abnormality has not yet been studied.
Even though we can quantify these abnormalities, a classification system has yet to be developed.
Furthermore, the impact of Spt6 breakdown on the accumulation of epigenetic abnormalities in cancer cells has yet to be evaluated.
Although some of these changes are known to occur in chemically induced tumors of experimental animals, the possible role of chemical carcinogens in the induction of genetic abnormalities in human cancers has yet to be determined.
Finally, the role of structural abnormalities in the development of arrhythmias in BrS has yet to be unraveled.
No convincing, definitive explanation has yet been found for the long persistence of these signal abnormalities.
