For these organs, common, possibly also endogenous, cancer risk factors could be postulated as contributing to the observed mutation spectrum.
It is worthwhile noticing that preoperative anxiety disorders, like post-traumatic stress disorder, were not associated with postoperative delirium in any of the previous studies [ 3], although surgery-related stress is postulated as contributing to delirium in the article by Mu and colleagues and in other articles.
Immune system dysfunction has been postulated as a contributing factor in the pathophysiology of BPD, as imbalances of "pro-inflammatory" and "anti-inflammatory" cytokines and impairment in the transition from the innate immune response mediated by neutrophils to the adaptive immune response mediated by T lymphocytes has been described [ 36].
RCAN1 is widely expressed in brain, both during development and in the adult and it has been postulated as a good candidate to contribute to mental disability in DS [5], [6], [7].
Abnormal development or migration of neural crest cells, possibly due to an underlying genetic defect, has been postulated as a mechanism that could contribute to both conditions [ 1, 11, 13, 28].
Mutations in the cell adhesion molecule CRELD1 (encoded by the CRELD1 gene on Hsa3) have been postulated as a risk factor for AVSD in the euploid population, and contribute to AVSD in DS (Maslen, 2004).
Although prevention of motoneuronal degeneration has been postulated as the primary target for a cure, accumulating evidence suggests that microglial accumulation contributes to disease progression.
Hepatic mitochondrial dysfunction has been postulated as an explanation for the development of LA in SS, although extra-hepatic mechanisms also contribute [8 16].
Since the core antigen has been postulated as target of cell mediated and humoral immunity, it is tempting to speculate, that core mutations contribute to a more severe course of the disease [ 12- 15].
