Hospitals with excess mortality should be encouraged to initiate further inquiries to reveal or debunk possible presence of suboptimal care. 1 In the literature, comprehensive improvement programmes and experiences have been reported for hospitals identified as outliers.
Although significantly altered gene expression has been reported for these areas, identifying the approximate number of genes expressed, and identifying similar expression patterns across regions, could lead to furthering our understanding of the functional and biological similarities and differences between cortical areas.
Some successes have been reported, for example, in identifying previously undetected risks of new drugs or procedures, but there remain doubts about the wider value of investments in developing and maintaining large-scale incident reporting systems.
An overlap of 70% has been reported for acetylation sites identified from mouse and human liver tissues, whereas the overlap with data from cell lines was only 14% (Zhao et al., 2010).
Unequivocal radiological data have been reported for cup inclination and anteversion, identifying minimal invasive approaches as a potential risk factor for cup malpositioning [ 6– 9].
Biological roles have not been reported for two species that we identified: an unusual sterol derivative and an ether/ester-linked phosphatidic acid (rather than a traditional diester).
In their review of QoL measures in children and adolescents Solans et al. [ 78] reported that acceptable sensitivity to change has been reported for only 10% of the identified generic instruments (CHQ, KIDSCREEN, KINDL and Peds-QL).
Remarkably, similar numbers have been reported for the frequency of ultrastructurally identified myoepithelial cells in breast cancer and for the expression of other markers such as oxytocin receptors, metallothionine, and connexin 43 [ 8, 9, 10, 27].
Chondrogenic differentiation capacity has long been reported for MSC and subsequently Sox9 was identified to be a master regulator of chondrogenic differentiation [ 17– 17].
Similar effects have been reported for other SOX2 mutant proteins previously identified in patients with hypopituitarism and eye defects [ Kelberman et al., 2006, 2008].
