The multivariate model that takes into account the interactions among vitamin D deficiency, presence/absence of CAC at 3-year visit, and VDR M1T genotype is shown in Table 3. Vitamin D deficiency predicted development of CAC among subjects free of CAC at the 3-year visit.
The development of CAC is a process which increases risk for future acute coronary events, [ 5] and CAC progression is a powerful predictor of mortality even among persons who already have CAC present; [ 6] However, calcification of a plaque itself does not promote plaque rupture [ 19].
The recent work from our laboratory characterized aldo-keto reductase 1B10 (asR1B10) as a novel risky factor of UC and CAC [ 2]. Almost all CRCs progress from a dysplastic precursor lesion, but the development of CAC is different in several important aspects from sporadic CRC [ 3].
These results suggest that the additive or synergistic actions of constitutive medicinal herbs contribute to the suppressive effect of daikenchuto on the development of CAC.
Using KampoDB, "Wnt signaling pathway", "T cell receptor signaling pathway", and "TNF signaling pathway" were predicted as candidates for target pathways associated with the underlying mechanisms of daikenchuto that contribute to the development of CAC.
Clearly, additional investigation of the impact of bacteria on development of CAC is needed.
