Consequently, it is plausible that various etiologies of AKI may also affect hepatic metabolism differently, as illustrated for diltiazem in Table 2. Furthermore, as shown in Table 3, not all hepatic cytochrome P450 (CYP) enzymes are affected by AKI, and the extent of the effect on hepatic clearance via CYP may depend on the mechanism of experimental kidney injury.
This overview is extremely speculative, but we hope it might serve to highlight possible regulatory mechanisms worthy of experimental investigation.
Our paper briefly discusses the underlying mechanisms of the experimental results.
To unravel the relative importance of these mechanisms, a range of experimental tools have been developed to quantify the network's mechanical non-linearity in systematic ways and relate the material micro-structure (network density and morphology, fiber behavior) to the mesoscopic stress-strain laws.
In an effort to understand the noise-source mechanisms, a suite of experimental measurements has been performed on a two-dimensional multi-element MD-30P30N aincludingncluding PIV, steady and unsteady surface pressure, and phased microphone array measurements.
This implies either direct AR-mediated regulation of cell proliferation or perhaps similar mechanisms involving induction of experimental tumors.
Bisphosphonates exert their anti-osteolytic effects by inhibiting osteoclast activity, and this mechanism is postulated to be the mechanism for prevention of experimental metastases [ 10, 11].
Contrast mechanism of the experimental results are backed up by Monte Carlo simulations based on the sphere cylinder birefringence model, which reveal the relationship between the pathological features in the cancerous tissues at the cellular level and the polarization parameters.
Therefore, the approach is useful both for a mechanism-based evaluation of experimental results and as a tool to explore transformation pathways in scenarios for which position-specific isotope data are not yet available.
