The authors consider a cellular CR network with base and terminal stations, where the interference between the SUs are not considered.
Determination of total cellular Cr by graphite furnace atomic absorption spectroscopy (GF-AAS) was based on a previously described procedure.
Cellular Cr was extracted with hot nitric acid and quantified by GF-AAS (AAnalyst 600 Atomic Absorption Spectrometer; PerkinElmer).
This rise in [Cr]i when Txnip mRNA levels were blunted by 50% confirms the role of Txnip as a negative regulator of cellular Cr entry.
Mice with myocardial CrT overexpression (CrT-OE) have elevated levels of cellular Cr in the heart, as previously reported (42, 29).
Further investigations of the molecular mechanisms of this interaction are merited, e.g., via redox signaling, posttranslational modification, or intracellular translocation of the Cr transporter, with a view to identifying new approaches for pharmacological control of cellular Cr homeostasis.
When Txnip was knocked down under basal conditions, we observed a reduction in cellular Cr uptake, suggesting that a certain level of Txnip expression is necessary to maintain normal CrT activity, in contrast to high levels of expression being associated with CrT inhibition.
At the cellular level, CR treatment is believed to enhance resistance to various forms of stress at least in part via the upregulation of sirtuins [ 38, 52– 52].
While the beneficial effects of CR on whole-body metabolism, including improved insulin and glucose profiles, have been described for decades, recent research has revealed that, on a cellular level, CR affects the same molecular pathways as current biological agents proposed for targeting cancer metabolism.
Though many applications of CR have been proposed for wireless mesh and in ad hoc and cellular networks, employing CR in vehicular (CRV) environments is a relatively novel research subject and some works in that direction have started to appear recently [28 35].
