We employed the "low-calcium" model of epilepsy in hippocampal slices to investigate the mobilization of these two proteins in CA1 pyramidal neurons.
Since a reduction of Ca2+ is expected to affect the interactions of CaM and Ng, we sought the "low-calcium" model of epilepsy in hippocampal slices (15− 17) to investigate the trafficking of these two proteins in CA1 pyramidal neurons.
In this "low-calcium" model of epilepsy in hippocampal slices, translocation of Ng and CaM from soma to dendrites may contribute to the development of epileptiform activity of CA1 pyramidal neurons.
All analyses were adjusted for age, sex (model 1), BMI, education, smoking, alcohol consumption, physical activity, study centre (model 2) and intake of calcium (model 3).
The mass-action formulation, while expanding the dimension of the P2 calcium model, regularized the mathematical structure.
To address uncertainty in the calcium model parameters, we estimated a family of possible parameter sets using a MOTE technique.
Considering the altered solid liquid equilibrium curve, an accelerated calcium leaching model of pure cement paste in 6 mol/L ammonium nitrate leaching solution was built up in this research.
In order to understand the conformational changes that occur when HsAPC-1 goes from the calcium-bound to the calcium-free state, models of the calcium-free state were generated based on deposited structures.
One model of calcium signaling in growth cone turning proposed that the amplitude of calcium gradients was higher in attractive growth cone turning but lower in repulsion (Wen et al., 2004).
Thanks to the detailed report by Mayer and Hurst [9] on how the secreted PTH is affected by the changes in the calcium level, we have been able to incorporate more precisely the PTH compartment into the difference equation model of calcium levels, making use of the Heaviside step function.
A novel model of calcium silicate hydrate (CSH /resin interface was modeled according to SEM and EDX analyses.
