On calcium-buffer dynamics within the excess buffer regime.

In intracellular calcium signaling, calcium buffers has been recognized for their role in reshaping and localizing the calcium concentration profile in the vicinity of the channel, as well as reducing the effective diffusion of free calcium. In the presence of an excess of endogenous or exogenous buffers, linearization of the reaction-diffusion system describing the calcium-buffer dynamics has been instrumental in understanding the extent of the microdomain formation and in quantifying the apparent diffusion of the free calcium. In these linearized models, the conclusions are usually drawn from the steady-state solutions upon the opening of the channel.

A task-specific validation of homogeneous non-linear optimisation approaches.

In biomechanics, musculoskeletal models are typically redundant. This situation is referred to as the distribution problem. Often, static, non-linear optimisation methods of the form "min: phi(f) subject to mechanical and muscular constraints" have been used to extract a unique set of muscle forces.

Microstructure-based Monte Carlo simulation of Ca2+ dynamics evoking cardiac calcium channel inactivation.

Ca(2+) dynamics underlying cardiac excitation-contraction coupling are essential for heart functions. In this study, we constructed microstructure-based models of Ca(2+) dynamics to simulate Ca(2+) influx through individual L-type Calcium channels (LCCs), an effective Ca(2+) diffusion within the cytoplasmic space and in the dyadic space, and the experimentally observed calcium-dependent inactivation (CDI) of the LCCs induced by local and global Ca(2+) sensing. The models consisted of LCCs with distal and proximal Ca(2+) (Calmodulin-Ca(2+) complex) binding sites.

Antagonistic activity of one-joint muscles in three-dimensions using non-linear optimisation.

Non-linear optimisation, such as the type presented by R.D. Crowninshield and R.