A platform for in silico modeling of physiological systems II. CellML compatibility and other extended capabilities.

The number of biological models published in peer reviewed journals and complexity of each of those models are rapidly increasing, making it difficult to reproduce simulation results of the published models and to reuse the models by third persons. This paper is a continuation of our previous report on a software platform development as a solution to such difficulties. We describe progresses of our development.

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.

A platform for in silico modeling of physiological systems.

This paper describes our challenge of developing base systems necessary and useful for a physiome typed platform for physiological modeling and simulation across multiple scales of time and size through diverse hierarchies of living organisms. Our base systems include a CellML compatible standardized description of structure and dynamic equations (rules for time evolution) of biological organisms in general. A database that can deal with the standardized description and APIs for large scale model constructions and their simulations are also considered.