Abstract
In the field of computational biology, in order to simulate multiscale biological systems, the Cellular Potts Model (CPM) has been used, which determines the actions that simulated cells can perform by determining a hamiltonian of energy that takes into account the influence that neighboring cells exert, under a wide range of parameters. There are some proposals in the literature that parallelize the CPM; in all cases, either lock-based techniques or other techniques that require large amounts of information to be disseminated among parallel tasks are used to preserve data coherence. In both cases, computational performance is limited. This work proposes an alternative approach for the parallelization of the model that uses transactional memory to maintain the coherence of the information. A Java implementation has been applied to the simulation of the ductal adenocarcinoma of breast in situ (DCIS). Times and speedups of the simulated execution of the model on the cluster of our university are analyzed. The results show a good speedup.
Highlights
The human breast is a tissue with a high architectural complexity, where the parenchyma branches out into networks of ducs formed in a cross-section(Figure 1) by an endoepithelium of luminal cells; myoepithelial cell rodeate that endoepithelium and a basement membrane subsume all the structure into the glandular stroma
In order to speed up the simulation of the Cellular Potts Model (CPM) model, we hava carried out an implementation that manages in parallel the tissue domain ζ in which, unlike other proposals [1], [5], [6], [7], [8], [9], the data structure is not divided between processing nodes, since this forces the propagation of information between threads that are responsible for bordering substructures, when a cell crosses the border between nodes, as a consequence of a mitosis or the extension of a pseudopod
To contrast the validity of the parallel implementation of the CPM model, we have developed two different experiments that simulate two different varieties of ductal carcinoma in situ (DCIS), and compared the outputs resulting from the execution with real histological slices:
Summary
The human breast is a tissue with a high architectural complexity, where the parenchyma branches out into networks of ducs formed in a cross-section(Figure 1) by an endoepithelium of luminal cells; myoepithelial cell rodeate that endoepithelium and a basement membrane subsume all the structure into the glandular stroma. The exchange of signals between the cells and their local microenvironment maintains the structure and function of the mammary epithelium The alteration of this signalling becomes, in a first phase, a ductal carcinoma in situ (DCIS), and in a second, an infiltrating ductal carcinoma (Figure 1). If DCIS is not treated, the infiltrating transformation occurs, which breaks the basement membrane and invades the glandular stroma. At present, it is not yet entirely clear how DCIS transforms into an infiltrating carcinoma, the presence of mutations in the BRCA1, BRCA2, PTEN and PT53 genes is a known cause.
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