Totally Corrective Multiclass Boosting with Binary Weak Learners

In this work, we propose a new optimization framework for multiclass boosting learning. In the literature, AdaBoost.MO and AdaBoost.ECC are the two successful multiclass boosting algorithms, which can use binary weak learners. We explicitly derive these two algorithms' Lagrange dual problems based on their regularized loss functions. We show that the Lagrange dual formulations enable us to design totally-corrective multiclass algorithms by using the primal-dual optimization technique. Experiments on benchmark data sets suggest that our multiclass boosting can achieve a comparable generalization capability with state-of-the-art, but the convergence speed is much faster than stage-wise gradient descent boosting. In other words, the new totally corrective algorithms can maximize the margin more aggressively.Comment: 11 page

Simulating non-small cell lung cancer with a multiscale agent-based model

Background The epidermal growth factor receptor (EGFR) is frequently overexpressed in many cancers, including non-small cell lung cancer (NSCLC). In silcio modeling is considered to be an increasingly promising tool to add useful insights into the dynamics of the EGFR signal transduction pathway. However, most of the previous modeling work focused on the molecular or the cellular level only, neglecting the crucial feedback between these scales as well as the interaction with the heterogeneous biochemical microenvironment. Results We developed a multiscale model for investigating expansion dynamics of NSCLC within a two-dimensional in silico microenvironment. At the molecular level, a specific EGFR-ERK intracellular signal transduction pathway was implemented. Dynamical alterations of these molecules were used to trigger phenotypic changes at the cellular level. Examining the relationship between extrinsic ligand concentrations, intrinsic molecular profiles and microscopic patterns, the results confirmed that increasing the amount of available growth factor leads to a spatially more aggressive cancer system. Moreover, for the cell closest to nutrient abundance, a phase-transition emerges where a minimal increase in extrinsic ligand abolishes the proliferative phenotype altogether. Conclusions Our in silico results indicate that, in NSCLC, in the presence of a strong extrinsic chemotactic stimulus, and depending on the cell's location, downstream EGFR-ERK signaling may be processed more efficiently, thereby yielding a migration-dominant cell phenotype and overall, an accelerated spatio-temporal expansion rate.Comment: 37 pages, 7 figure

RORS: Enhanced Rule-based OWL Reasoning on Spark

The rule-based OWL reasoning is to compute the deductive closure of an ontology by applying RDF/RDFS and OWL entailment rules. The performance of the rule-based OWL reasoning is often sensitive to the rule execution order. In this paper, we present an approach to enhancing the performance of the rule-based OWL reasoning on Spark based on a locally optimal executable strategy. Firstly, we divide all rules (27 in total) into four main classes, namely, SPO rules (5 rules), type rules (7 rules), sameAs rules (7 rules), and schema rules (8 rules) since, as we investigated, those triples corresponding to the first three classes of rules are overwhelming (e.g., over 99% in the LUBM dataset) in our practical world. Secondly, based on the interdependence among those entailment rules in each class, we pick out an optimal rule executable order of each class and then combine them into a new rule execution order of all rules. Finally, we implement the new rule execution order on Spark in a prototype called RORS. The experimental results show that the running time of RORS is improved by about 30% as compared to Kim & Park's algorithm (2015) using the LUBM200 (27.6 million triples).Comment: 12 page

Simulating Brain Tumor Heterogeneity with a Multiscale Agent-Based Model: Linking Molecular Signatures, Phenotypes and Expansion Rate

We have extended our previously developed 3D multi-scale agent-based brain tumor model to simulate cancer heterogeneity and to analyze its impact across the scales of interest. While our algorithm continues to employ an epidermal growth factor receptor (EGFR) gene-protein interaction network to determine the cells' phenotype, it now adds an explicit treatment of tumor cell adhesion related to the model's biochemical microenvironment. We simulate a simplified tumor progression pathway that leads to the emergence of five distinct glioma cell clones with different EGFR density and cell 'search precisions'. The in silico results show that microscopic tumor heterogeneity can impact the tumor system's multicellular growth patterns. Our findings further confirm that EGFR density results in the more aggressive clonal populations switching earlier from proliferation-dominated to a more migratory phenotype. Moreover, analyzing the dynamic molecular profile that triggers the phenotypic switch between proliferation and migration, our in silico oncogenomics data display spatial and temporal diversity in documenting the regional impact of tumorigenesis, and thus support the added value of multi-site and repeated assessments in vitro and in vivo. Potential implications from this in silico work for experimental and computational studies are discussed.Comment: 37 pages, 10 figure