An experimental test of Lanchester's models of combat in the neotropical termite Nasutitermes corniger (Blattodea: Termitidae).

Lanchester's models of combat have been invoked to explain the mechanics of group fighting in social animals. Specifically, Lanchester's square law posits that the fighting ability of the group is proportional to the square of the number of combatants. Although used to explain a variety of ecological phenomena, the models have not been thoroughly tested. We tested the Lanchester models using group battles between colonies of the termite Nasutitermes corniger. Our main goals were to determine if mortality rates fit the Lanchester models, and if so, whether the behavioural mechanisms underlying a group's success match those used in deriving the model. We initiated battles between pairs of colonies with different ratios of fighters and recorded deaths over time. We found that the numerically larger army has an advantage, but that the advantage is not as pronounced as predicted by Lanchester's square law. We also video-recorded battles to analyse individual behaviour, which did not support the mechanisms invoked by Lanchester. Instead, the killing power of an individual is increased by the presence of nest-mates, giving the larger group a disproportionate advantage. Although the behavioural mechanisms leading to the advantage may differ, our results still support some of the proposed ecological phenomena.

Dysregulation in Actin Cytoskeletal Organization Drives Increased Stiffness and Migratory Persistence in Polyploidal Giant Cancer Cells.

Polyploidal giant cancer cells (PGCCs) have been observed by pathologists in patient tumor samples and are especially prominent in late stage, high grade disease or after chemotherapy. However, they are often overlooked due to their apparent dormancy. Recent research has shown PGCCs to be chemoresistant and express stem-like features, traits associated with disease progression and relapse. Here, we show the preferential survival of PGCCs during Paclitaxel (PTX) treatment and used multiple particle tracking analysis to probe their unique biophysical phenotype. We show that PGCCs have higher inherent cytoplasmic and nuclear stiffness in order to withstand the mechanical stress associated with their increased size and the chemical stress from PTX treatment. Inhibitor studies show the involvement of a dysregulated RhoA-Rock1 pathway and overall actin cytoskeletal network as the underlying mechanism for the altered biophysical phenotype of PGCCs. Furthermore, PGCCs exhibit a slow but persistent migratory phenotype, a trait commonly associated with metastatic dissemination and invasiveness. This work demonstrates the clinical relevance and the need to study this subpopulation, in order to devise therapeutic strategies to combat disease relapse. By highlighting the unique biophysical phenotype of PGCCs, we hope to provide unique avenues for therapeutic targeting of these cells in disease treatment.