Namiko Mitarai

This study develops a stochastic model to analyze how tail fiber configuration affects bacteriophage adsorption efficiency, finding an optimal number of fibers balancing binding stability and mobility.

The paper studies how mechanical forces, bacterial growth, and viral infection dynamics interact during the expansion of an E. coli colony, revealing phage hitchhiking and anisotropic spread.

The paper models how phage lysis timing in response to host physiology affects competition under fluctuating nutrient conditions, showing delayed lysis is advantageous in feast-famine environments.

This study shows that wrinkles in biofilms arise from matrix complementarity and mechanical discontinuity between bacterial strains.

The paper shows how spatial organization and mechanical pushing enable susceptible bacteria to survive antibiotic stress through collective behavior.

The paper shows that stochastic infection dynamics in motile bacteria-phage populations lead to irregular spatial patterns, with front roughness controlled by burst size and adsorption rate.

The paper develops an individual-based model to simulate T-even phage lysis dynamics under varying multiplicity of infection, showing how spatial dynamics and secondary adsorption thresholds influence phage-host interactions.

The paper shows longer bacterial cells gain a competitive advantage during range expansion through collective alignment, blocking shorter cells from resources.

The paper shows that spontaneous dormancy in bacteria is advantageous only when antibiotic application and feast periods are decoupled, and combining both dormancy types is optimal with stochastic antibiotic timing.

The paper measures how host metabolic state affects viral adsorption rates and shows that energy-limited conditions reduce infection commitment for some phages.

The paper models phage-bacteria coexistence in microcolonies, showing that external bacterial influx affects colony size distribution and steady-state dynamics.

The paper introduces a simplified bacterial growth model to simulate the formation of dormant subpopulations under various conditions.

This study uses a mathematical model to analyze how lysis inhibition in T-even phages provides competitive advantages in different environments.

The paper explains Gompertzian mortality patterns using a systems model that incorporates inter-dependent subsystems and their temporal failure, providing insights into biological aging and heterogeneity.

The paper constructs a kinetic model of E. coli central carbon metabolism to show how perturbations can lead to distinct metabolic states resembling growth and dormancy.

The paper identifies three structural features of chemical reaction networks that predict out-of-steady-state relaxation dynamics, applicable to both artificial and biological systems.

The paper develops a theoretical framework to determine optimal bacterial waking-up strategies during antibiotic exposure, showing that optimal lag times can exhibit discontinuous transitions under varying antibiotic severeness.

The paper models the slow processing of toxin mRNAs in type-I TA systems to explain post-segregational killing and noise filtering mechanisms.