Yusuke Himeoka

The paper uses a mechanistic model to explain the bell-shaped protein production profile in the PURE system, showing that excess EF-Tu sequesters tRNAfMet, and confirms this by experimental validation.

The paper models microbial nutrient utilization strategies, showing that growth-death trade-offs determine whether generalists or specialists dominate under fluctuating nutrient conditions.

The paper examines how temperature changes affect a kinetic model of E. coli metabolism and identifies strategies to maintain ATP production efficiency.

The paper presents a theoretical framework for cell death by modeling it as a controllability problem in dynamical systems, using stoichiometric rays to define life-death boundaries.

The paper analyzes how bacterial metabolic systems respond to perturbations using kinetic models, finding that cofactors and network sparsity significantly influence responsiveness.

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.

The paper develops a theoretical model to explain transitions between bacterial growth phases, showing lag time follows the square root of starvation time and is inversely related to growth rate.