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Introduction: After myocardial infarction (MI), the heart undergoes necrosis, inflammation, scar formation, and remodeling. While restoring blood flow is crucial, it can cause ischemia-reperfusion (IR) injury, driven by reactive oxygen species (ROSs), which exacerbate cell death and tissue damage. This study introduces a mathematical model capturing key post-MI dynamics, including inflammatory responses, IR injury, cardiac remodeling, and stem cell therapy. The model uses nonlinear ordinary differential equations to simulate these processes under varying conditions, offering a predictive tool to understand MI pathophysiology better and optimize treatments. Methods: After myocardial infarction (MI), left ventricular remodeling progresses through three distinct yet interconnected phases. The first phase captures the immediate dynamics following MI, prior to any medical intervention. This stage is mathematically modeled using the system of ordinary differential equations: The second and third stages of the remodeling process account for the system dynamics of medical treatments, including oxygen restoration and subsequent stem cell injection at the injury site. Results: We simulate heart tissue and immune cell dynamics over 30 days for mild and severe MI using the novel mathematical model under medical treatment. The treatment involves no intervention until 2 h post-MI, followed by oxygen restoration and stem cell injection at day 7, which is shown experimentallyand numerically to be optimal. The simulation incorporates a baseline ROS threshold (Rc) where subcritical ROS levels do not cause cell damage. Conclusion: This study presents a novel mathematical model that extends a previously published framework by incorporating three clinically relevant parameters: oxygen restoration rate (ω), patient risk factors (γ), and neutrophil recruitment profile (δ). The model accounts for post-MI inflammatory dynamics, ROS-mediated ischemia-reperfusion (IR) injury, cardiac remodeling, and stem cell therapy. The model’s sensitivity highlights critical clinical insights: while oxygen restoration is vital, excessive rates may exacerbate ROS-driven IR injury. Additionally, heightened patient risk factors (e.g., smoking, obesity) and immunodeficiency significantly impact tissue damage and recovery. This predictive tool offers valuable insights into MI pathology and aids in optimizing treatment strategies to mitigate IR injury and improve post-MI outcomes. 

The development of low-cost, high-performance anode materials for Li-ion batteries (LIBs) is imperative to meet the ever-increasing demands for advanced power sources. Here we report our findings on the design, synthesis, and characterization of a new cation-disordered ZnSiP 2 anode. When tested in LIBs, the disordered phase of ZnSiP 2 demonstrates faster reaction kinetics and higher energy efficiency than the cation-ordered phase of ZnSiP 2 . The superior performance is attributed to the greater electronic and ionic conductivity and better tolerance against volume variation during cycling, as confirmed by theoretical calculations and experimental measurements. Moreover, the cation-disordered ZnSiP 2 /C composite exhibits excellent cycle stability and superior rate capability. The performance surpasses all reported multi-phase anodes studied. Further, a number of the cation-disordered phases in the Zn(Cu)–Si–P family with a wide range of cation ratios show similar performance, achieving large specific capacities and high first-cycle coulombic efficiency while maintaining desirable working potentials for enhanced safety.