A finite element-guided mathematical surrogate modeling approach for assessing occupant injury trends across variations in simplified vehicular impact conditions.

A finite element (FE)-guided mathematical surrogate modeling methodology is presented for evaluating relative injury trends across varied vehicular impact conditions. The prevalence of crash-induced injuries necessitates the quantification of the human body's response to impacts. FE modeling is often used for crash analyses but requires time and computational cost. However, surrogate modeling can predict injury trends between the FE data, requiring fewer FE simulations to evaluate the complete testing range. To determine the viability of this methodology for injury assessment, crash-induced occupant head injury criterion (HIC15) trends were predicted from Kriging models across varied impact velocities (10-45 mph; 16.1-72.4 km/h), locations (near side, far side, front, and rear), and angles (-45 to 45°) and compared to previously published data. These response trends were analyzed to locate high-risk target regions. Impact velocity and location were the most influential factors, with HIC15 increasing alongside the velocity and proximity to the driver. The impact angle was dependent on the location and was minimally influential, often producing greater HIC15 under oblique angles. These model-based head injury trends were consistent with previously published data, demonstrating great promise for the proposed methodology, which provides effective and efficient quantification of human response across a wide variety of car crash scenarios, simultaneously. This study presents a finite element-guided mathematical surrogate modeling methodology to evaluate occupant injury response trends for a wide range of impact velocities (10-45 mph), locations, and angles (-45 to 45°). Head injury response trends were predicted and compared to previously published data to assess the efficacy of the methodology for assessing occupant response to variations in impact conditions. Velocity and location were the most influential factors on the head injury response, with the risk increasing alongside greater impact velocity and locational proximity to the driver. Additionally, the angle of impact variable was dependent on the location and, thus, had minimal independent influence on the head injury risk.

A Mechanical Brain Damage Framework Used to Model Abnormal Brain Tau Protein Accumulations of National Football League Players.

A mechanics-based brain damage framework is used to model the abnormal accumulation of hyperphosphorylated p-tau associated with chronic traumatic encephalopathy within the brains of deceased National Football League (NFL) players studied at Boston University and to provide a framework for understanding the damage mechanisms. p-tau damage is formulated as the multiplicative decomposition of three independently evolving damage internal state variables (ISVs): nucleation related to number density, growth related to the average area, and coalescence related to the nearest neighbor distance. The ISVs evolve under different rates for three well known mechanical boundary conditions, which in themselves introduce three different rates making a total of nine scenarios, that we postulate are related to brain damage progression: (1) monotonic overloads, (2) cyclic fatigue which corresponds to repetitive impacts, and (3) creep which is correlated to damage accumulation over time. Different NFL player positions are described to capture the different types of damage progression. Skill position players, such as quarterbacks, are expected to exhibit a greater p-tau protein accumulation during low cycle fatigue (higher amplitude impacts with a lesser number), and linemen who exhibit a greater p-tau protein accumulation during high cycle fatigue (lower amplitude impacts with a greater number of impacts). This mechanics-based damage framework presents a foundation for developing a multiscale model for traumatic brain injury that combines mechanics with biology.

Activation of estrogen response elements is mediated both via estrogen and muscle contractions in rat skeletal muscle myotubes.

The aim of the present study was to investigate the activation of estrogen response elements (EREs) by estrogen and muscle contractions in rat myotubes in culture and to assess whether the activation is dependent on the estrogen receptors (ERs). In addition, the effect of estrogen and contraction on the mRNA levels of ERalpha and ERbeta was studied to determine the functional consequence of the transactivation. Myoblasts were isolated from rat skeletal muscle and transfected with a vector consisting of sequences of EREs coupled to the gene for luciferase. The transfected myoblasts were then differentiated into myotubes and subjected to either estrogen or electrical stimulation. Activation of the ERE sequence was determined by measurement of luciferase activity. The results show that both ERalpha and ERbeta are expressed in myotubes from rats. Both estrogen stimulation and muscle contraction increased (P < 0.05) transactivation of the ERE sequence and enhanced ERbeta mRNA, whereas ERalpha was unaffected by estrogen and attenuated (P < 0.05) by muscle contraction. Use of ER antagonists showed that, whereas the estrogen-induced transactivation is mediated via ERs, the effect of muscle contraction is ER independent. The muscle contraction-induced transactivation of ERE and increase in ERbeta mRNA were instead found to be MAP kinase (MAPK) dependent. This study demonstrates for the first time that muscle contractions have a similar functional effect as estrogen in skeletal muscle myotubes, causing ERE activation and an enhancement in ERbeta mRNA. However, in contrast to estrogen, the effect is independent of ERs and dependent on MAPK, suggesting activation via the estrogen related receptor (ERR).