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An investigation of the mechanical strain rate, inelastic behavior, and microstructural evolution under deformation for an as-cast pearlitic gray cast iron (GCI) is presented. A complex network of graphite, pearlite, steadite, and particle inclusions was stereologically quantified using standard techniques to identify the potential constituents that define the structure-property relationships, with the primary focus being strain rate sensitivity (SRS) of the stress-strain behavior. Volume fractions for pearlite, graphite, steadite, and particles were determined as 74%, 16%, 9%, and 1%, respectively. Secondary dendrite arm spacing (SDAS) was quantified as 22.50 μm ± 6.07 μm. Graphite flake lengths and widths were averaged as 199 μm ± 175 μm and 4.9 μm ± 2.3 μm, respectively. Particle inclusions comprised of manganese and sulfur with an average size of 13.5 μm ± 9.9 μm. The experimental data showed that as the strain rate increased from 10-3 to 103 s-1, the averaged strength increased 15-20%. As the stress state changed from torsion to tension to compression at a strain of 0.003 mm/mm, the stress asymmetry increased ~470% and ~670% for strain rates of 10-3 and 103 s-1, respectively. As the strain increased, the stress asymmetry differences increased further. Coalescence of cracks emanating from the graphite flake tips exacerbated the stress asymmetry differences. An internal state variable (ISV) plasticity-damage model that separately accounts for damage nucleation, growth, and coalescence was calibrated and used to give insight into the damage and work hardening relationship. [ABSTRACT FROM AUTHOR]

We induced mild blunt and blast injuries in rats using a custom-built device and utilized in-house diffusion tensor imaging (DTI) software to reconstruct 3-D fiber tracts in brains before and after injury (1, 4, and 7 days). DTI measures such as fiber count, fiber length, and fractional anisotropy (FA) were selected to characterize axonal integrity. In-house image analysis software also showed changes in parameters including the area fraction (AF) and nearest neighbor distance (NND), which corresponded to variations in the microstructure of Hematoxylin and Eosin (H&E) brain sections. Both blunt and blast injuries produced lower fiber counts, but neither injury case significantly changed the fiber length. Compared to controls, blunt injury produced a lower FA, which may correspond to an early onset of diffuse axonal injury (DAI). However, blast injury generated a higher FA compared to controls. This increase in FA has been linked previously to various phenomena including edema, neuroplasticity, and even recovery. Subsequent image analysis revealed that both blunt and blast injuries produced a significantly higher AF and significantly lower NND, which correlated to voids formed by the reduced fluid retention within injured axons. In conclusion, DTI can detect subtle pathophysiological changes in axonal fiber structure after mild blunt and blast trauma. Our injury model and DTI method provide a practical basis for studying mild traumatic brain injury (mTBI) in a controllable manner and for tracking injury progression. Knowledge gained from our approach could lead to enhanced mTBI diagnoses, biofidelic constitutive brain models, and specialized pharmaceutical treatments. [ABSTRACT FROM AUTHOR]