Fig. 1

Injury models and experimental design schematic. Adult male Sprague-Dawley rats (400–500 g) either received (1) head-on whole-body blast overpressure exposure [120 kPa; BOP], (2) a partial-thickness cutaneous thermal burn [BU], (3) BOP+BU, (4) complex extremity trauma involving closed femoral fracture and soft-tissue crush injury, 3 h of prolonged tourniquet-induced limb ischemia and limb amputation through the zone of injury [CEI+tI+HLA], or (5) BOP+CEI plus delayed hind limb amputation [BOP+CEI+dHLA]. Age- and sex-matched naïve rats (n = 7) served as controls. Following injury, whole blood obtained from tail vein venipuncture was obtained from each cohort (1, 3, or 72 hpi) at the timepoint that preceded euthanasia. At 6, 24, and 168 h postinjury (hpi), cohorts of rats (n = 5–7 timepoint/injury paradigm) were euthanized, and eight anatomic regions of the brain were dissected and profiled for neuroinflammatory-neurodegeneration gene expression signatures using a custom low-density RT‒qPCR microarray. The molecular heterogeneity of the gene profiles of the trauma-induced changes in the brain over time was compared with that of the naïve steady state of control animals. This scientific illustration was created in the Biorender web interface