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Background Trauma can result in systemic inflammation that leads to organ dysfunction, but the impact on the brain, particularly following extracranial insults, has been largely overlooked. Methods Building upon our prior findings, we aimed to understand the impact of systemic inflammation on neuroinflammatory gene transcripts in eight brain regions in rats exposed to (1) blast overpressure exposure [BOP], (2) cutaneous thermal injury [BU], (3) complex extremity injury, 3 hours (h) of tourniquet-induced ischemia, and hind limb amputation [CEI+tI+HLA], (4) BOP+BU or (5) BOP+CEI and delayed HLA [BOP+CEI+dHLA] at 6, 24, and 168 h post-injury (hpi). Results Globally, the number and magnitude of differentially expressed genes (DEGs) correlated with injury severity, systemic inflammation markers, and end-organ damage, driven by several chemokines/cytokines ( Csf3, Cxcr2, Il16, and Tgfb2 ), neurosteroids/prostaglandins ( Cyp19a1, Ptger2, and Ptger3 ), and markers of neurodegeneration ( Gfap , Grin2b , and Homer1 ). Regional neuroinflammatory activity was least impacted following BOP. Non-blast trauma (in the BU and CEI+tI+HLA groups) contributed to an earlier, robust and diverse neuroinflammatory response across brain regions (up to 2–50-fold greater than that in the BOP group), while combined trauma (in the BOP+CEI+dHLA group) significantly advanced neuroinflammation in all regions except for the cerebellum. In contrast, BOP+BU resulted in differential activity of several critical neuroinflammatory-neurodegenerative markers compared to BU. t-SNE plots of DEGs demonstrated that the onset, extent, and duration of the inflammatory response are brain region dependent. Regardless of injury type, the thalamus and hypothalamus, which are critical for maintaining homeostasis, had the most DEGs. Our results indicate that neuroinflammation in all groups progressively increased or remained at peak levels over the study duration, while markers of end-organ dysfunction decreased or otherwise resolved. Conclusions Collectively, these findings emphasize the brain's sensitivity to mediators of systemic inflammation and provide an example of immune-brain crosstalk. Follow-on molecular and behavioral investigations are warranted to understand the short- to long-term pathophysiological consequences on the brain, particularly the mechanism of blood–brain barrier breakdown, immune cell penetration–activation, and microglial activation.

Purpose Three-column osteotomies (3COs), such as pedicle subtraction osteotomy (PSO) and vertebral column resection (VCR), are used to surgically correct rigid adult spinal deformity (ASD). While extensive research exists about complications associated with 3COs, there remains a paucity of studies analyzing risk factors for mortality following 3CO. We believe the mortality rate after 3-column osteotomy will be low with specific identifiable demographic or medical risk factors. Methods A retrospective analysis was conducted using the National Surgical Quality Improvement Program (NSQIP) database. Patients undergoing 3CO were identified via CPT codes. The primary outcome of interest was 30-day postoperative mortality. Univariate statistical analysis was performed, followed by multivariable logistic regression controlling for age, sex, and body mass index (BMI). Results The analysis included 1,441 patients. 446 patients had thoracic osteotomies, 996 patients had lumbar osteotomies, and 226 had multilevel osteotomies. The overall 30-day mortality rate was 1.2% (18 patients). On univariate analysis, mortality was more likely in patients with diabetes (2.8% vs. 1.2%, P  = 0.029) and COPD (7.0% vs. 1.2%, P  < 0.001). Mortality was associated with higher 5-factor modified frailty index ( P  = 0.004). After controlling for age, sex, and BMI, multivariable analysis revealed that mortality rates were independently associated with longer operative times (OR = 1.28, 95% CI:1.06–1.54, P  = 0.010) and COPD (OR = 10.36, 95% CI: [2.17–49.47], P  = 0.003). Conclusion Thirty-day mortality after 3CO is 1.2% globally. The greatest univariate risk factors are diabetes, COPD, and frailty. Regardless of age, sex, or BMI, it was found that COPD and duration of surgery were independently associated with increased rates of mortality.