26dkou618 10.3205/26dkou618 urn:nbn:de:0183-26dkou6185 Meeting Abstract Heller Heller Raban R

German Armed Forces Hospital Ulm, Department for Trauma Surgery and Orthopaedics, Reconstructive and Septic Surgery, Sportstraumatology, Ulm, Deutschland Charité – Universitätsmedizin Berlin, Institute for Experimental Endocrinology, Berlin, Deutschland Technische Universität Berlin, Department of Food Chemistry and Toxicology, Berlin, Deutschland

author Chillon Chillon Thilo T

Charité – Universitätsmedizin Berlin, Institute for Experimental Endocrinology, Berlin, Deutschland

author Alhalabi Alhalabi Obada T. OT

Heidelberg University Hospital, Department of Neurosurgery, Heidelberg, Deutschland Heidelberg University, Medical Faculty, Heidelberg, Deutschland

author Bauer Bauer Andreas A

German Armed Forces Hospital Ulm, Department for Trauma Surgery and Orthopaedics, Reconstructive and Septic Surgery, Sportstraumatology, Ulm, Deutschland

author Krieg Krieg Sandro M. SM

Heidelberg University Hospital, Department of Neurosurgery, Heidelberg, Deutschland Heidelberg University, Medical Faculty, Heidelberg, Deutschland

author Achatz Achatz Gerhard G

German Armed Forces Hospital Ulm, Department for Trauma Surgery and Orthopaedics, Reconstructive and Septic Surgery, Sportstraumatology, Ulm, Deutschland

author Haase Haase Hajo H

Technische Universität Berlin, Department of Food Chemistry and Toxicology, Berlin, Deutschland

author Schomburg Schomburg Lutz L

Charité – Universitätsmedizin Berlin, Institute for Experimental Endocrinology, Berlin, Deutschland

author Moghaddam Moghaddam Arash A

Orthopedic and Trauma Surgery, Aschaffenburg, Deutschland

author Younsi Younsi Alexander A

Heidelberg University Hospital, Department of Neurosurgery, Heidelberg, Deutschland Heidelberg University, Medical Faculty, Heidelberg, Deutschland BG Trauma Centre Ludwigshafen, Department of Neurosurgery, Ludwigshafen, Deutschland

author Biglari Biglari Bahram B

BG Trauma Centre Ludwigshafen, Department of Paraplegiology, Ludwigshafen, Deutschland

author German Medical Science GMS Publishing House

Düsseldorf

610 20261020 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0659 618 Deutsche Gesellschaft für Orthopädie und Unfallchirurgie Deutsche Gesellschaft für Orthopädie und Orthopädische Chirurgie Deutsche Gesellschaft für Unfallchirurgie Berufsverband für Orthopädie und Unfallchirurgie Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2026) Posterpreise experimentell Berlin 20261020 20261023 DKOU26_Abs_2456 TextObjectives and questions: Trace elements modulate secondary injury cascades following traumatic spinal cord injury (TSCI). Selenium is a central regulator of redox homeostasis and immune signaling; however, its translational behavior between animal models and humans remains poorly defined. We aimed to model cross-species serum selenium dynamics after TSCI and compare them with spinal column injuries without neurological deficits.Material and methods: Serum selenium concentrations were analyzed in a rat thoracic compression–contusion spinal cord injury model (n=120; 80 SCI, 40 controls; all female) and a prospective human cohort (n=59; 49 TSCI, 10 controls; 17 female; median age 50 years, IQR 32–64). Sampling followed a harmonized cross-species protocol at 1, 3, 7, 14, and 28 days post injury (dpi). Values were z-standardized and compared to controls. Linear regression modeled temporal trajectories per species and jointly. Cross-species transferability was evaluated using RMSE, MAE, and R2.Results: Both species showed significant selenium depression at 1 dpi compared to controls (animal: p < 0.001; human: p = 0.016). Temporal modeling identified a significant time effect without improvement from injury subclassification. The joint model demonstrated a species-dependent intercept shift but conserved temporal structure. Cross-prediction revealed asymmetric transfer: the animal model moderately predicted human data (R2 = 0.24, RMSE=0.90), whereas the human model poorly predicted animal dynamics (R2 = 0.04, RMSE=1.02). Residual diagnostics confirmed stable model assumptions.Discussion and conclusions: Selenium exhibits conserved early injury dynamics across species, supporting translational relevance of experimental SCI models and underscoring its link to trauma immunology. However, asymmetric prediction indicates additional human-specific variability. Cross-species modeling provides a quantitative framework for evaluating biomarker translation in TSCI. 0 0 0 0