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A population-based trauma register was used to develop a risk-adjustment model in order to compare mortality between university and emergency hospitals in clinically relevant subsets of trauma patients (multiple blunt trauma, penetrating truncal trauma, and severe traumatic brain injury). The results suggest that university hospitals outperform emergency hospitals when it comes to the treatment of traumatic brain injury, but the differences in outcome following extracranial trauma appear more uniform. We recommend monitoring of risk-adjusted mortality in clinically relevant subsets for the continuous evaluation of quality of trauma care. Background Risk-adjusted mortality (RAM) analysis and comparisons of clinically relevant subsets of trauma patients allow hospitals to assess performance in different processes of care. The aim of the study was to develop a RAM model and compare RAM ratio (RAMR) in subsets of severely injured adult patients treated in university hospitals (UHs) and emergency hospitals (EHs) in Sweden. Methods This was a retrospective study of the Swedish trauma registry data (2013 to 2017) comparing RAMR in patients (aged 15 years or older and New Injury Severity Score (NISS) of more than 15) in the total population (TP) and in multisystem blunt (MB), truncal penetrating (PEN), and severe traumatic brain injury (STBI) subsets treated in UHs and EHs. The RAM model included the variables age, NISS, ASA Physical Status Classification System Score, and physiology on arrival. Results In total, 6690 patients were included in the study (4485 from UHs and 2205 from EHs). The logistic regression model showed a good fit. RAMR was 4.0, 3.8, 7.4, and 8.5 percentage points lower in UH versus EH for TP (P < 0.001), MB (P < 0.001), PEN (P = 0.096), and STBI (P = 0.005), respectively. The TP and MB subsets were subgrouped in with (+) and without (-) traumatic brain injury (TBI). RAMR was 7.5 and 7.0, respectively, percentage points lower in UHs than in EHs in

Serum alanine aminotransferase (ALT) is used asa clinical marker to detect hepatic damage and hepatoxicity.Two isoforms of ALT have been identified, ALT1 and ALT2,which have identical enzymatic capacities and are detectedsimultaneously in human serum/plasma using classical clinicalchemical assays. Differences exist in the expression patterns ofthe ALT1 and ALT2 proteins in different organs which suggestthat changes in the proportion of ALT1 and ALT2 in plasmamay arise and reflect damage to different human organs.However, this has not been previously studied due to the lackof a selective methodology that can quantify both ALT1 andALT2 isoforms in the total ALT activity normally measuredin clinical samples. To the best of our knowledge, our currentstudy reveals for the first time, that under 3 different conditionsof liver damage (non-alcoholic fatty liver disease, hepatitis Cand during liver surgery) the leakage of ALT1 activity intoplasma greatly exceeds that of ALT2, and that the measurementof ALT1 during liver damage is equal to the measurement oftotal ALT activity. By contrast, during skeletal muscle injury,induced in volunteers by physical exertion, the leakage ofALT2 exceeds that of ALT1 and the proportion of circulatingALT isoforms changes accordingly. The ALT isoform changesoccurring in plasma reflect previously demonstrated relativecontents of ALT1 and ALT2 activities in human liver and skeletalmuscle. These data suggest that assessing the percentagecontribution of ALT1 and ALT2 activities to total ALT activityin plasma may distinguish hepatic from extrahepatic injuryusing the same standard analytical platform.