This week in research.

In Chuckwagon racing, teams of four Thoroughbred horses pull wagons at high speeds. Movement symmetry is a key locomotion metric linked to force production, racing direction, and lameness. Racehorse symmetry in trot during on-track warmups and cooldowns was assessed. Over 10 days, 60 horses (average 8 per day) were fitted with Global Navigation Satellite Systems combined with Inertial Measurement Unit (GNSS-IMU) sensors. Weight-bearing asymmetry was quantified using the minimum difference (MnD) in vertical trunk displacement between diagonal limb pairs, and push-off asymmetry was quantified using the upwards difference (UpD). Absolute (mm) and normalized (% ROM) asymmetries were compared between warmups and cooldowns using linear mixed models. Mean MnD was similar between warmup (6.2 mm; 17.6%) and cooldown (6.4 mm, 19.7%). Mean UpD increased from warmup (11.3 mm, 31.7%) to cooldown (12.8 mm, 38.0%), with UpD% significantly higher in cooldown (p = 0.046). No other differences were significant (all p ≥ 0.202). One horse sustained a catastrophic musculoskeletal (MSK) injury. This horse’s UpD ranged from 3.3–29.7 mm (11.4–69.3%) during warmups and 24.3–25.5 mm (47.8–76.4%) during cooldowns. Push-off asymmetry may increase after Chuckwagon racing. The injured horse showed high asymmetries, but high values also occurred in uninjured horses. Further work needs to establish normal asymmetry ranges in Chuckwagon racing and identify patterns associated with MSK injuries.

Severe burns provoke a systemic "genomic storm," yet cell states associated with divergent outcomes remain unclear. We profiled blood cells by single-cell RNA-Sequencing (73,014 cells) from adult burn patients within post-burn day 17 (n=4) and healthy donors (n=5), integrated data with bulk signatures of burn size, inhalation injury, and mortality, and evaluated clinical associations in the ABA National Burn Repository. Burn was associated with emergency hematopoiesis marked by expansion of hematopoietic stem/progenitor-like cells, immature neutrophils, and plasmablast/plasma cell states, alongside depletion of naïve CD4+/CD8+ T cells and dendritic cells. Larger burns (>20% TBSA) showed enrichment of humoral transcriptional programs, including plasmablast/plasma cell activation and suppression of cytotoxic CD8+ T-cell states. In multivariable models, inhalation injury was a stronger predictor of death (adjusted OR 1.9) than burn size (adjusted OR 1.1) and shared greater overlap with the most perturbed single cells in non-survivors; 55% of co-perturbed cells were neutrophils, implicating granulocyte dysregulation as a common lethal axis. We identified a neutrophil-specific 5-gene panel (OLFM4, RETN, LCN2, ARG1, BTNL3) that discriminated survivors vs non-survivors after burns (AUC >0.9) and generalized to trauma (n=158; AUC 0.81) and ICU COVID-19 (n=103; AUC 0.75), providing information orthogonal to conventional biomarkers and severity scores. Cytomorphology corroborated transcriptomic immaturity, with ~2-fold higher band neutrophils and larger neutrophil size in a fatal case. Computational drug-reversal analysis highlighted galectin-1 inhibition as a candidate modulator of mortality-associated neutrophil programs. Together, our findings suggest that immature neutrophils represent a shared immune feature across severe burns and other forms of critical illness. Structured Abstract Objective: To define cell-specific immune programs associated with burn size, severity, inhalation injury, and fatal trajectories. BACKGROUND: Large burns provoke a "genomic storm" yet cellular drivers of divergent clinical outcomes remain unknown. METHODS: We profiled 73,014 immune cells (scRNA-seq) from 4 adult burn patients and 5 healthy donors, mapping TBSA, inhalation injury, and mortality signatures from bulk datasets onto single-cell atlas. Clinical patterns were validated using ABA NBR. 5-gene neutrophil panel was developed to predict burn mortality and tested in trauma (n=158) and ICU COVID-19 (n=103) cohorts. RESULTS: Burns were associated with emergency hematopoiesis, expanding HSPCs, immature neutrophils, and plasmablasts while depleting naïve CD4+/CD8+ T cells. Large burns (>20% TBSA) showed enrichment of humoral responses by activating plasmablasts and plasma cells at the expense of CD8+ T-mediated immunity. While >20% TBSA increased mortality (OR 1.1), inhalation injury was a stronger independent predictor (OR 1.9) and shared 55% of its most perturbed cells with non-survivors, converging on neutrophils as the dominant transcriptional state. 5-gene immature neutrophil signature predicted burn mortality with AUC >0.9, generalized to trauma (AUC 0.81) and COVID-19 (AUC 0.75), and was orthogonal to conventional biomarkers and severity scores. Non-survivor had ~2-fold greater band neutrophils, supporting neutrophil nuclear segmentation and size as potential indicators of burn severity. In silico screening identified galectin-1 inhibition as a potential suppressor of death-associated neutrophil programs. CONCLUSION: Immature neutrophil surges associate with mortality in burns, trauma, and COVID-19. 5-gene panel may identify this risk and therapeutic modulation of these cells will reveal whether they are modifiable features of critical illness.

Performance-based assessments (PBAs) are essential tools in veterinary medical education for evaluating students’ clinical and professional competencies. This reflection on assessment is grounded in the first author’s experience as a veterinary educator navigating the complexities of PBAs and in the second author’s experience as a psychometrician studying validity claims about raters’ cognitive processes as they use PBAs. By integrating personal insights with existing literature, this work contributes to the ongoing discourse on assessment design and defensibility in health professional education. Our aim is to highlight the need to explore how rater response processes influence assessment outcomes and to advocate for more robust, contextually relevant validity evidence in veterinary medical education. While multiple sources of validity evidence are needed to support decisions based on PBA scores, the response processes of raters—how they interpret and apply assessment criteria—remain underexplored in health profession education. Without this type of evidence, the defensibility of assessment scores, as well as the decisions based on them, may be compromised. We argue that understanding rater decision making is crucial for strengthening the validity argument of PBAs.