Citations

ABSTRACT Objectives To evaluate how academic emergency departments (EDs) support procedural skill maintenance for faculty physicians, particularly in environments where learners often perform procedures. We aimed to characterize training strategies, barriers to participation, and the inclusion of high‐acuity, low‐occurrence (HALO) procedures. Methods We conducted a cross‐sectional survey of department chairs, vice chairs, and chair emeriti attending the 2025 Association of Academic Chairs of Emergency Medicine (AACEM) retreat. The survey assessed institutional approaches to procedural training, frequency of offerings, training modalities, inclusion of HALO procedures, and perceived barriers. Descriptive statistics and chi‐square tests were used to analyze differences in training frequency and procedural coverage. Results Of 81 academic departments represented, 49 responded (60.5%). Most (87.8%) offered procedural training, yet only 32.6% required participation. Hands‐on training was most common (93%), followed by in‐person (79%) and virtual (16%) sessions. While 100% of departments covered point‐of‐care ultrasound and 93% airway management, fewer addressed HALO procedures: only 27.9% covered all HALO categories (e.g., surgical airway, thoracostomy, pericardiocentesis). Time constraints and clinical schedules were the most‐commonly reported barriers to participation. Conclusions Procedural skill maintenance for EM attendings varies widely across academic EDs. Despite the specialty's procedural intensity, most academic departments lack comprehensive, mandatory training, particularly for infrequent but critical procedures. Findings highlight variability in departmental approaches and the need to further explore best practices for procedural skill maintenance.

Abstract INTRODUCTION Sleep and circadian rest–activity rhythm (RAR) disruption may bidirectionally relate to Alzheimer's disease (AD). Down syndrome (DS), the most common genetic cause of AD, presents sleep disorders, yet RAR patterns across the DS‐associated AD continuum remain uncharacterized. METHODS We analyzed 7‐day wrist actigraphy in 140 adults with DS (108 asymptomatic; 32 AD dementia) and 41 unimpaired controls. General linear models, adjusted for age, sex, sleep efficiency, and obstructive sleep apnea (OSA) severity, tested group differences, with interaction terms included to evaluate group‐specific associations. RESULTS DS showed lower relative amplitude and higher nocturnal activity, already in asymptomatic individuals. Rhythm strength declined further with AD progression, while regularity and phase timing remained preserved until dementia. Findings were independent of sleep duration and OSA. DISCUSSION Adults with DS showed early RAR disturbance that progressed across the AD continuum, paralleling sporadic AD. Circadian RAR features may be scalable biomarkers of AD progression.

Vitamin D deficiency is frequently reported in hidradenitis suppurativa (HS), but its clinical significance remains unclear. In a retrospective cohort of 503 patients, deficiency was common and associated with demographic and metabolic factors but not with treatment-defined severity. Vitamin D deficiency was independently associated with elevated C-reactive protein, suggesting a link with systemic inflammation.

Abstract Spatial transcriptomics links gene expression to tissue architecture, providing a mechanistic view of cellular organization. Yet existing datasets cover few donors and miss the complexity of human disease. Experimental costs remain prohibitive, and large-scale profiling is impractically slow for population-level studies. Accurate computational methods are urgently needed. Predicting gene expression from standard histology, however, remains an open problem, as current approaches transfer poorly to unseen cohorts and diseases. Here, we present Phoenix, a (latent) flow matching generative model that infers pan-cancer spatially resolved single-cell gene expression with high accuracy. Phoenix analyzes treatment response in silico: Applied to 763 head and neck cancer patients, it identified three new spatial biomarkers that we validated across two cancers (breast cancer, n = 84; ovarian cancer, n = 157) and treatment regimens (platinum, trastuzumab). Phoenix generalizes beyond carcinomas: In a large sarcoma cohort (802 tissue microarray cores), it accurately predicted cell-type-specific signatures in held-out samples and captured chemotherapy-induced immune remodeling. Phoenix also extends across species: In a mouse model, it accurately predicted the expression of pancreatic cancer lineage markers and the mutant mKras^G12D allele in silico. In total, we evaluated Phoenix on over 10,000 patients. Our results establish virtual spatial transcriptomics as a scalable framework for studying tissue organization, therapeutic response, and disease mechanisms.

Purpose of review To review recent advances in infectious myelopathies and integrate them into a practical, syndrome-based approach that supports early recognition, guides testing, and avoids pitfalls. Recent findings Advances in MRI pattern recognition and pathogen-specific diagnostics have refined the evaluation of infectious myelopathies, with strategies tailored to geographic epidemiology, host susceptibility, and distinction from immune-mediated causes. During the COVID-19 pandemic, SARS-CoV-2-associated myelopathy emerged as a rare para- or postinfectious cause of myelitis. The pandemic coincided with a decline in enterovirus outbreaks and acute flaccid myelitis, which are now re-emerging, underscoring the importance of epidemiologic surveillance. Metagenomic next-generation sequencing is useful in suspected infectious myelopathy because it can identify unexpected pathogens from cerebrospinal fluid, but its imperfect sensitivity and contamination risk mean it should complement rather than replace conventional testing. Growing recognition of compartmentalized central nervous system inflammation and cerebrospinal fluid viral escape in HIV myelopathy has shifted management toward antiretroviral resistance patterns and treatment optimization. Therapeutic advances remain limited and largely pathogen-specific, although targeted approaches such as mogamulizumab for HTLV-1-associated myelopathy are promising. Summary Recent progress in infectious myelopathies has been driven by improved pathogen detection and more tailored diagnostic strategies, although treatment advances are beginning to emerge.

Abstract Aims Lipoprotein(a) [Lp(a)] is a causal risk factor for cardiovascular events. However, the effect of Lp(a) on coronary plaque composition and high-risk plaque features has not been fully characterized. This study aimed to investigate the association between Lp(a) and coronary atherosclerotic plaque phenotype at the plaque level. Methods and results This study included 710 patients who underwent coronary computed tomography angiography (CCTA) and had Lp(a) measured between 2008 and 2024. CCTA scans were analysed with a previously validated artificial intelligence-based algorithm (AI-QCT, Cleerly Inc.). The association of Lp(a) with non-calcified and calcified plaque volumes and HRP features was evaluated at the plaque level using generalized estimating equation models adjusted for traditional cardiovascular risk factors. Among the 710 patients, the mean age was 56 ± 10 years and 379 (53%) were male. In total, 3642 plaques were identified. In the adjusted plaque-level analysis, elevated Lp(a) (≥150 nmol/L) was associated with an increase in non-calcified plaque volume per plaque (P = 0.009), but not with an increase in calcified plaque volume (P = 0.81). Furthermore, elevated Lp(a) (≥150 nmol/L) was strongly associated with the presence of high-risk plaque at the plaque level (adjusted odds ratio: 1.78, 95% CI: 1.25–2.54, P = 0.001), whereas low-density lipoprotein-cholesterol and high-sensitivity C-reactive protein were not (P > 0.05). Conclusion In this plaque-level CCTA study of 3642 individual plaques, elevated Lp(a) levels were independently associated with increased non-calcified plaque volume and with the presence of high-risk plaque, but not with calcified plaque volume. These findings elucidate the impact of Lp(a) on unstable plaque phenotypes, even in patients without prior cardiovascular events.