Lab-grown heart muscle enters failing hearts; traffic causes most brain injuries in low-tier areas; delayed adjuvant strengthens mRNA vaccine

Lab-grown heart muscle enters failing hearts

10 of the 20 patients with advanced heart failure received intramyocardial injections of allogeneic heart muscle cells derived from human induced pluripotent stem cells alongside coronary bypass surgery; the trial's primary endpoint was safety, and neither sustained ventricular tachycardia nor tumour formation appeared over 12 months. Randomisation was to injection or no injection, and both groups underwent coronary artery bypass grafting, so the comparison is not blinded. All 10 patients in the cell group developed accelerated idioventricular rhythm, typically 5 to 7 days after transplantation. Clinically significant ventricular tachycardia above 140 beats per minute occurred in 2 patients, peaked at 2 to 3 weeks and resolved completely after cardioversion. Secondary analyses showed larger gains in 6-minute walk distance, global myocardial perfusion and relative wall thickening in the cell group, while left ventricular ejection fraction, ventricular volumes, scar size and New York Heart Association class did not differ between the groups.^[1]

Traffic causes most brain injuries where development is low

The Global Neurosurgical Study-1 prospectively followed 2,165 patients with traumatic brain injury at 100 hospitals in 29 countries between 2019 and 2022, covering operated and non-operated cases together. Traffic injuries accounted for 65.8 per cent of injuries in the low human development tier, while falls reached 66 per cent in the very high tier. 69.3 per cent of low-tier patients arrived by private vehicle against 13 per cent in the very high tier. Median age ranged from 32 years in the high tier to 63 years in the very high tier. The authors report no dose-response relationship between mortality and development level and attribute the differences to injury mechanism, patient age and prehospital access.^[2]

Delayed adjuvant switches on after antigen production

STING agonists strengthen mRNA vaccines but also suppress translation of the antigen mRNA delivered with them. The authors packed antigen mRNA, mRNA encoding full-length STING and a delayed-release activator called DMXAA into one lipid nanoparticle, so the adjuvant switches on after the antigen has been made. In humanised STING mice tested with human papillomavirus E7 and ovalbumin antigens, intratumoral or subcutaneous particles were taken up mainly by myeloid cells, keeping antigen expression intact while confining STING activation to antigen-presenting cells. The vaccine slowed tumour growth and lengthened survival with little anti-STING immunity. All results come from mouse models, so nothing here establishes efficacy in people.^[3]