A team of researchers at the University of Oxford have unveiled a pioneering ‘microstent’ which could revolutionise treatment for glaucoma, a common but debilitating condition. The study has been published in The Innovation journal, Cell Press.

Cerebrovascular diseases, often driven by vascular stenosis, are notoriously difficult to study due to the complexity of brain vessel physiology. Traditional lab models fail to capture the structural and mechanical nuances of human vasculature. Now, researchers have developed a 3D-bioprinted brain vessel model that not only mimics anatomical features but also recreates realistic blood flow. This breakthrough platform offers an unprecedented opportunity to decode disease mechanisms and test therapies in a more accurate, human-relevant setting.

Stroke often results in persistent gait impairments, limiting mobility and reducing quality of life. This study evaluated FAST walk, a novel electromyography-triggered system that combines transcutaneous spinal cord and hip extensor stimulation to support walking recovery in patients with chronic stroke. In a randomized controlled trial, FAST walk produced greater improvements in gait speed than spinal stimulation or treadmill training alone, highlighting its potential as a safe, non-invasive, and time-efficient approach for real-world stroke rehabilitation.

As bones weaken with age, the culprits may be the aging cells within. A new review uncovers how cellular changes—like senescence, inflammation, and loss of regenerative capacity—disrupt the delicate balance of bone formation and breakdown. By mapping these age-related mechanisms across multiple skeletal diseases, the study offers a clearer picture of how bones decline over time, and where potential therapies might intervene to slow or even reverse the process.

The dengue early warning system was piloted in Barbados in June 2024 for the Cricket World Cup, prompting public health interventions to mitigate potential outbreak risk in advance of the tournament.

Led by researchers at the Barcelona Supercomputing Center and co-developed with Caribbean health and meteorological agencies and an international team of researchers, the study marks a milestone in disease prediction modelling with climate information.

For decades, the destruction of pancreatic β-cell functionality has been recognized as the hallmark of Type 1 Diabetes (T1D), yet the involvement of inter-organ metabolic crosstalk remained unexplored. A multicenter research team led by Xinran Ma (ECNU), Lingyan Xu (ECNU), Yang Xiao (Xiangya Second Hospital), and Weiping Zhang (Naval Medical University) has uncovered an unappreciated contributor in T1D disease progression - the zinc finger protein ZNF638 in brown adipose tissue (BAT). Their recent study, published in Science Bulletin, demonstrates that BAT-derived ZNF638 suppresses retinol-binding protein 4 (RBP4), thereby disrupting the protective all-trans retinoic acid (ATRA) signaling essential for β-cell survival. Clinically, RBP4 levels and retinol levels were decreased in the serum of T1D patients compared to healthy controls. Via genetic and pharmacological interventions in mouse models, the team demonstrated that either ZNF638 inhibition or ATRA treatment effectively preserves pancreatic islet function and normalizes blood glucose levels. Overall, the study reveals the unappreciated crosstalk between brown adipocytes and β-cells and suggests that targeting brown fat ZNF638 to affect the RBP4-retinol-ARTA axis significantly alleviates T1D progression.