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.

The research project “BARB – Biomedical Applications of Radioactive Ion Beams” funded by a prestigious ERC Advanced Grant to Professor Marco Durante, head of the Biophysics Department at the GSI Helmholtzzentrum für Schwerionenforschung, has reached an important milestone: the first treatment of an animal tumor with radioactive ion beams has been demonstrated and published in Nature Physics. The study marks a decisive step towards the further development of particle therapy and is based on intensive collaboration between different GSI departments and FAIR pillars and with the Ludwig-Maximilians-Universität in Munich (LMU), Department of Medical Physics, who contributes to the BARB project as Associated Partner with a team led by Professor Katia Parodi.

Professor Ogawa, Mr. Echigo (PhD student), and their colleagues in Kanazawa University report in Eur J Nucl Med Mol Imaging that combination of an At-211-labeled agent with immune checkpoint blockade significantly enhances its therapeutic effect. This strategy represents a promising advancement in the development of next-generation cancer therapies that combine targeted alpha therapy and immunotherapy.

POSTECH & ImmunoBiome identify gut–immune–brain axis as key driver beyond genetics.

SRPX2 is a chondroitin sulfate proteoglycan (CSPG) exhibiting significant N-glycosylation, which influences its conformation, interactions, and functions, as evidenced by the enhanced glycosylation and functional impact of the N327S mutation. It plays versatile roles in multiple diseases. SRPX2 promotes cancer progression (e.g., gastric, pancreatic, thyroid, glioblastoma) by enhancing proliferation, migration, invasion, and chemoresistance via pathways like TGF-β, PI3K/AKT, Wnt/β-catenin, and FAK/SRC/ERK, correlating with poor prognosis. SRPX2 also plays critical roles in neurodevelopment; mutations are linked to language disorders, autism spectrum disorder (ASD), and potentially Rolandic epilepsy (though evidence is complex and may involve interactions like GRIN2A). SRPX2, a protein characterized by sushi repeat domains, plays a crucial role in synaptogenesis and modulates complement-mediated synaptic pruning processes. Additionally, SRPX2 contributes to idiopathic pulmonary fibrosis via TGF-β signaling, angiogenesis via μPAR/integrin signaling, myocardial infarction protection by inhibiting PI3K/AKT/mTOR, and other conditions. Its context-dependent roles, e.g., pro-fibrotic in lungs vs. protective in heart, and involvement in key signaling pathways highlight its potential as a therapeutic target, though challenges like inhibitor specificity remain.