Scientists observe matter-wave diffraction in positronium, confirming quantum interference in a unique antimatter system.
A team at Japan’s National Institutes for Quantum Science and Technology (QST) has published a field-defining Perspective that places the societal payoff of quantum technologies front and center: earlier disease detection, faster drug development, and new routes to clean energy. Their paper has been published online in the journal ACS Nano on December 18, 2025.
Sometimes, in genetics, two wrongs do make a right. A research team has recently shown that two harmful genetic variants, when occurring together in a gene, can restore function—proving a decades-old hypothesis originally proposed by Nobel laureate Francis Crick.
Their study, to be published in the Proceedings of the National Academy of Sciences, not only experimentally validated this theory but also introduced a powerful artificial intelligence (AI)-driven approach to genetic interpretation led by George Mason University researchers.
The project began when Aimée Dudley, a geneticist at the Pacific Northwest Research Institute (PNRI), approached George Mason University Chief AI Officer Amarda Shehu after following her lab’s work on frontier AI models for predicting the functional impact of genetic variation. That conversation sparked a collaboration that married PNRI’s experimental expertise with George Mason’s computational innovation to discover some surprising ways variant combinations can shape human health.
Pioneering research by experts at the University of Sydney, the Baird Institute and the Royal Prince Alfred Hospital in Sydney has shown that heart muscle cells regrow after a heart attack, opening up the possibility of new regenerative treatments for cardiovascular disease.
Following the publication of the study in Circulation Research, first author Dr. Robert Hume, from the Faculty of Medicine and Health and Charles Perkins Center, and Lead of Translational Research at the Baird Institute for Applied Heart and Lung Research, explained the significance of the finding: Until now we’ve thought that, because heart cells die after a heart attack, those areas of the heart were irreparably damaged, leaving the heart less able to pump blood to the body’s organs.
Our research shows that while the heart is left scarred after a heart attack, it produces new muscle cells, which opens up new possibilities.
Common diabetes drugs may do more than regulate blood sugar—they could also influence how cancers grow, spread, or slow down. Researchers are now unraveling how these medications affect immune function, inflammation, and tumor biology, with intriguing but still uncertain implications.
Researchers are taking a closer look at how medications used to treat diabetes may also influence cancer. While diabetes itself has long been associated with higher cancer risk, scientists are now investigating whether diabetes drugs play a direct role beyond controlling blood sugar levels and body weight. A recent review examines how widely used treatments such as metformin, SGLT2 inhibitors, and GLP-1 receptor agonists may affect cancer growth by changing how cells multiply, how the immune system responds, and how inflammation develops. These insights point to possible new treatment strategies while also highlighting how much remains unknown.
Type 2 Diabetes (T2DM) has been linked to a higher likelihood of developing several types of cancer, including liver, colorectal, and breast cancer. Managing blood glucose and body weight remains essential for people with diabetes, but growing evidence suggests these factors alone do not fully explain the increased cancer risk. This has led scientists to explore how diabetes medications themselves might influence cancer, either by reducing risk or, in some cases, creating unintended effects. Understanding this connection could help clarify how diabetes treatments fit into cancer prevention and care, though further research is still needed to unravel the underlying biology.
Reduced blood flow to the brain is thought to be a key factor in many forms of dementia, including Alzheimer’s, and scientists have just identified a new mechanism regulating this flow, which may also help explain how it goes wrong.
A fat molecule helps maintain the system’s balance, researchers at the University of Vermont discovered, and in mouse models of Alzheimer’s disease, disruption of this balance led to problems.
Fixing the imbalance restored more normal blood flow, offering a hopeful new target for understanding and treating dementia-related brain changes.
Here, Vivian L. Weiss & team highlight stromal tumor-dynamics occurring across the spatial evolution of thyroid cancer from indolent to lethal disease, identifying a prognostic invasive cell subtype:
The figure shows two distinct patterns associated with anaplastic thyroid carcinoma.
6The Francis Crick Institute, London, United Kingdom.
7Institute of Interdisciplinary Research (IRIBHM), Universite Libre de Bruxelles, Brussels, Belgium.
8Department of Laboratory Medicine and Pathology, University of Washington School of Medicine, Seattle, Washington, USA.
3. Pathology as Network Dysregulation.
In recent years, a transformative view of physiology has emerged: the body operates not as isolated organs, but as an integrated communication network in which signals flow bidirectionally between the brain, the immune system, the gut, and peripheral organs. This comprehensive review synthesizes current mechanistic insights into this “organ cross-talk” and frames them within systems biology and neuroscience.
At its core, organ cross-talk encompasses neural, endocrine, metabolic, and immune signaling between organs that coordinate homeostasis and orchestrate responses to stress and disease. From a neuroscience vantage point, three themes stand out:
1. The Brain as a Communication Hub.
2. Peripheral Feedback to the CNS.