Because the method does not require a needle, it could offer an alternative for people who are uncomfortable with injections. Researchers also believe it may make large scale vaccination campaigns easier and faster, particularly in settings where traditional injections are more difficult to administer.
Before human testing began, animal studies showed the vaccine could generate strong immune responses against multiple coronaviruses.
Inflammation, especially chronic inflammation, plays a pivotal role in tumorigenesis and metastasis through various mechanisms and is now recognized as a hallmark of cancer and an attractive therapeutic target in cancer. In this review, we discuss recent advances in molecular mechanisms of how inflammation promotes tumorigenesis and metastasis and suppresses anti-tumor immunity in various types of solid tumors, including esophageal, gastric, colorectal, liver, and pancreatic cancer as well as hematopoietic malignancies.
Therapy resistance is a major obstacle to durable clinical responses. While genetic alterations and signalling rewiring are primary drivers of resistance, metabolic adaptation, which is closely intertwined with these processes, enables tumour persistence under therapeutic pressure and directly contributes to resistance. Peroxisomes are metabolic organelles with a role in controlling lipid metabolism, together with redox signalling and homeostasis—processes that intersect with pathways governing cancer behaviour and therapy response. Indeed, peroxisomal functions are remodelled to support metabolic plasticity and redox buffering under therapeutic stress.
In 2025, the European Medicines Agency approved two antibodies for Alzheimer’s disease: lecanemab (LeqembiTM, from Biogen) and donanemab (Kisunla, from Eli Lilly and Co.), both based on immunotherapy (the use of molecules from the immune system to treat diseases). These antibodies, obtained in the laboratory, act against the Aβ peptide, a protein fragment that accumulates in the brains of patients with Alzheimer’s disease. Elimination of this protein by the immune system helps slow the characteristic cognitive decline of the disease.
These two antibodies are the first disease-modifying therapies for Alzheimer’s. They stop and, in some cases, even partially reverse this devastating condition. However, a frequent and characteristic side effect of these drugs is cerebral bleeding, detectable by magnetic resonance imaging. The brain does not have the molecules and cells that make up the systemic immune system, so the entry of antibodies into the brain is not desirable under healthy conditions, although it is necessary for these treatments to be effective.
The incidence of bleeding in clinical trials ranged from 10% to 27% of treated patients, with a particularly high incidence in individuals carrying a specific apolipoprotein allele: APOEε4. In Europe, these treatments can be administered only to people with one or no copy of the APOEε4 allele, a genetic variant associated with a higher risk of Alzheimer’s.
Non-invasive eye scans allow doctors a zoomed-in, three-dimensional look beneath the eye’s surface without causing discomfort or pain to the patient. Used routinely in clinics worldwide, the scans produce detailed views of individual layers of the eye’s interior to help diagnose conditions that threaten vision. But with that level of precision comes a flood of data—hundreds of images per scan that physicians have to review manually, a time-consuming process that is vulnerable to human error.
Now, researchers at Washington University School of Medicine in St. Louis, in collaboration with colleagues at the University of Washington in Seattle and Genentech, Inc., have developed an experimental artificial intelligence (AI) system that can speed the scan review process and help doctors spot subtle signs of eye disease sooner. The technology, called OCTCube-M, includes a family of three AI models that are designed to read and interpret 3D images of the eye’s retina as well as other types of eye scans.
In a new study, the researchers found that, compared with older models, the new AI system more accurately identified eight different retinal diseases, including age-related macular degeneration, a common disease that damages the retina and is the leading cause of blindness in people over 50. It also was more accurate in its predictions of how fast a severe form of this condition, called geographic atrophy, would progress.
Creatine, the organic acid that is popularly taken as a supplement by athletes and bodybuilders, supercharges a critical class of immune cells that activate and prepare the body’s key cancer-fighters, according to new UCLA research.
The study, conducted in mouse models and human cells and published in iScience, builds directly on earlier work from the same lab showing that creatine powers killer T cells in their battle against tumors. Now, the team has discovered that creatine also fuels dendritic cells, specialized immune cells that capture tumor fragments and direct killer T cells to attack.
Most approved cancer immunotherapies work by targeting killer T cells directly, yet only about 20%–40% of patients respond to them. Bolstering the dendritic cells that train and activate T cells could potentially offer a way to bring the benefits of immunotherapy to more patients.
Efficient brain-wide communication requires neural activity to traverse long anatomical distances rapidly. Here we examine how propagation timing is jointly associated with spatial geometry, functional network organization, and long-range white-matter pathways and their microstructural properties. And we ask whether the same rules govern epileptiform and physiological activity. Using stereo-EEG and diffusion spectrum imaging from 47 epilepsy patients (26 males and 21 females), we quantified inter-regional propagation with two complementary delay estimators: event-based interictal epileptiform discharge (IED) traveling waves and continuous lagged-correlation delays during IED-free periods. We found that IED propagation traversing gray and white matter formed reproducible spatiotemporal motifs that deviated from randomized null models, indicating structured routing rather than random spread. Epileptiform and physiological propagation delays increased over short ranges but saturated at longer distances, indicating that geometry alone cannot account for long-range fast propagation. Beyond geometry, stronger structural connectivity and higher functional connectivity were associated with shorter delays, and intrinsic functional modules facilitated efficient communication: within-network propagation was faster than between-network propagation. Crucially, diffusion-derived quantitative anisotropy (QA) revealed a microstructural mechanism for long-range fast propagation: long-range white-matter tracts showed higher QA, and QA was positively associated with apparent propagation velocity. Together, these results identify convergent, architecture-dependent constraints on propagation timing that generalize across epileptiform and normal activity, providing a principled bridge between macroscale connectome organization and fast intracranial spatiotemporal dynamics.
Significance statement Efficient communication across long anatomical distances is fundamental for the human brain. By integrating stereo-EEG with diffusion spectrum imaging, this study shows that brain-wide information propagation is not determined by distance alone, but is critically supported by long-range white-matter pathways, their microstructural properties, and intrinsic functional network organization. We also find that both pathological epileptiform discharges and physiological spontaneous activity follow shared propagation rules, exhibiting distance saturation, structural facilitation, and preferential within-network transmission. These findings provide a microstructure-grounded account of how the human brain achieves fast, efficient large-scale communication, bridging macroscale connectome architecture with millisecond-scale neural dynamics.
