Improvements in the Articulate Medical Intelligence Explorer, a large language model designed for diagnostic dialogue, enable the model to request, interpret and reason about multimodal medical data.
Researchers at Tampere University, Finland, have developed a groundbreaking 3D-printed ceramic implant material that closely mimics real human bone. The findings advance the development of personalized bone regeneration and may lead to more effective and accessible treatments for bone defects.
The research article, titled “Biomimetic bone calcium phosphate-based scaffolds fabricated via ceramic vat photopolymerization: Effect of porosity, sintering temperature, mineralogical phases and trace elements on the osteogenic potential,” was published in Materials Today Bio.
Bone grafting is the second most common tissue transplantation procedure worldwide, with more than 2 million operations performed annually. Current treatments often rely on bone taken from the patient or a donor, approaches that are limited in availability and may involve additional surgery, lengthy recovery times and complications. As populations age, the need for safer and more effective alternatives is growing rapidly.
In this study, we identify an unexpected and previously unrecognized role for PI3Kδ in promoting stromal fibrosis in PDAC, expanding its known function beyond immune regulation. Through mechanistic and preclinical studies, we show that PI3Kδ controls the biosynthesis of LPA in cancer cells and stromal fibroblasts, establishing an immunometabolic axis that sustains both fibrosis and immune evasion in PDAC.
Strikingly, PI3Kδ inhibition alone was sufficient to suppress tumor growth, reduce fibrosis, restore antitumor immune responses, and prolong survival across multiple PDAC models. Dual inhibition of PI3Kδ and ATX produced additive effects on stromal remodeling and immune activation, significantly enhancing responsiveness to chemotherapy and PD-1 blockade. These findings position PI3Kδ as a central regulator of the PDAC tumor microenvironment and highlight its therapeutic targeting, alone or in combination, as a promising strategy to treat PDAC.
A pioneering treatment which could slow or reverse liver failure and offer a potential alternative to liver transplants has shown positive results in a medical trial.
70% of end-stage liver disease patients who were treated with macrophage cell therapy in the MATCH trial did not need a liver transplant after four years, compared with just 40% who didn’t receive the treatment.
The cell therapy takes immune cells from the patients’ blood and turns them into mature macrophages – a white blood cell – which is then re-injected back into the patient. The macrophages travel to the liver, where they break down scar tissue, reduce inflammation, and encourage the growth of healthy liver cells.
Researchers from A*STAR Genome Institute of Singapore (A*STAR GIS) have developed a new method to study individual RNA molecules and reveal how their structures influence gene regulation, a fundamental process that affects how cells function in health and disease. Their work was published in Nature Methods.
RNA is best known for carrying genetic instructions from DNA to make proteins. However, RNA does more than act as a messenger. Like a string that can bend, fold and interact with other molecules, RNA can adopt different shapes that affect how it behaves in the cell. These shapes can influence how efficiently proteins are produced, how long RNA molecules last, and how diseases such as viral infections progress.
Until now, studying these structures in detail has been difficult because RNA is highly flexible and dynamic. Most existing methods only provide an average picture across many RNA molecules, making it harder to see how individual RNA molecules may fold differently, even when they come from the same gene.
Engineers have developed a new ultra-thin membrane that allows fuel cells to operate more efficiently at high temperatures by enabling proton transport without water, overcoming a key limitation in clean energy technologies.
The breakthrough, reported in Science Advances, could expand the use of fuel cells in transport, heavy industry, and future clean energy systems.
Fuel cells convert chemical energy directly into electricity, producing water and heat as the main by-products. They are already used in hydrogen-powered vehicles, backup power systems for hospitals and data centers, and space missions where lightweight, reliable energy is essential.
A routine experiment with a new single-cell DNA sequencing method turned into a surprising scientific twist when researchers stumbled upon a bizarre genetic code in a microscopic pond organism. Instead of following the near-universal “rules” of life, this newly identified protist rewrites how genes signal their end. This unexpected discovery challenges long-held assumptions about how genetic translation works and hints that nature may be far more flexible—and mysterious—than scientists realized.
A newly developed targeted radiopharmaceutical treatment can effectively slow tumor growth in pancreatic ductal adenocarcinoma (PDAC), according to new research published in the May issue of The Journal of Nuclear Medicine. In preclinical models, the treatment achieved complete remission of the disease, highlighting its potential to transform care for this highly aggressive cancer.
PDAC accounts for more than 90% of pancreatic cancer cases and remains one of the most lethal malignancies, with a five-year survival rate of less than 5% in patients with metastatic disease. Although surgery is the only curative approach, it is feasible only in 10%–20% of patients with localized disease.
“PDAC is very difficult to treat, and new options are urgently needed,” said Marika Nestor, professor in the Department of Immunology, Genetics and Pathology at Uppsala University in Sweden. “Our previous findings suggest a possible new targeted treatment approach for pancreatic cancer patients whose tumors express CD44v6, which may help make treatment more precise and effective.”
This study aimed to explore the alleviating effects of fisetin, a polyphenolic flavonoid, on ovarian dysfunction in a D-galactose (D-gal)-induced aging mouse model, as well as the underlying mechanisms, using both in vivo and in vitro experiments. Mice were subcutaneously injected with D-gal (100 mg/kg/day) for 60 days to establish the ovarian aging model; during the final 30 days, fisetin (10, 20, 30 mg/kg/day) was given orally. In addition, a senescent model of granulosa cell (GC) was established using D-gal and treated with fisetin. Fisetin supplementation improved ovarian endocrine function and reproductive capacity in aging mice, as reflected by regularized estrous cycles, elevated estradiol levels, and increased embryo numbers. Furthermore, fisetin reduced the number of atretic follicles and the extent of ovarian fibrosis and senescence, while simultaneously restoring the proliferation-apoptosis balance in follicular GCs, as well as alleviating oxidative stress. RNA-sequencing revealed that AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR) signaling and mitophagy were involved in the protective effects of fisetin against ovarian aging. Consistently, fisetin treatment promoted mitophagy, accompanied by AMPK/mTOR activation in ovarian tissues and GCs following D-gal exposure. Inhibition of AMPK attenuated the effect of fisetin on mitophagy. Additionally, blockage of mitophagy also reversed the beneficial effects of fisetin on mitochondrial injury, oxidative stress, cell cycle arrest, and cellular senescence in D-gal-induced senescent GCs. These findings indicate that fisetin prevents ovarian aging by suppressing follicular GC oxidative damage and ameliorating cell cycle arrest via activation of AMPK/mTOR-mediated mitophagy, thereby preserving female fertility.
Researchers at UCLA Health have identified a key gene that may help explain why women are more likely than men to develop a certain type of artery plaque linked to heart disease.
In a study published in Circulation Research, investigators found that a gene known as MYH9 plays an important role in the formation of fibrous plaques. These buildups in the arteries are generally more stable than those more prone to rupture, but they can still lead to heart attacks and other serious cardiac events through plaque erosion.
Atherosclerosis, the buildup of plaque in the arteries, is the underlying cause of most heart disease. Research has mainly focused on unstable plaques, which can rupture and trigger heart attacks. Fibrous, scar-like plaques tend to have thicker caps and different biological characteristics.