Researchers at the University of Basel have developed a gene therapy that could potentially treat a rare and currently fatal muscle disease in children. The study shows in animal models that a single treatment is sufficient to stabilize muscles and nerves and to halt disease progression. The challenge now is to bring this promising therapy into the clinic.

The powerhouse of the cells – known as mitochondria – appear to be able to influence the number of lipid droplets in the cell. A mechanism that is actually intended for a completely different purpose plays a central role in this. This is shown by a recent study by the University of Bonn and University Hospital Bonn and the University of Freiburg. The results have now been published in the journal Nature Cell Biology.

Biochemical and structural biological analysis of a hypothetical gene (protein) within a gene cluster related to metabolic pathway of L-threonate, a four-carbon sugar acid, revealed it’s enzyme function as a L-threonate 3-dehydrogenase and physiological role for metabolic diversity. Although the existence of this enzyme itself was reported in the same academic journal in 1964, the molecular identity of which has remained unknown for over 60 years.

Researchers from the Critical Analytics for Manufacturing Personalized-Medicine (CAMP), an interdisciplinary research group (IRG) of Singapore-MIT Alliance for Research and Technology (SMART), supported by SMART Antimicrobial Resistance (AMR) IRG and in collaboration with Massachusetts Institute of Technology (MIT) and National University of Singapore (NUS), have developed a first-of-its-kind rapid, non-destructive method to monitor iron flux — the movement and rate at which cells take in, store, use and release iron — in mesenchymal stromal cells (MSCs), which can provide insights within a minute on the cell’s ability to grow cartilage tissue for cartilage repair. This breakthrough offers a promising pathway toward more consistent and efficient manufacturing of high‑quality MSCs used in regenerative therapies, which are used to treat joint diseases such as osteoarthritis, chronic joint degeneration conditions, and cartilage injuries.

A new study highlights how the wild can be a “death trap” for animals that are released from captivity after previously being rescued.

Published in the journal Global Ecology and Conservation, the study follows the fate of nine slow lorises, the world’s only venomous primate, which were released into a forest in Bangladesh – a site previously used for a number of slow loris reintroductions.

Seven of the nine died within six months and the study highlights the importance of fully understanding an animal’s behaviour, its time spent in captivity and crucially the density of resident populations at the release site before sending rescued animals back into the wild.

Scripps Research scientists discover that some membrane-less compartments are built from tiny filaments—a finding that could shape drug development.

Even in the womb, where all oxygen is provided by the parental placenta, fetuses can—and do—yawn. More yawns during observation were associated with a lower weight at birth—potentially indicating mild fetal stress in the womb, according to a study published February 25, 2026 in the open-access journal PLOS One by Damiano Menin, of the Università degli Studi di Ferrara in Italy, and colleagues.