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Category: biotech/medical – Page 37

Dreams drain energy: The REM sleep paradox

The brain demands a lot of energy compared with other organs. However, it can also make do when energy supplies are scarce, flexibly processing information using what is available. How the brain resourcefully allocates this limited energy across internal states remains a key question in neuroscience.

Sleep provides a useful window into answering this question. Although sleep is associated with rest, the brain remains highly active. This is especially true during rapid eye movement (REM) sleep, the stage closely linked to dreaming and memory processing. REM sleep is sometimes called “paradoxical sleep” because the body is largely still while the brain shows wake-like activity. Researchers at Tohoku University have now uncovered another paradox within REM sleep: While energy supply to the dreaming brain appears to rise, the energy molecule used directly by neurons falls. The findings are published in Communications Biology.

“Ever felt exhausted after a vivid dream?” asks Professor Ko Matsui of Tohoku University. “Sleep may appear peaceful, but the brain is highly active—especially when dreaming. We were intrigued by this paradox and wanted to look into the scientific basis behind why dreaming is somehow tiring.”

Scientists decipher how T cells sense enemies—such as cancer—at point of contact

Every encounter between a T cell and a potential target—especially when that target is a developing tumor—begins with a rapid series of molecular decisions. Within seconds, the immune cell must determine whether to launch an attack or stand down. T cells are so potent, so potentially devastating, that misreading the situation can cause serious tissue injury.

But cancer cells come equipped with a bag of tricks that allows them to disarm these powerful warriors of the immune system. All of these activities, whether mediated by T cells or their targets, occur at split-second speed and unfold at the point of cell-to-cell contact.

Now, scientists have identified tiny nanoscale contact points where those decisions are made, revealing how activation and inhibitory signals are integrated at the first moments of a cell-to-cell encounter.

AI finds tiny gene editor changes that reduce unintended DNA edits

Gene editing is a highly precise and powerful technology that allows scientists to insert, delete, modify or replace DNA bases in living organisms. It has a variety of uses, including correcting disease-causing mutations and improving crops. Tools like CRISPR act as molecular scissors that target specific places in a genome to make these changes. But the technology is not perfect and can accidentally edit the wrong pieces of DNA or RNA.

In research published in Nature, scientists describe a new framework that uses AI to make these tools more accurate. Hoi Yee Chu and Alan S.L. Wong of the University of Hong Kong published a News and Views piece in the same journal on the significance of this research.

Faster fracture tests offer path to more sustainable material choices

Recycled materials promise a cleaner future, but recycled content alone does not necessarily make a product sustainable. At Georgia Tech’s Daedalus Lab, assistant professor Christos Athanasiou and postdoctoral researcher Danqi Sun are working to provide greater certainty to designers and engineers by rethinking how materials are tested for their fracture characteristics.

Their article in Science Advances details a new testing protocol that reduces costs, increases speed and simulates real-world conditions.

Materials shape nearly every part of modern life, from packaging and consumer products to bridges and medical devices. Choosing the right material involves balancing durability, cost, manufacturability and environmental impact. Yet those decisions are not always guided by a clear understanding of how materials age and fail under real-world conditions, especially for recycled materials like plastics.

Chinese researchers map epigenetic control of congenital heart defects

The findings have direct implications for clinical practice and future research. For genetic screening, the study provides a clear priority: CHD7 for outflow‑tract defects, CHD4 for chamber‑patterning anomalies, and CHD8 for ventricular dysfunction. This prioritization can improve diagnostic efficiency. Therapeutically, while directly targeting remodelers is risky due to their broad expression, identifying their downstream pathways—such as those regulating cardiomyocyte proliferation or metabolism—may offer safer drug targets. Furthermore, future studies combining time‑resolved multi‑omics and combinatorial genetics could uncover how these proteins coordinate across development, potentially paving the way for precise, temporally controlled epigenetic therapies.

A team from China has published (DOI: 10.1007/s12519-026–01049-y) this definitive synthesis in World Journal of Pediatrics. The review systematically evaluates the current evidence from human genetics, animal models, and stem‑cell systems to assign specific cardiac functions to different CHD family members. The findings offer a new conceptual map for understanding the epigenetic control of heart development and disease.

The study’s key contribution is its systematic analysis of the evidence, which reveals a clear division of labor among CHD proteins. CHD7, the gene most frequently mutated in CHARGE syndrome (an acronym for Coloboma, Heart defects, Atresia choanae, Retarded growth, Genital abnormalities, and Ear abnormalities) syndrome, shows the strongest link to cardiac development, playing a dominant role in building the heart’s early structure. In contrast, CHD3 and CHD4 act as “identity guardians,” ensuring that heart cells commit to the correct fate during chamber formation. For CHD8, while evidence is still emerging, it appears to regulate later ventricular growth and functional maturation. Notably, although these proteins seem to act at different stages—CHD7 early, CHD4 mid, and CHD8 late—the review emphasizes that direct proof of their coordinated action is lacking.

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