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New mechanism reveals how heart cells resist regenerative reprogramming

Specialized cells in the human body make biological trade-offs to perform certain jobs. To support the large, hardworking hearts that power other organs, heart cells have evolved to be extremely efficient and resilient. Because the adult human heart cannot repair itself the way skin does, scientists have studied ways to “reprogram” heart cells to regenerate after heart attacks. Heart cells have very stable identities, however, and are resistant to reprogramming.

Scientists at Sanford Burnham Prebys Medical Discovery Institute and collaborators at Johns Hopkins University School of Medicine published findings in Nature Communications that cover a new mechanism cells use to protect their identities and ward off reprogramming attempts. Continued study of the obstacles to cellular reprogramming may lead to treatments that can help the heart repair itself after injury.

Stable DNA building blocks enable faster oligonucleotide synthesis without oxidation

The chemical synthesis of oligonucleotides (ONs) is central to modern molecular biology, diagnostics and nucleic acid therapeutics. While demand for high-quality ONs is increasing, the conventional synthetic method has long-standing efficiency challenges. Widely adopted P(III)-phosphoramidite-based ON synthesis requires an oxidation step after every nucleotide coupling cycle and uses moisture-sensitive building blocks, adding complexity to the workflow and slowing the process.

Early studies of ON synthesis showed that pentavalent phosphorus [P(V)] chemistry could form linkages between nucleotides. However, practical limitations, including unstable intermediates, slow coupling, harsh deprotection or poor performance during chain elongation, prevented these methods from replacing P(III)-based phosphoramidite chemistry.

A recent study led by Associate Professor Noriko Saito-Tarashima of the Graduate School of Pharmaceutical Sciences at Tokushima University in Japan, along with Nana Mihara, a doctoral student from the same institution, investigated whether nucleoside 3′-phosphorofluoridates [P(V)–F] could be used as stable building blocks for ON synthesis without requiring a separate oxidation step.

Misfolded insulin may be quietly driving diabetes

As prediabetes advances toward diabetes, this delicate process can begin to break down. Misfolded and defective proteins accumulate inside cells, creating stress that can damage the pancreatic cells responsible for producing insulin.

Researchers from Sanford Burnham Prebys Medical Discovery Institute and the University of Michigan reported new details about this process on June 1, 2026, in the Proceedings of the National Academy of Sciences. Their findings reveal how insulin-producing cells coordinate protein folding and what happens when that system falls out of balance. The work suggests that strengthening the cellular machinery responsible for folding proteins could help protect these cells from damage.

Too little or too much iodine may push immunity off balance

This narrative review finds that adequate iodine supports thyroid hormone signaling, leukocyte metabolism, antioxidant defenses, and antimicrobial activity in humans and domesticated mammals. Both deficiency and sustained excess may impair immunity or promote thyroid inflammation, but precise immune-specific intake thresholds remain uncertain.

UCLA researchers may have discovered how to heal damaged kidneys

A drug previously developed at UCLA to help heart tissue repair itself after a heart attack might also help kidney tissue repair and regenerate, researchers have found.

The drug, called AD-NP1, which was recently approved by the FDA for a Phase 1 clinical trial in humans, works in heart tissue by blocking a protein that disrupts healing and prevents internal organs from fully recovering. Researchers have now found that blocking this protein in kidney tissue speeds repair after kidney injury in mice.

The new finding, published in Cell Stem Cell, builds upon many years of research in the laboratory of UCLA cardiovascular scientist Arjun Deb.

Bloodstream-delivered cell therapy slows muscle decline in young people with Duchenne muscular dystrophy, trial finds

A cell therapy called deramiocel could slow muscle weakening in boys and young men with advanced Duchenne muscular dystrophy (DMD) and may also slow heart damage in those who already have heart muscle disease, a Phase III clinical trial published in The Lancet has found.

It is the first Phase III trial of a cell therapy made from donor cells and administered through the bloodstream to treat a genetic disease, and the first such trial in boys and young men whose DMD is already advanced. The therapy is grown from heart cells that were donated for transplant but could not be used.

There is no cure for DMD, a serious genetic condition that causes the muscles, including the heart, to gradually weaken and waste away. It almost exclusively affects boys and young men because the gene involved sits on the X chromosome. As the disease progresses, most patients lose the ability to walk and come to depend on their arms and hands for everyday tasks and independence.

Two meteor showers peak this week. Here’s how to watch

A double meteor shower peak will occur this week — but sky-gazers might have a difficult time catching a glimpse of the cosmic activity.

The Alpha Capricornids are active from early July to mid-August, and the Southern Delta Aquariids are active from mid-July to mid-August, but both are expected to reach their peaks — the point at which Earth will pass through the densest part of the shower — Thursday night into Friday, according to the American Meteor Society.

A third meteor shower, the Perseids, will also be active this week, though it won’t peak until mid-August.

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