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Evolutionary comparison points to pigs as superior models for human pancreas and diabetes research

Pancreas development in pigs resembles humans much more closely than does the established mouse model. An international team headed by Helmholtz Munich and the German Center for Diabetes Research (DZD) has now produced a comprehensive evolutionary comparison of single-cell atlases of pancreas development. The results open up new prospects for regenerative therapies.

For decades, the pancreas and its development have been a major focus of diabetes and . Until now, the science was almost exclusively based on mouse models. However, mice differ from humans in many respects—from developmental duration to metabolism and .

“Particularly for complex diseases such as diabetes mellitus, we need models that truly resemble humans,” therefore emphasizes Prof. Heiko Lickert. The DZD researcher is the director of the Institute of Diabetes and Regeneration Research at Helmholtz Munich and professor at the Technical University of Munich (TUM).

The right dose for the brain: Selenomethionine’s role in protecting dopaminergic neurons

Dopamine is often called the brain’s “motivation molecule,” but for me, it represents something deeper, a window into how fragile our neurons can be. The cells that produce dopamine, known as dopaminergic neurons, are among the first to die in Parkinson’s disease, leading to the motor symptoms that gradually rob patients of movement and independence.

To understand what makes these neurons so vulnerable, I used an in-vitro model where I exposed N27 dopaminergic cells to 6-hydroxydopamine (6-OHDA), a toxin that triggers oxidative stress, like what occurs in the Parkinsonian brain. Then, I introduced Selenomethionine (SeMet), an organic form of selenium, to test whether this compound could counteract the damage and help the neurons survive.

Selenium has long intrigued scientists for its paradoxical nature. It is a trace element essential for antioxidant defense, yet in excess it can become toxic. I wanted to see whether a specific range of SeMet concentrations could offer meaningful protection without tipping that balance. My study, carried out at Charles University and the National Institute of Mental Health (NUDZ) in the Czech Republic, set out to define that “safe and effective window.” It is published in the journal In vitro models.

Pan-immunotherapy biomarker for treatment monitoring

The ability of immune cells—particularly CD8+ T cells—to launch a rapid burst of proliferation inside tumors is key to the success of modern day cancer immunotherapies. However, the factors and mechanisms that drive this burst in proliferation remain poorly understood, making it difficult to predict which patients will benefit from treatment. A deeper understanding of this T cell burst could also guide the development of new therapies that enhance T cell proliferation and improve treatment outcomes.

To tackle this challenge, an international team of researchers developed a novel approach to monitor CD8 ⁺ T cell activity over time. Their findings, recently published in the journal Nature Communications, sheds new light on how T cells expand in the tumor—and how their expansion can be predicted, and ultimately, therapeutically reactivated.

“The development of immunotherapies has been hindered by our inability to comprehensively monitor their effects on immune cells—particularly cancer-fighting T cells—over time,” explainsthe author. “Building on our previous work, we developed a method to track these cells longitudinally in the tumor, allowing us to gain deeper insights into the burst of proliferation that drives effective anti-tumor responses.”

How a tiny RNA molecule in the kidney triggers a deadly autoimmune disease

Researchers at the University Hospital Bonn (UKB) and the University of Bonn have discovered how a small, naturally occurring RNA molecule in the kidney activates a mutated immune receptor, triggering a chain reaction.

In cooperation with Nanyang Technological University Singapore and the University Hospital Würzburg, among others, the study provides an explanation of how a in the immune receptor RIG-I transforms the body’s defense system into a self-destructive force and causes severe organ-specific autoimmune diseases.

The results have been published in the journal Science Immunology.

A gene from 100-year-olds could help kids who age too fast

Scientists have uncovered a breakthrough in the fight against a rare genetic condition that causes children to age much faster than normal. The discovery involves “longevity genes” found in people who live exceptionally long lives, often beyond 100 years. Researchers from the University of Bristol and IRCCS MultiMedica found that these genes, which help maintain the health of the heart and blood vessels during aging, could reverse some of the damage caused by this devastating disease.

The study, published in Signal Transduction and Targeted Therapy, is the first to show that a gene from long-lived individuals can slow down heart aging in a model of Progeria. Known scientifically as Hutchinson-Gilford Progeria Syndrome (HGPS), this rare and fatal disorder causes children to exhibit signs of “accelerated aging.”

Progeria stems from a mutation in the LMNA gene, which leads to the creation of a harmful protein called progerin. This protein disrupts normal cell function, particularly in the heart and blood vessels. Most affected children die in their teenage years from heart complications, though some, like Sammy Basso — the oldest known person with Progeria — live longer. Sammy passed away on October 24, 2024, at the age of 28.

Artificial muscles use ultrasound-activated microbubbles to move

Researchers at ETH Zurich have developed artificial muscles that contain microbubbles and can be controlled with ultrasound. In the future, these muscles could be deployed in technical and medical settings as gripper arms, tissue patches, targeted drug delivery, or robots.

It might look like a simple material experiment at first glance, as a brief ultrasound stimulation induces a thin strip of silicone to start bending and arching. But that’s just the beginning. A team led by Daniel Ahmed, Professor of Acoustic Robotics for Life Sciences and Healthcare, has developed a new class of : flexible membranes that respond to ultrasound with the help of thousands of microbubbles.

The work is published in the journal Nature.

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