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A disrupted protein degradation process in heart muscle cells can lead to a range of severe heart diseases. In the case of dilated cardiomyopathy, a pathological enlargement of the heart chambers, researchers at the Max Planck Institute for Heart and Lung Research in Bad Nauheim have now identified a cause: a low level of the enzyme Ubiquitin-specific peptidase 5 (USP5) leads to an accumulation of Ubiquitin in heart muscle cells and the formation of protein aggregates, which trigger heart diseases. Increasing USP5 levels in heart muscle cells protects the heart from harmful degradation processes, offering a perspective for new therapies.

Dilated cardiomyopathy is a pathological enlargement of one or both heart chambers, including the atria. The resulting restriction of heart function is caused by structural damage to . The consequence is , which can lead to death without a heart transplant. Existing can usually not stop or reverse the progression of the disease.

In search of new therapeutic approaches, researchers from the department of Thomas Braun at the Max Planck Institute for Heart and Lung Research have investigated the molecular processes of protein degradation in heart muscle cells. Yvonne Eibach and Silke Kreher, both first authors of the study published in Science Advances, together with their research partners, discovered disturbances in the process that serves the disposal of defective or no longer needed proteins.

An international team of scientists, including researchers from Harvard University and the University of Zurich, analyzed clinical trial results 777 elderly Swiss adults to test the potential anti-aging benefits of supplements and exercise.

While there’s no perfect way to measure biological aging, the researchers used tools that help measure age-related decline in the cells and organs, including factors like brain health and heart health.

They looked at participants who underwent one of eight longevity treatments over three years, including exercising and supplementing omega-3s, vitamin D, or both.

The term “nanoscale” refers to dimensions that are measured in nanometers (nm), with one nanometer equaling one-billionth of a meter. This scale encompasses sizes from approximately 1 to 100 nanometers, where unique physical, chemical, and biological properties emerge that are not present in bulk materials. At the nanoscale, materials exhibit phenomena such as quantum effects and increased surface area to volume ratios, which can significantly alter their optical, electrical, and magnetic behaviors. These characteristics make nanoscale materials highly valuable for a wide range of applications, including electronics, medicine, and materials science.

DNA (deoxyribonucleic acid), the molecular “blueprint” carrying the genetic instructions that influence the growth, development, reproduction and predispositions of individual humans, can undergo different types of mechanical stress inside cells. For instance, it can be twisted or stretched, impacting its overall structure and dynamics.

Researchers at the University of York recently explored how DNA behaves under torsion and tension using molecular dynamics simulations. These atomic-scale simulations yielded interesting new findings, which were published in a paper in Physical Review Letters.

“I have always been interested in studying how DNA behaves inside the cell,” Dr. Agnes Noy, senior author of the paper, told Phys.org. “We are used to thinking of DNA as a relaxed ‘perfect’ , but the reality is far from that. Inside cells, DNA is under/overtwisted, resulting in the formation of ‘supercoiled’ loops, resembling what can happen to long cords or garden hoses in our homes.”

A metabolomics study pinpointed the differences between leukemia stem cells (LSCs) and their normal counterparts, and suggests elevated levels of spermidine are a signature and a targetable weakness in LSCs.


Spermidine is essential for the function of leukemia stem and progenitor cells through the regulation of KAT7 expression.

Tissue processing advance can label proteins at the level of individual cells across whole, intact rodent brains and other large samples just as fast and uniformly as in dissociated single cells.

Scientists at UC San Francisco have pioneered a groundbreaking approach to fighting cancer using engineered fat cells.

By transforming ordinary fat into high-energy beige fat using CRISPR, they created a cell type that voraciously consumes nutrients — outcompeting and starving tumors.

Revolutionizing cancer treatment: engineered fat cells starve tumors.

Sorry, you’re not Neo and this isn’t “The Matrix.” Michio Kaku gets real about simulation theory.

Up next, Is reality real? These neuroscientists don’t think so ► https://youtu.be/RZdfE_7cde0?si=2-isNPeC1lVvgbiu.

Are we all just living in an elaborate simulation?

After movies like “The Matrix” (1999) posited the existence of a superficial world layered over our own, human imagination has run abound with theories about the nature of our reality. To a small but passionate minority, the red pill that can awaken us to this illusion is right at our fingertips.

World-renowned physicist Michio Kaku isn’t quite ready to take that pill. In fact, he’s skeptical that the pills even exist. He explains why.

Go Deeper with Big Think:

The proportion of people who have never smoked being diagnosed with lung cancer is rising, with new research pointing to air pollution as a growing contributor to lung cancer around the world.

Researchers from the International Agency for Research on Cancer said for never-smokers, lung cancer was the fifth largest leading cause of cancer deaths worldwide. Those cases were nearly exclusively the subtype adenocarcinoma — a tumour that forms in the glandular tissue — and largely in women and Asian populations.

The research, published in The Lancet Respiratory Medicine journal, found nearly 200,000 or about 15 per cent of all adenocarcinoma cases in 2022 were a result of air pollution, suggesting the risk of lung cancer linked to air pollution was also on the rise, particularly in east Asia and China.