Scientists Discover Key Protein That May Reverse Aging at the Cellular Level

 Researchers from Osaka University have discovered that the protein subunit AP2A1 may play a role in the unique structural organization of senescent cells.

There are countless products on the market that claim to restore a youthful appearance by reducing wrinkles or tightening the jawline. But what if aging could be reversed at the cellular level? Researchers in Japan may have uncovered a way to do just that.

A recent study published in Cellular Signaling by scientists at Osaka University identifies a key protein that regulates the transition between “young” and “old” cell states.

As the body ages, senescent cells—older, less active cells—accumulate in various organs. These cells are significantly larger than younger ones and display structural changes, including altered organization of stress fibers, which are essential for movement and interaction with their environment.

“We still don’t understand how these senescent cells can maintain their huge size,” says lead author of the study Pirawan Chantachotikul. “One intriguing clue is that stress fibers are much thicker in senescent cells than in young cells, suggesting that proteins within these fibers help support their size.”

The Role of AP2A1 in Cellular Senescence

To explore this possibility, the researchers examined AP2A1 (Adaptor Protein Complex 2, Alpha 1 Subunit). AP2A1 is a protein that is upregulated in the stress fibers of senescent cells, including fibroblasts, which create and maintain the skin’s structural and mechanical characteristics, and epithelial cells. The researchers eliminated AP2A1 expression in older cells and overexpressed AP2A1 in young cells to determine the effect on senescence-like behaviors.

“The results were very intriguing,” explains Shinji Deguchi, senior author. “Suppressing AP2A1 in older cells reversed senescence and promoted cellular rejuvenation, while AP2A1 overexpression in young cells advanced senescence.”

Furthermore, the researchers found that AP2A1 is often closely associated with integrin β1, a protein that helps cells latch onto the scaffolding-like collagen matrix that surrounds them, and that both AP2A1 and integrin β1 move along stress fibers within cells. In addition, integrin β1 strengthened cell–substrate adhesions in fibroblasts; this might explain the cause of the raised or thickened structures characteristic of senescent cells.

“Our findings suggest that senescent cells maintain their large size through improved adhesion to the extracellular matrix via AP2A1 and integrin β1 movement along enlarged stress fibers,” concludes Chantachotikul.

Given that AP2A1 expression is so closely linked to signs of aging in senescent cells, it could potentially be used as a marker for cellular aging. The research team’s work may also provide a new treatment target for diseases that are associated with old age.

Website: popularscientist.com

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Quantum Computers Keep Losing Qubits but Scientists Just Found a Fix

 

Vanishing atoms can ruin quantum calculations. Scientists have a new plan to locate leaks.

Quantum computers face a major challenge: atoms, which serve as their qubits, can vanish without warning, corrupting calculations. Researchers have developed a groundbreaking method to detect this problem in neutral-atom quantum systems without disrupting their state. This discovery helps overcome a key hurdle in making quantum computing reliable on a large scale.

Quantum Computing’s Hidden Problem: Atom Loss

Atoms inside quantum computers can sometimes disappear without warning, disrupting calculations and corrupting data. This issue, known as atom loss, has been a major challenge in quantum computing — until now.

For the first time, researchers from Sandia National Laboratories and the University of New Mexico have developed a practical method to detect these “leakage errors” in neutral-atom quantum computers. Their breakthrough removes a key obstacle in the field, bringing scientists closer to unlocking the full potential of quantum technology. Many experts believe these advanced computers could reveal insights about the universe that are beyond the reach of current systems.

“We can now detect the loss of an atom without disturbing its quantum state,” said Yuan-Yu Jau, Sandia atomic physicist and principal investigator of the experiment team.

The team’s method, detailed in a recent paper in PRX Quantum, achieved 93.4% accuracy in detecting lost atoms. By identifying and flagging these errors, researchers can take steps to correct them, improving the stability of quantum computers.

This research was supported by Sandia’s Laboratory Directed Research and Development program.

A Looming Crisis for Future Quantum Machines

Atoms are squirrely little things. Scientists control them in some quantum computers by freezing them at just above absolute zero, about minus-460 degrees Fahrenheit. A thousandth of a degree too warm and they spring free. Even at the right temperature, they can escape through random chance.

If an atom slips away in the middle of a calculation, “The result can be completely useless. It’s like garbage,” Yuan-Yu said.

A detection scheme can tell researchers whether they can trust the result and could lead to a way of correcting errors by filling in detected gaps.

Neutral-Atom Computers Now Have a Fighting Chance

Matthew Chow, who led the research, said atom loss is a manageable nuisance in small-scale machines because they have relatively few qubits, so the odds of losing one at any given moment are generally small.

But the future has been looking bleak. Useful quantum computers will need millions of qubits. With so many, the odds of losing them mid-program spikes. Atoms would be silently walking off the jobsite en masse, leaving scientists with the futile task of trying to use a computer that is literally vanishing before their eyes.

“This is super important because if we don’t have a solution for this, I don’t think there’s a way to keep moving forward,” Yuan-Yu said.

Researchers have found ways to detect atom loss and other kinds of leakage errors in different quantum computing platforms, like those using electrically charged atoms, called trapped ion qubits, instead of neutral ones. The New Mexico-based team is the first to non-destructively detect atom loss in neutral-atom systems. By implementing simple circuit-based techniques to detect leakage errors, the team is helping avert the crisis of uncontrollable future leakage.

The Challenge: Detecting Atoms Without Looking

The dilemma of detecting atom loss is that scientists cannot look at the atoms they need to preserve during computation.

“Quantum calculations are extremely fragile,” Yuan-Yu said.

The operation falls apart if researchers do anything at all to observe the state of a qubit while it’s working.

Austrian physicist Erwin Schrödinger famously compared this concept to having a cat inside a box with something that will randomly kill it. According to quantum physics, Schrödinger explained, the cat can be thought of as simultaneously dead and alive until you open the box.

“It’s very easy to have a mathematical description of everything in terms of quantum computing. But to visualize entangled quantum information, it’s hard,” Yuan-Yu said.

So how do you check that an atom is in the processor without observing it?

“The idea is analogous to having Schrödinger’s cat in a box, and putting that box on a scale, where the weight of the box tells you whether or not there’s a cat, but it doesn’t tell you whether the cat’s dead or alive,” Chow said.

A Surprising Discovery Sparks a Breakthrough

Chow, a University of New Mexico doctoral student and Sandia intern at the time of the research, said he never expected this breakthrough.

“This was certainly not a paper that we had planned to write,” he said.

He was debugging a small bit of quantum computing code at Sandia for his dissertation. The code diagnoses the entangling interaction — a unique quantum process that links the states of atoms — by repeatedly applying an operation and comparing the results when two atoms interact versus when only one atom is present. When the atoms interact, the repeated application of the operation makes them switch between entangled and disentangled states. In this comparison, he observed a key pattern.

Every other run, when the atoms were disentangled, the outcome for the two-atom case was markedly different from the solo-atom case.

Turning an Accidental Finding into a Quantum Tool

Without trying, Chow realized, he had found a subtle signal to indicate a neighboring atom was present in a quantum computer without observing it directly. The oscillating measurement was the scale to measure whether the cat is still in the box.

“This was the thing that got me really excited — that made me show it to Vikas.”

Vikas Buchemmavari, another doctoral student at UNM and a frequent collaborator, knew more quantum theory than Chow. He works in a research group led by the director of UNM’s Center for Quantum Information and Control, Ivan Deutsch.

“I was simultaneously very impressed by the gate quality and very excited about what the idea meant: We could detect if the atom was there or not without damaging the information in it,” Buchemmavari said.

Testing and Verifying the New Method

He went to work formalizing the idea into a set of code tailored to detect atom loss. It would use a second atom, not involved in any calculation, to indirectly detect whether an atom of interest is missing.

“Quantum systems are very error-prone. To build useful quantum computers, we need quantum error correction techniques that correct the errors and make the calculations reliable. Atom loss — and leakage errors — are some of the worst kinds of errors to deal with,” he said.

The two then developed ways to test their idea.

“You need to test not only your ability to detect an atom, but to detect an atom that starts in many different states,” Chow said. “And then the second part is to check that it doesn’t disturb that state of the first atom.”

Chow’s Sandia team jumped onboard, too, helping test the new routine and verify its results by comparing them to a method of directly observing the atoms.

“We had the capability at Sandia to verify it was working because we have this measurement where we can say the atom is in the one state or the zero state or it’s gone. A lot of people don’t have that third option,” Sandia’s Bethany Little said.

The Future of Correcting Atom Loss

Looking ahead, Buchemmavari said, “We hope this work serves as a guide for other groups implementing these techniques to overcome these errors in their systems. We also hope this spurs deeper research into the advantages and trade-offs of these techniques in real systems.”

Chow, who has since earned his doctoral degree and now works at HRL Laboratories, said he is proud of the discovery because it shows the problem of atom loss is solvable, even if future quantum computers do not use his exact method.

“If you’re careful to keep your eyes open, you might spot something really useful.”

website: popularscientist.com

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A Real-Time Blood Test for Cancer Tumors

 

A newly published study from Yale University shows that liquid biopsies offer a real-time blood test for solid lung cancer tumors.

In the rapidly changing world of molecular profiling for genetic diseases, cancer researchers are increasingly optimistic about the reality of a simple blood test to monitor and treat solid tumor cancers.

Recent studies show that liquid biopsy, conducted through a blood test, could be a surrogate for standard tissue biopsies in assessing genomic changes in certain non-small cell lung cancer tumors, according to an editorial by Yale cancer researchers Dr. Roy S. Herbst, Katerina Politi, and co-author Dr. Daniel Morgensztern of Washington University in St. Louis, published February 26 in JAMA Oncology. Specifically, the authors commented on a study looking at non-small cell lung tumors with particular genetic alterations that could be detected in blood.

The findings of that study have significant implications for other types of solid tumors, said Herbst, professor of medicine and pharmacology, and chief of medical oncology at Yale Cancer Center and Smilow Cancer Hospital. A blood test offers a less-invasive and less-expensive way to rebiopsy patients at various points during treatment, he noted. Patients could avoid additional surgeries, and oncologists could make more timely decisions about which drugs are the best match given a tumor’s genetic profile.

“Until recently, profiling tumors using blood serum wasn’t accurate enough to detect the complexities of solid tumors in a way that would allow us take meaningful action,” Herbst said. “This real-time monitoring means we will know what’s happening with a tumor as it changes, for better or worse.”

Historically, blood biopsy has been used for molecular profiling of blood cancers and other genetic diseases like Down syndrome. Yale is investigating how liquid biopsies can be used to track response and resistance to cancer therapies. A key issue will be the sensitivity and specificity of the test, which Yale researchers will continue to explore.

Website: popularscientist.com

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Scientists Just Discovered an RNA That Repairs DNA Damage – And It’s a Game-Changer

 

Our DNA is constantly under threat — from cell division errors to external factors like sunlight and smoking. Fortunately, cells have intricate repair mechanisms to counteract this damage.

Scientists have uncovered a surprising role played by long non-coding RNA, particularly NEAT1, in stabilizing the genome. Their findings suggest that NEAT1, when highly methylated, helps the cell recognize and repair broken DNA strands more efficiently. This discovery could pave the way for new cancer treatments targeting tumors with high NEAT1 expression.

Genome Instability and Disease Risk

Every time a cell divides, its DNA is at risk of damage. To complete division, the cell must copy its entire genetic code — billions of letters long — which can lead to occasional errors. But cell division isn’t the only threat. Over time, exposure to factors like sunlight, alcohol, and cigarette smoke can also harm DNA, increasing the risk of cancer and other diseases.

Fortunately, cells have built-in repair systems to counteract this damage. This process, known as the DNA damage response (DDR), activates specific signaling pathways that detect and fix errors. These mechanisms help maintain genetic stability and ensure the cell’s survival.

A New Look at the DNA Damage Response

A team of scientists from Julius-Maximilians-Universität Würzburg (JMU) in Bavaria, Germany, has now taken a closer look at one of these signaling pathways. The group has identified a new mechanism of the DNA damage response that is mediated via an RNA transcript. Their results help to broaden the conceptual view on the DNA damage response and to link it more closely with RNA metabolism.

Dr. Kaspar Burger, junior research group leader at the Department of Biochemistry and Molecular Biology, was responsible for this study. The group has published the results of their investigations in the journal Genes & Development.

RNA Transcripts as Key Regulators

“In our study, we focused on so-called long non-coding RNA transcripts. Previous data suggest that some of these transcripts act as regulators of genome stability,” says Kaspar Burger, explaining the background to the work. The study focused on the nuclear enriched abundant transcript 1 — also known as NEAT1 — which is found in high concentrations in many tumor cells. NEAT1 is also known to react to DNA damage and to cellular stress. However, its exact role in the DNA damage response was previously unclear.

“Our hypothesis was that RNA metabolism involves NEAT1 in the DNA damage response in order to ensure the stability of the genome,” says Burger. To test this hypothesis, the research group experimentally investigated how NEAT1 reacts to serious damage to the genome — so-called DNA double-strand breaks — in human bone cancer cells. The result: “We were able to show that DNA double-strand breaks increase both the number of NEAT1 transcripts and the amount of N6-methyladenosine marks on NEAT1,” says the scientist.

RNA Modification and Cancer Connections

Methyladenosine marks on RNA transcripts are a topic that scientists have not been dealing with for very long. They fall into the area of epitranscriptomics — the field of biology that deals with the question of how RNA modifications are involved in the regulation of gene expression. Methyl groups play a key role in this. It is known, for example, that RNA modifications are often misplaced in cancer cells.

NEAT1’s Surprising Role in DNA Repair

The experiments conducted by Kaspar Burger and his team show that the frequent occurrence of DNA double-strand breaks causes excessive methylation of NEAT1, which leads to changes in the NEAT1 secondary structure. As a result, highly methylated NEAT1 accumulates at some of these lesions to drive the recognition of broken DNA. In turn, experimentally induced suppression of NEAT1 levels delayed the DNA damage response, resulting in increased amounts of DNA damage.

NEAT1 itself does not repair DNA damage. However, as the Würzburg team discovered, it enables the controlled release and activation of an RNA-binding DNA repair factor. In this way, the cell can recognize and repair DNA damage highly efficiently.

New Avenues for Cancer Therapy

According to the scientists, knowledge about the role of NEAT1 methylation in the recognition and repair of DNA damage could open up new therapeutic options for tumors with high NEAT1 expression. However, it must first be clarified whether these results, which were obtained in simple cell systems, can also be transferred to complex tumor models.

website: popularscientist.com

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