Category: 7. Science

Quantum computers, often hailed as the next frontier in computing, promise transformative capabilities far beyond the reach of classical machines.

From revolutionising drug discovery and optimisation problems to securing communication systems and accelerating clean energy research, the potential of quantum computing is staggering.

However, a persistent technical challenge has kept these machines from reaching their full potential: decoherence – the process where fragile quantum information degrades due to environmental interference.

Now, a groundbreaking development by scientists at the National Physical Laboratory (NPL), in partnership with Chalmers University of Technology and Royal Holloway University of London, may offer a vital key to solving this issue.

For the first time, researchers have successfully imaged individual defects in superconducting quantum circuits, a crucial step toward building more stable and reliable quantum systems.

Tiny flaws in superconducting quantum circuits

Superconducting circuits are one of the leading architectures for quantum processors, favoured by tech giants and academic researchers alike.

These quantum circuits rely on maintaining extremely low temperatures – near absolute zero – to function without electrical resistance. But hidden within these circuits are minute imperfections known as two-level system (TLS) defects.

Although scientists have suspected these defects of causing decoherence for over 50 years, it had never been possible to visually detect and study them inside an operational quantum device – until now.

A new instrument that sees the unseeable

To overcome this long-standing obstacle, NPL scientists have developed an innovative instrument capable of locating and analysing individual TLS defects within functioning quantum circuits.

The tool combines advanced scanning microscopy with cryogenic engineering, operating inside a completely light-tight chamber at temperatures just above absolute zero.

This ensures minimal external interference, allowing for the real-time observation of the defects’ effects on quantum coherence.

The imaging system produces visual patterns resembling ripples caused by raindrops, where each ring indicates the presence and influence of a defect.

By capturing this data, researchers can now quantify how each TLS defect interacts with the circuit and contributes to quantum noise and instability.

Paving the path to fault-tolerant quantum computing

This pioneering research marks a significant leap forward in quantum technology. For the first time, scientists can go beyond theoretical understanding and physically map the noise landscape of superconducting quantum circuits.

The implications are enormous. With this imaging capability, future work can focus on the chemical identification and elimination of these defects, potentially leading to quantum chips that are far more robust and scalable.

By addressing the root cause of decoherence, engineers can inch closer to creating fault-tolerant quantum computers, a milestone necessary for real-world applications in everything from machine learning to materials science.

Dr Riju Banerjee, a senior scientist at NPL and one of the lead authors of the paper, added: “For years, people have believed that TLS defects perturb quantum circuits.

“It is remarkable to finally be able to visualise the fluctuations and decoherence each TLS defect causes as it interacts with the circuit.

“We now have a new tool with which we can learn so much more about these nasty defects that plague quantum circuits. It can now help us find ways to get rid of these defects in the future.”

A new era for quantum circuits

This discovery isn’t just a technical triumph – it’s a paradigm shift.

As quantum computing edges closer to practical reality, innovations like this imaging breakthrough are critical to overcoming the engineering bottlenecks that have slowed progress for decades.

With the ability to see and eventually control TLS defects, scientists are now equipped to fine-tune quantum circuits at an unprecedented level.

This marks a decisive step toward a future where quantum computers no longer live solely in the lab, but in industries, research centres, and even healthcare systems worldwide.

In short, the quantum revolution just became a lot clearer, one defect at a time.

The research strengthens the potential of MCL-1 as a cancer drug target, which is currently the subject of clinical trials all over the world.

While drug compounds targeting MCL-1 that have been developed to date are considered extremely effective at combating cancer, they have unfortunately also caused significant side effects in early clinical trials, particularly in the heart.

Co-senior researcher Professor Andreas Strasser said the findings could help resolve the safety issues of drugs targeting MCL-1 that have hindered these promising treatments.

“If we can direct MCL-1 inhibitors preferentially to tumour cells and away from the cells of the heart and other healthy tissues, we may be able to selectively kill cancer cells while sparing healthy tissues,” Prof Strasser, a WEHI laboratory head, said.

The study also lays the groundwork for better combination therapies. By understanding the distinct pathways the protein influences, researchers can design smarter dosing strategies and pair MCL-1 inhibitors with other treatments to reduce toxicity.

“This work exemplifies the power of discovery science,” said co-senior researcher Professor Marco Herold, CEO of the Olivia Newton-John Cancer Research Institute (ONJCRI).

“The sophisticated preclinical models we developed allow us to interrogate the precise function of MCL-1, and to address fundamental biological questions that have direct relevance to human disease.”

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Slow-motion earthquakes, as you might guess from the name, involve the release of pent-up geological energy over the course of days or weeks rather than minutes – and scientists have now recorded some as they were happening.

These quakes, also known as slow slip earthquakes or just slow earthquakes, are typically too gentle to cause immediate danger. However, they can help scientists predict full-speed earthquakes or tsunamis, which can of course be far more dangerous.

A team led by researchers from the University of Texas Institute for Geophysics (UTIG) tracked two separate slow slip events (SSEs) in real time – one in 2015 and another in 2020.

Special borehole sensors were positioned deep underwater, close to the Nankai Trough subduction zone off the coast of Japan. There, the Philippine Sea plate is pushing under the Eurasian plate. The researchers describe the activity of the slow quakes as being like a tectonic shock absorber.

“It’s like a ripple moving across the plate interface,” says hydrogeophysicist Josh Edgington, from UTIG.

Related: Earthquakes Today Could Be Echoes of Powerful Quakes Centuries Ago

The measurements confirm what scientists had previously thought about these slow-motion earthquakes, which were only recently discovered: that they can be significant in releasing (or building) stress around a faultline.

This subduction zone is part of the Pacific Ring of Fire, an extensive collection of volcanoes and faults surrounding the Pacific Ocean. It’s responsible for many of the largest earthquakes and tsunamis on record.

And the findings here, about the shock absorber effect, will be crucial in understanding when and where future earthquakes could hit. Other faults lack this kind of tectonic protection, including Cascadia off the western coast of North America.

“This is a place that we know has hosted magnitude 9 earthquakes and can spawn deadly tsunamis,” says geophysicist Demian Saffer, from UTIG. “Are there creaks and groans that indicate the release of accumulated strain, or is the fault near the trench deadly silent?”

“Cascadia is a clear top-priority area for the kind of high-precision monitoring approach that we’ve demonstrated is so valuable at Nankai.”

It’s only possible to measure these SSEs because of advances in sensor technology, meaning shakes of much lower strength – sometimes only shifting the ground a few millimeters at a time – can be detected.

Through their analysis, the researchers were able to determine that slow earthquakes may be related to high geologic fluid pressures, and that the upper part of the fault can release pressure independently of the rest of it.

All of this helps to inform models predicting earthquakes and tsunamis – with the potential to save thousands of lives. The last major Nankai Trough quake happened in 1946, with the loss of tens of thousands of properties and causing more than 1,300 deaths.

Predicting earthquakes isn’t an exact science, with a host of variables involved, but it’s something we’re getting better at. With each study and technological upgrade, seismologists are improving their models, and adding in data from slow earthquake activity could help greatly.

“The patterns of strain accumulation and release along the offshore reaches of subduction megathrusts are particularly important toward understanding hazards associated with shallow coseismic slip and tsunamigenesis,” write the researchers in their published paper.

The research has been published in Science.

KNOXVILLE, TN, July 08, 2025 /24-7PressRelease/ — Researchers explore how 6-PPD quinone (6-PPDQ), an environmental contaminant derived from tire antioxidant N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD), affects the citric acid cycle in C. elegans at environmentally relevant concentrations. The research reveals significant reduction in the citric acid cycle intermediates and key enzyme gene expressions by 6-PPDQ exposure, highlighting the its potential exposure risk on citric acid cycle metabolism.

6-PPDQ, has emerged as an environmental concern due to its widespread detection and toxic effects. In a study published in Environmental Chemistry and Ecotoxicology, researchers from Southeast University in China explored the effects of 6-PPDQ on the citric acid cycle and underlying mechanism in C. elegans. The citric acid cycle, a crucial metabolic pathway occurring in the mitochondria, plays a central role in cellular metabolism by linking carbohydrate, fat, and amino acid metabolisms. It provides intermediates for the synthesis of amino acids, fatty acids, and glycogen, which are essential for sustaining life activities.

The study reveals how 6-PPDQ at environmentally relevant concentrations (0.1–10 μg/L) disrupted the citric acid cycle by reducing intermediate metabolites, including citric acid, α-ketoglutarate, succinate, fumarate, malate, and oxaloacetate. Additionally, the reduction of these intermediate metabolites was due to the inhibition of relevant key enzyme gene expressions. Exposure to 6-PPDQ suppressed genes encoding citrate synthase (cts-1), isocitrate dehydrogenase 2 (idh-2), and α-ketoglutarate dehydrogenase complex (dlst-1, dld-1). As explained by the researchers, “exposure to 6-PPDQ significantly impacts the citric acid cycle in C. elegans, which is crucial for understanding the potential risks of this contaminant to both environmental and human health.”

The researchers also observed that 6-PPDQ exposure decreased acetyl CoA and pyruvate contents, which are important for the control of citric acid cycle. Acetyl CoA generated from pyruvate is a key substrate for the cycle. The study found that among the genes encoding components of the pyruvate dehydrogenase complex, which controls acetyl CoA synthesis, only dlat-1 and dld-1 expressions were decreased by 6-PPDQ. The expressions of genes pyk-1 and pyk-2 associated with pyruvate generation were also reduced. RNA interference (RNAi) of these genes further exacerbated the cycle’s disruption, highlighting the crucial contribution of these alterations to 6-PPDQ-induced toxicity.

The study also demonstrated that the disruption in citric acid cycle and reduction in acetyl CoA and pyruvate contents contributed to mitochondrial dysfunction, as indicated by increased oxygen consumption rates and decreased ATP content in 6-PPDQ exposed nematodes. Furthermore, the researchers investigated the protective effects of sodium pyruvate treatment, finding that it could suppress toxic effects of 6-PPDQ. “Our results suggest that sodium pyruvate treatment may be a promising approach to against 6-PPDQ toxicity,” the researchers concluded.

This study provides valuable insights into the mechanisms by which 6-PPDQ disrupts metabolic process of citric acid cycle and highlights the potential risks of this contaminant. The findings underscore the importance of further research to fully understand the implications of 6-PPDQ exposure for both environmental and human health.

References

DOI

10.1016/j.enceco.2025.05.022

Original Source URL

https://doi.org/10.1016/j.enceco.2025.05.022

Journal

Environmental Chemistry and Ecotoxicology

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Scientists have identified a new type of protein in bacteria that could change our understanding of how these organisms interact with their environments.

A new study, published in Nature Communications, focuses on a protein called PopA, found in the bacterial predator Bdellovibrio bacteriovorus. The protein forms a unique fivefold structure, unlike the usual single or three-part structures seen in similar proteins.

Supported by the Wellcome Trust, BBSRC, ERC, MRC, and EPSRC an international research team, led by University of Birmingham scientists, used advanced imaging techniques to reveal that PopA has a bowl-like shape that can trap parts of the bacterial membrane inside it.

When PopA – an outer membrane protein (OMP) – is introduced into E. coli bacteria, it causes damage to their membranes. This suggests that PopA might play a role in how Bdellovibrio attacks and consumes other bacteria, whilst its ability to trap lipids (fats) suggests a new way bacteria might interact with their surroundings.

Structural analysis and AI-driven searches showed that PopA homologues – found across diverse bacterial species – form tetramers, hexamers, and even nonamers, all sharing the signature lipid‑trapping features. This suggests a widespread, previously unrecognised ‘superfamily’ of proteins.

Our discovery is significant because it challenges what scientists thought they knew about bacterial proteins. The unique structure and function of PopA suggest that bacteria have more complex ways of interacting with their environments than previously understood.

This could open new possibilities for understanding how bacteria function and interact with their environments – leading to new ways to target harmful bacteria with important implications for medicine and biotechnology.”

Professor Andrew Lovering, Lead Author, University of Birmingham

The study also identified another new family of proteins that form ring-like structures, further expanding our knowledge of bacterial proteins and suggesting that the mechanism to combine into rings might be more common than previously thought.

Using a combination of X‑ray crystallography, cryo-electron microscopy, and molecular dynamics, the team demonstrated that PopA, previously known as Bd0427, forms a central lipid-trapping cavity which is unusual given that the textbook model of membrane protein formation is centred on excluding lipids.

OMPs perform a wide range of functions including signalling, host cell adhesion, catalysis of crucial reactions, and transport of solutes/nutrients into and out of organelles within the human body. Understanding the natural variability of OMPs may have benefits ranging from antibacterial development to synthetic biology.

CAGLIARI, Sardinia, Italy, 8 July 2025 – In a comprehensive Genomic Press Interview published today in Genomic Psychiatry, Dr. Mirko Manchia opens up about his transformative journey from a small Sardinian city to becoming a leading voice in psychiatric pharmacogenomics, revealing how personal family experiences with mental illness sparked a lifelong quest to understand why psychiatric medications work brilliantly for some patients while failing others.

The Associate Professor of Psychiatry at the University of Cagliari has spent decades unraveling one of psychiatry’s most perplexing puzzles: why does lithium, psychiatry’s oldest mood stabilizer, transform some bipolar patients’ lives while leaving others searching for alternatives?

From Personal Experience to Scientific Breakthrough

Growing up in Sassari with no medical background in his family, Dr. Manchia’s path into neuroscience began with what he describes as “profound familial events” during adolescence that connected him deeply with mental health. This personal connection would later fuel groundbreaking research that culminated in a landmark publication in The Lancet, identifying genome-wide significant associations for lithium response in bipolar patients.

“I saw patients who had severe illness trajectories and who had remained well after several years of treatment with mood stabilizers, especially lithium, while others experienced continuous recurrences with dire consequences on their lives,” Dr. Manchia reflects in the interview. This observation became the cornerstone of his research philosophy.

Building International Collaborations

As a co-investigator and founding member of the International Consortium on Lithium Genetics (ConLiGen), Dr. Manchia has helped coordinate one of psychiatry’s most ambitious pharmacogenetic efforts. His meticulous phenotypic analysis of patient samples has been instrumental in identifying genetic markers that could predict treatment response before patients endure months of trial-and-error medication adjustments.

The impact extends far beyond lithium. With 230 peer-reviewed publications spanning molecular genetics and clinical psychiatry, Dr. Manchia has established himself as a bridge between laboratory discoveries and real-world patient care. His dual appointments at Cagliari and Dalhousie University in Canada reflect this international reach.

Precision Medicine Takes Center Stage

Currently serving as chair of the European College of Neuropsychopharmacology (ECNP) Bipolar Disorders Network, Dr. Manchia envisions a future where genetic testing becomes routine in psychiatric care. “We are at a point in psychiatric genetics where clinical utility is emerging,” he states. His current focus includes developing healthcare pathways that integrate pharmacogenetic testing for treatment-resistant depression and implementing AI-based predictive tools.

What makes this vision particularly compelling is its practical application. Rather than pursuing abstract genetic associations, Dr. Manchia’s work centers on questions every psychiatrist faces: Which patient will respond to this medication? How can we minimize the devastating trial-and-error period that often characterizes psychiatric treatment? Can we predict and prevent treatment resistance before it develops?

Addressing Research Disparities

The interview also highlights a critical challenge facing psychiatric research: chronic underfunding compared to other medical specialties. Dr. Manchia advocates for increased investment, noting that oncology’s transformation followed massive research funding. “This could also be achieved in psychiatry, but we need to act in a harmonized way, involving all stakeholders, particularly patient and family associations,” he emphasizes.

His approach to this challenge reflects the same patient-centered philosophy that drives his research. By involving patient organizations in research development and dissemination, Dr. Manchia believes the field can build the public support necessary for sustained funding increases.

Looking Ahead: Digital Integration and Beyond

The interview reveals Dr. Manchia’s vision for psychiatry’s future, where digital monitoring, psychometric assessments, genomics, and brain imaging converge into comprehensive predictive models. Within 20 years, he predicts, these integrated approaches will fundamentally transform how mental health is managed and delivered.

Yet despite these technological advances, Dr. Manchia’s motivations remain deeply human. When asked about his greatest passion beyond science, he mentions Roman history, classical music, and playing guitar – reminders that even cutting-edge researchers need balance and perspective.

Dr. Mirko Manchia’s Genomic Press interview is part of a larger series called Innovators & Ideas that highlights the people behind today’s most influential scientific breakthroughs. Each interview in the series offers a blend of cutting-edge research and personal reflections, providing readers with a comprehensive view of the scientists shaping the future. By combining a focus on professional achievements with personal insights, this interview style invites a richer narrative that both engages and educates readers. This format provides an ideal starting point for profiles that explore the scientist’s impact on the field, while also touching on broader human themes. More information on the research leaders and rising stars featured in our Innovators & Ideas – Genomic Press Interview series can be found in our publications website: https://genomicpress.kglmeridian.com/.

The Genomic Press Interview in Genomic Psychiatry titled “Mirko Manchia: Exploring the biological landscape of psychiatric disorders to innovate clinical management with precision medicine approaches,” is freely available via Open Access on 8 July 2025 in Genomic Psychiatry at the following hyperlink: https://doi.org/10.61373/gp025k.0071.

About Genomic Psychiatry: Genomic Psychiatry: Advancing Science from Genes to Society (ISSN: 2997-2388, online and 2997-254X, print) represents a paradigm shift in genetics journals by interweaving advances in genomics and genetics with progress in all other areas of contemporary psychiatry. Genomic Psychiatry publishes high-quality medical research articles of the highest quality from any area within the continuum that goes from genes and molecules to neuroscience, clinical psychiatry, and public health.

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Landmark research on MCL-1, a critical protein that is an attractive target for cancer drug development, helps explain why some promising cancer treatments are causing serious side effects, and offers a roadmap for designing safer, more targeted therapies. 

The WEHI-led discovery, published in Science, has uncovered a critical new role for MCL-1, revealing it not only prevents cell death but also provides cells with the energy they need to function. 

The findings reshape our understanding of how cells survive and thrive, with implications for both cancer treatment and developmental biology. 

At a glance 

• Landmark research shows the protein MCL-1, in addition to its well-understood role in preventing cell death, plays a second essential role in helping cells function by supporting energy production. 
• Drugs targeting MCL-1 have shown great promise as a future cancer treatment, but have been shown to harm healthy tissues, especially in organs with high energy demand like the heart and liver. 
• The findings published in Science pave the way for safer, more targeted cancer therapies targeting MCL-1. 

First author Dr. Kerstin Brinkmann said that while previous research in cell cultures had hinted at the metabolic role of MCL-1 in providing energy to cells, it was unclear whether this mattered in living organisms. 

This is the first time MCL-1’s metabolic function has been shown to be critical in a living organism.

It’s a fundamental shift in how we understand what this protein does. 

The findings open up a completely new way of thinking about the intersection between programmed cell death and metabolism – something that’s been speculated on for years but never been shown in a living organism until now.” 

Dr. Kerstin Brinkmann, WEHI researcher

Cancer drug target 

The research strengthens the potential of MCL-1 as a cancer drug target, which is currently the subject of clinical trials all over the world. 

While drug compounds targeting MCL-1 that have been developed to date are considered extremely effective at combating cancer, they have unfortunately also caused significant side effects in early clinical trials, particularly in the heart. 

Co-senior researcher Professor Andreas Strasser said the findings could help resolve the safety issues of drugs targeting MCL-1 that have hindered these promising treatments. 

“If we can direct MCL-1 inhibitors preferentially to tumour cells and away from the cells of the heart and other healthy tissues, we may be able to selectively kill cancer cells while sparing healthy tissues,” Prof Strasser, a WEHI laboratory head, said. 

The study also lays the groundwork for better combination therapies. By understanding the distinct pathways the protein influences, researchers can design smarter dosing strategies and pair MCL-1 inhibitors with other treatments to reduce toxicity. 

“This work exemplifies the power of discovery science,” said co-senior researcher Professor Marco Herold, CEO of the Olivia Newton-John Cancer Research Institute (ONJCRI). 

“The sophisticated preclinical models we developed allow us to interrogate the precise function of MCL-1, and to address fundamental biological questions that have direct relevance to human disease.” 

Protein link to rare, fatal diseases 

MCL-1’s role in energy production could help explain fatal metabolic diseases in infants, such as mitochondrial disorders. These rare conditions, often caused by mutations in genes that stop cells from generating enough energy, can be lethal in early life. 

The study suggests MCL-1 may play a previously unrecognised role in these diseases, offering a potential new target for future therapies. 

Another key outcome of the study is the creation of a system that allows researchers to compare the functions of pro-survival proteins like MCL-1, BCL-XL and BCL-2. 

These new tools will help identify which roles are shared and which are unique – knowledge that could inform future drug development across multiple targets. 

A collaborative discovery 

The project was made possible by WEHI’s collaborative research environment, bringing together experts in cancer biology, metabolism, developmental biology and gene editing. 

Co-senior authors Prof Herold (from the ONJCRI), Associate Professor Tim Thomas and Professor Anne Voss played key roles in the study. 

“This kind of discovery only happens when you have the right mix of people and expertise,” said Prof Strasser. 

“It’s a powerful example of how fundamental science drives future medical breakthroughs. 

“This came from a simple biological question – not a drug development project. It shows why we need to support curiosity-driven science. That’s where the big insights come from.”